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SYSTEMATIC REVIEW article

Front. Oncol., 30 January 2026

Sec. Cancer Epidemiology and Prevention

Volume 16 - 2026 | https://doi.org/10.3389/fonc.2026.1740352

This article is part of the Research TopicCancer Epidemiology and Etiology Evaluation in Latin American PopulationView all 8 articles

Research on potential biomarkers of prostate cancer in Latin America and the Caribbean: a scoping review

  • 1Grupo de Investigaciones Clínicas, Instituto Nacional de Cancerología, Bogotá, Colombia
  • 2Departamento de Patología, Instituto Nacional de Cancerología, Bogotá, Colombia
  • 3Grupo de Investigación en Biología del Cáncer, Instituto Nacional de Cancerología, Bogotá, Colombia
  • 4Grupo Vigilancia Epidemiológica del Cáncer, Instituto Nacional de Cancerología, Bogotá, Colombia
  • 5Instituto de Investigación, Fundación Universitaria de Ciencias de la Salud-FUCS, Bogotá, Colombia
  • 6Departamento de Urología, Instituto Nacional de Cancerología, Bogotá, Colombia
  • 7Facultad de Medicina, Universidad Nacional de Colombia, Bogotá, Colombia
  • 8Departamento de Química, Facultad de Ciencias, Universidad Nacional de Colombia, Bogotá, Colombia

Background: Latin America and the Caribbean (LAC) have higher prostate cancer (PCa) mortality rates than other regions, possibly due to disparities in detection and treatment, as well as differences in tumor biology and behavior. This scoping review aimed to identify studies conducted in LAC that evaluated potential biomarkers associated with PCa.

Methods: A search was conducted in PubMed, Scopus, Embase, LILACS, and Web of Science, including original studies conducted in LAC that evaluated the presence of potential biomarkers in relation to PCa. Due to the heterogeneity of the studies, a descriptive analysis of the data was performed.

Results: A total of 138 articles were included, evaluating 342 potential biomarkers across 17 countries/territories of LAC. Articles were classified into one or more of the following categories of potential biomarkers: risk of developing PCa (n=74), screening, early detection, and diagnosis (n=13), prognosis (n=48), treatment (n=10) and others (n=12). The countries with the most publications were Brazil, Mexico, and Chile.

Conclusion: Most studies analyzed the relationship between various potential biomarkers and the risk of developing PCa as well as its prognosis. The majority of studies came from continental countries with lower percentages of African ancestry and lower PCa mortality rates, highlighting the need to strengthen research in LAC while improving access to healthcare. Systematic review registration:

1 Introduction

Cancer is currently one of the main social, economic, and public‐health challenges (1). Globally, prostate cancer (PCa) was the second most prevalent cancer among men and ranked as the fifth leading cause of cancer‐related mortality in 2022 (1). PCa incidence varies widely between regions, with the highest rates reported in North America and Oceania, and the lowest in Africa and Asia (1). Regarding mortality, this pattern shifts markedly. In regions of Africa and parts of the Caribbean, mortality rates are high despite low incidence, in contrast to highly developed areas such as Northern Europe and North America, where, despite high incidence, mortality remains low (1).

Latin America and the Caribbean (LAC) is a region comprising 49 countries and territories (the term “territories” groups overseas and unincorporated areas) and can be subdivided into three subregions based on geographic location: Central America (8 countries), South America (12 countries and 1 territory), and the Caribbean (13 countries and 15 territories). In LAC the estimated PCa incidence and mortality rates are 58.0 and 13.9 per 100,000 men, respectively, compared with 73.5 and 8.3 in Northern America, 71.9 and 11.5 in Oceania, and 59.9 and 11.2 in Europe (2). This contrast with Asia, where incidence and mortality rates are 12.6 and 3.8, respectively (2). Within LAC, the highest PCa incidence and mortality rates were seen in the Caribbean, followed by South America, and, at the lowest level, Central America (Figure 1A) (2). The trend in PCa mortality between 1990 and 2020, based on Globocan data, for South America and Central America and the only two Caribbean countries with available data (Cuba and Puerto Rico), shows a striking increase in Cuba and a decrease in Puerto Rico, both Caribbean islands but with distinct geopolitical statuses, since Puerto Rico is an unincorporated territory of the United States, whereas Cuba is an independent state (Figure 1B) (2).

Figure 1
Three sections represent cancer incidence and mortality data in the Americas. Section A shows bar charts comparing incidence and mortality per 100,000 in the Caribbean, South America, and Central America. Section B presents a line graph illustrating cancer trends from 1990 to 2018 for Puerto Rico, South America, Central America, and Cuba. Section C comprises detailed bar charts showing cancer incidence and mortality rates for individual countries, alongside a table of ethnic composition percentages for each country.

Figure 1. Prostate cancer incidence and mortality in Latin America and the Carribean in 2022, in relation to ethic composition. (A) By subrgions. (B) Mortality trends from 1990 to 2020 in South America, Central America, Cuba, and Puerto Rico. (C) By contries/territories, specifying AFRICAN, EUROPEAN, AND Native American ethnic components. Blue Barsrepresents incidence and red bars represent mortality. NA, Not data available; ASR, Age-Standardized Rate. Modified from Globocan (3).

PCa incidence and mortality rates (1), and reported ethnic composition for each LAC country or overseas territory, are presented in descending order of mortality (326) (Figure 1C), where a potential association between higher mortality rates and a greater proportion of African ethnic ancestry is observed. Countries with the highest mortality were primarily Caribbean islands, except for Guadeloupe (a French overseas territory), which does not rank among them despite the fact that 85% of its population is of African descent. Interestingly, Martinique (also a French overseas territory) did not show particularly high mortality, although ethnicity data are not available for this territory. Furthermore, countries with the highest proportion of Native American ancestry, mostly located in Central America, tend to have a lower proportion of African ancestry and lower PCa mortality rates (Figure 1C).

The influence of ancestry on tumor biology and behavior suggests underlying differences in tumor profiles, especially in PCa. Multiple studies have reported a higher burden of PCa in men of African ancestry, linked to their West and West-Central African heritage from the transatlantic slave trade, which has been associated with earlier onset and more aggressive tumor behavior compared with men of other ancestries (27, 28). This burden is even greater in Black Caribbean populations and is also evident in the United Kingdom, where most Black men are of Afro-Caribbean or West African descent (29). These patterns likely reflect complex interactions between population-specific genetic ancestry and mixed heritage across regions, together with environmental factors, like the socioeconomic environment, that have been shown to modulate how genetic ancestry influences prostate cancer risk (28, 30). These complex interactions highlight the need for targeted strategies that extend beyond self-reported race and incorporate biomarkers, like West African ancestry–associated SNPs, which have been associated with improved prediction of biopsy positivity and clinically significant disease in African American men, highlighting the role of biomarkers in refining risk stratification and improving early detection in high-risk populations (31).

Traditionally, the term biomarker is defined as a characteristic that can be measured precisely and reproducibly, and that indicate normal or pathological biological processes, or responses to exposures or interventions (32, 33). However, due to the complexity of tumor biology, not all of these characteristics have undergone a formal validation process, and some remain at an exploratory stage. Therefore, in this review, the term potential biomarkers will be used to encompass all these findings, ranging from well-established biomarkers like PSA or PCA3 to emerging ones that are currently being studied, not only as susceptibility biomarkers but also in other areas like prognosis or treatment selection (34, 35).

LAC is characterized by high PCa mortality rates in certain areas and marked ancestral heterogeneity, with populations exhibiting varying proportions of Afro-Caribbean, Native American, and European ancestry shaped by historical processes such as colonization and the transatlantic slave trade. In this context and given the relevance of the molecular landscape for the management of this disease, this article aims to conduct a scoping review of studies on potential biomarkers related to PCa carried out in LAC countries/territories. This review will highlight the interests and advances in this field within the region, while also identifying the needs and knowledge gaps that must be addressed.

2 Materials and methods

This scoping review was conducted based on the PRISMA-Scr (Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews) guidelines (36).

2.1 Search strategy

A search was conducted up to 2025 April 23 in the Medline, Embase, Scopus, LILACS and Web of Science databases, without restrictions on language or publication date. The search included terms such as “prostatic neoplasms”, “biomarker”, “Latin America” and “Caribbean”; the full search strategy is detailed in Supplementary Table S1. Additionally, articles identified through manual searches and from the reference lists of retrieved studies were also included.

2.2 Inclusion and exclusion criteria

We included original studies assessing potential biomarkers in patients with a confirmed diagnosis of PCa at any stage, residing in LAC countries/territories. The following exclusion criteria were applied: a) studies that included patients residing outside LAC and did not report disaggregated results specifically for the LAC population, b) preliminary studies whose results were part of larger studies, and c) studies with discrepancies between the methodology and the results presented.

2.3 Study selection and data extraction

After removing duplicates, a screening based on title and abstract was conducted. Subsequently, a full text review was performed, and the studies were classified according to their primary biomarker category, following the definitions of BEST (Biomarkers, EndpointS, and other Tools) Resource (32). The categories were adapted, for illustrative purposes, as follows: 1) related to the risk of developing PCa, 2) screening, early detection, and diagnosis, 3) prognosis, 4) treatment, and 5) others. The treatment category includes associations related to medical products, like response, predictive or safety. The others category was used for articles/biomarkers that did not directly evaluate associations with any of the previous categories. In cases where articles addressed more than one focus, they were included in all relevant categories.

Discrepancies were resolved by consensus among the authors. Information from each article was extracted into tables, including country, year of publication, authors, number of patients, study type, potential biomarker, and the technique used for its evaluation, as well as the type of association, outcome, effect measure, and/or p-value. Statistical significance was defined according to the criteria used in each article. The full data were included in the Supplementary Tables, while the main article contains summarized versions of the tables showing the potential biomarkers, type of association with PCa, country, and reference. These were organized according to the functional groups of the evaluated biomarkers and countries.

3 Results

A total of 1979 articles were identified. After excluding duplicates and screening titles and abstracts, 270 articles underwent full-text review, and 138 of these met the inclusion criteria and were finally included. The detailed search and selection process is visually represented in the PRISMA flow diagram (Figure 2).

Figure 2
Flowchart depicting the process of study selection. Initially, 1,965 records were identified through database searching, and 14 through other sources. After removing duplicates, 1,126 records were screened by title and abstract, with 856 excluded. Full-text screening was applied to 270 articles, resulting in the exclusion of 132 articles for various reasons. Ultimately, 138 studies were included for descriptive analysis. The diagram follows a hierarchical structure with sections labeled: Identification, Screening, Eligibility, and Included.

Figure 2. PRISMA diagram summarizing the systematic search and final selection of articles.

These articles were conducted in 17 LAC countries/territories: 7 from the Caribbean, 7 from South America, and 3 from Central America. The number of articles and potential biomarkers studied, classified by category and country, are presented in Table 1. The articles were categorized as follows: related to the risk of developing PCa (n=74); screening, early detection, and diagnosis (n=13); prognosis (n=48); treatment (n=10); and others (n=12). A total of 19 articles were classified into more than one category. Similarly, 342 potential biomarkers were reported and classified as follows: 146 related to the risk of developing PCa; 20 to screening, early detection, and diagnosis; 147 associated with prognosis; 14 linked to treatment; and 59 to the “others” group. A total of 44 biomarkers were classified into more than one category.

Table 1
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Table 1. Articles and potential biomarkers associated with prostate cancer in Latin America and the Caribbean, by country and focus category.

The results are described below, grouped according to their category.

3.1 Potential biomarkers associated with risk of developing PCa

A total of 146 potential biomarkers associated with the risk of developing PCa were identified across 74 studies from 12 countries/territories (Table 2, Supplementary Table 2) (37110). These were mostly case–control studies evaluating DNA polymorphisms, including one ancestry analysis, as well as expression levels measured as RNA, serum levels of proteins and vitamins, and other potential biomarkers. Most of these were SNPs and were assessed in blood and prostate tissue. The countries/territories with the highest number of publications and potential biomarkers studied were Brazil, with 27 studies and 58 biomarkers analyzed; Mexico, with 12 studies and 14 biomarkers; and Jamaica, with 10 studies and 49 biomarkers.

Table 2
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Table 2. Potential biomarkers associated with risk of developing PCa in Latin America and the Caribbean.

The potential biomarkers were categorized into the following functional groups: immune regulation and inflammatory response (56), xenobiotic metabolism (14), gene expression regulation (13), cell adhesion and tissue remodeling (12), endobiotic metabolism (7), involved in prostate tissue physiology (7), related to sex steroid hormones (6), DNA replication and repair (3), apoptosis (4) and others (16). Biomarkers studied in more than one country included those related to the androgen receptor (AR), ribonuclease L (RNASEL), glutathione S-transferase enzymes T1, M1, and P1 (GSTM1, GSTT1, and GSTP1), cytochrome P450, 3-oxo-5α-steroid 4-dehydrogenase 2 (SRD5A2), vitamin D receptor (VDR), and the non-coding region at 8q24.21.

3.2 Potential biomarkers associated with PCa screening, early detection, and diagnosis

A total of 20 potential biomarkers with possible applications in the screening, early detection, and diagnosis of PCa were identified in 13 articles from four countries (Table 3, Supplementary Table 3) (111123). These biomarkers were mainly related or compared to PSA levels as early detection biomarkers, with the aim of increasing specificity relative to PSA and thereby help determine whether a biopsy was necessary. Detailed information available from the included articles for each of these biomarkers is provided in Supplementary Table 3. Study designs comprised case–control, cohort, and cross-sectional studies (Supplementary Table 3).

Table 3
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Table 3. Potential biomarkers associated with PCa screening, early detection, and diagnosis in Latin America and the Caribbean.

The potential biomarkers analyzed included DNA polymorphisms, gene expression levels quantified as mRNA and proteins, and metabolites, as well as methylation markers, microRNAs, and malignant primary circulating prostate cells. The analyses were based not only on blood and prostate tissue, but also on urinary sediment cells. The only related biomarkers studied in more than one country were those associated with the AR, as a protein in prostate tissue in Brazil, and as a CAG repeat length polymorphism in Mexico. The number of studies and potential biomarkers analyzed by country was as follows: Brazil, 4 studies and 12 biomarkers; Chile, 6 studies and 2 biomarkers; Mexico, 2 studies and 5 biomarkers; and Barbados, 1 study and 1 biomarker.

3.3 Potential biomarkers associated with PCa prognosis

A total of 48 articles (Table 4, Supplementary Table 4) (50, 58, 59, 61, 63, 64, 70, 71, 73, 74, 80, 86, 88, 109, 110, 113, 124155) evaluating 147 potential biomarkers related to PCa prognosis were identified across 11 countries/territories. The analyses included DNA polymorphisms, protein expression levels assessed by immunohistochemistry, genotypes determined by restriction enzymes, point mutations, immune cell infiltration, DNA damage response, gene methylation, and circulating tumor DNA concentrations. These biomarkers were assessed in blood or tumor tissue.

Table 4
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Table 4. Potential biomarkers associated with PCa prognosis in Latin America and the Caribbean.

The countries/territories with the highest number of publications and potential biomarkers evaluated were Brazil, with 23 studies and 78 biomarkers; Chile, with 6 studies and 18 biomarkers; Colombia, with 6 studies and 12 biomarkers; and Mexico, with 5 studies and 11 biomarkers. The biomarkers were categorized into functional groups: endobiotic metabolism (33), cell adhesion and tissue remodeling (19), DNA replication and repair (12), related to sex steroid hormones (11), immune regulation and inflammatory response (6), xenobiotic metabolism (5), involved in prostate tissue physiology (5), gene expression regulation (4), apoptosis (1) and others (39).

3.4 Potential biomarkers associated with PCa treatment

A total of 10 articles from 6 countries were identified, reporting on 14 potential biomarkers related to PCa treatment (Table 5, Supplementary Table 5) (156165). Seven of these studies had an experimental focus and evaluated the application of innovative therapies in the treatment of PCa. Although the search retrieved multicenter clinical trials that included LAC centers (166, 167), these were not incorporated as they did not focus on the region or present disaggregated results for their LAC population.

Table 5
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Table 5. Potential biomarkers associated with PCa treatment in Latin America and the Caribbean.

The distribution of studies and potential biomarkers analyzed by country was as follows: Brazil, 6 studies and 11 biomarkers; Mexico, 2 studies and 4 biomarkers; Chile, 1 study and 2 biomarkers; and Argentina, Colombia and Cuba, with 1 study and 1 biomarker each. The study by Pacheco-Orozco et al. (161) was assigned to more than one country, as it was a hypothetical cost‐analysis study that evaluated the utility of the androgen receptor splice variant 7 biomarker in Argentina, Colombia and Mexico.

3.5 Other potential biomarkers associated with PCa

In the others category, a total of 12 articles (138, 154, 155, 168176) were included, evaluating 59 potential biomarkers related to PCa (Supplementary Table 6); the majority were studies on the prevalence of germline and/or somatic mutations. The countries/territories with the highest number of publications and potential biomarkers evaluated were Brazil, with 8 studies and 53 biomarkers; Mexico, with 3 studies and 34 biomarkers; and Colombia, with 3 studies and 33 biomarkers. Among these, two multicenter studies (155, 174) stood out, evaluating the prevalence of genetic mutations in five and seven LAC countries, respectively.

4 Discussion

The populations of LAC have a genetic admixture of Indigenous, European, and African ancestry which, along with other factors, may influence the behavior of PCa. In this context, the aim of this study was to identify the available regional evidence in published studies on potential biomarkers associated with PCa. Across different focus categories and countries/territories, the most studied biomarkers were those related to AR, the genes GSTM1, GSTT1 and GSTP1, and vitamin D metabolism.

Regarding AR, 5 studies from Brazil, Mexico, and Ecuador evaluated the association between CAG repeat length in the AR gene and the risk of PCa, three of which reported an increased risk with ≤21 CAGs (49, 66) y <19 CAGs (67). This partially aligns with the meta-analysis by Qin et al. (177), which included 51 studies from America, Africa, Asia, and Europe, and found an association between ≤20 CAGs and a higher risk of PCa. However, the other two studies did not find significant associations (99, 109). Likewise, the relationship of this biomarker with prognosis and diagnosis was also investigated; in Martinique, an association between >20 CAGs and lower PCa aggressiveness was reported (74), and in Mexico, its ability to differentiate PCa from BPH was observed (112). Similarly, other related potential biomarkers, such as AR protein expression levels in prostate tissue, and AR variant 7, were evaluated as diagnostic biomarkers and predictors of treatment response, respectively (111, 161).

With respect to glutathione S-transferases, they catalyze the conjugation of reduced glutathione to diverse compounds, enabling the detoxification of xenobiotic-derived substances, yet they can also activate oxidative metabolites with carcinogenic potential. In this review, several studies evaluated the GSTM1 gene, and although most did not yield significant results, a study from Chile by Acevedo et al. (46) found that the Null genotype was associated with increased susceptibility to PCa. In Guadeloupe, two studies associated a higher risk with the presence of at least one functional allele of GSTT1 (47) and with having more than two copies of this same gene (48). The meta-analysis by Gong et al. al (178)., which included studies involving Caucasian, African, and Asian individuals, found that the Null genotypes of GSTM1 and GSTT1 were associated with a higher risk of PCa. While Malik et al. (179) reported that the genotype Null of GSTM1 was associated with increased risk in Asian and European populations, and genotype Null of GSTT1 only in African populations. This may indicate differential behavior of these genes in PCa susceptibility, linked to the continental ancestry of each population.

The relationship between glutathione S-transferase genes and PCa prognosis was also studied, with the study by Acevedo et al. (135) in Chile standing out, which reported higher overall mortality in patients with the Null genotype of GSTM1, an association not previously described in other studies. Similarly, the study by Cotignola et al. (136) in Argentina found an association between a polymorphism of GSTP1 and a lower biochemical recurrence-free survival. Although no significant association was found with polymorphisms of GSTT1 and GSTM1, lower biochemical recurrence-free survival and higher recurrence were observed in patients when combining the genotypes of all three GST genes in multivariable models. This contrasts with the study by Nock et al. (180) in the United States, which found no differences in biochemical recurrence related to GSTP1 gene polymorphisms in African American subjects, but did report a significant association with the Null genotype of GSTT1. These findings could also suggest differences in PCa prognosis based on the ancestry of the respective populations.

As for vitamin D metabolism, several potential biomarkers related to the VDR, such as the rs2238135 (57) polymorphism and the presence of more than 20 adenine repeats in the 3’ untranslated region of the gene, were associated with a higher risk of PCa (74); the latter was also linked to greater aggressiveness (74). These findings are consistent with studies conducted in populations from the United States (181, 182). Likewise, high serum levels of 25-hydroxyvitamin D were associated with a higher risk of PCa in Jamaica (76), which aligns with the meta-analysis by Xu et al. (183), showing a similar association in studies from Europe and the United States. This could be explained by the fact that levels of calcidiol, an intermediate metabolite generated in the liver from calcifediol, have been correlated with high levels of insulin-like growth factor 1 (184), which activates the mitogen-activated protein kinase and phosphoinositide 3-kinase pathways, and promotes cell proliferation in PCa (183, 185).

In relation to the potential biomarkers associated with PCa screening, early detection, and diagnosis, these biomarkers were primarily evaluated in relation to PSA levels ≥ 4.0 ng/mL as early detection biomarkers. This is largely due to their high sensitivity (0.90) but low specificity (0.20), which leads to a substantial number of unnecessary biopsies, as reported in reviews included in clinical practice guidelines. The primary application evaluated for these biomarkers would be to increase the specificity of PSA and thereby reduce unnecessary biopsies (186188). Detailed information from the included articles regarding each of these biomarkers in relation to PSA is provided in Supplementary Table 3. Among the biomarkers included in this study, PCA3 is the only one currently addressed in clinical practice guidelines at the level of early detection; however, its usefulness in guiding biopsy decisions remains uncertain, and the supporting evidence is considered weak (186). This underscores the importance of conducting further studies to determine whether PCA3 has clinical utility in LAC.

Regarding the articles associated with treatment, there was a lack of randomized clinical trials in the final selection of studies. Although some identified studies included centers in LAC, they were excluded because they did not report results disaggregated for the LAC population (166, 167). This is particularly concerning in light of evidence showing low enrollment of individuals from minority groups in clinical trials and the resulting lack of population-specific data (189). On the other hand, although a hypothetical cost-analysis study suggested a potential cost-saving role for androgen receptor splice variant 7, direct clinical evidence in LAC is still required, as its use is not routinely recommended in clinical practice guidelines, even though some evidence suggests its utility (161, 186). Lastly, it is worth highlighting the development of trials based on innovative therapies developed within the region, which are on par with those conducted in high-income countries, such as dendritic cell-based vaccines used as neoadjuvant treatment, demonstrating the region’s potential to develop therapies tailored to its population (190, 191).

Overall, most of the studies identified were conducted individually in continental countries such as Brazil, Chile, Argentina, México, Ecuador and Colombia, which have a lower proportion of African ancestry compared to island nations like Haiti or The Bahamas (Figure 1). This may be explained by the lower investment in research in these insular countries/territories, with some exceptions such as Puerto Rico (192). This highlights a significant knowledge gap regarding the genetic profiles and specific characteristics of these populations, which could be linked to their higher PCa mortality rates and represent potential areas for the implementation of preventive and/or therapeutic measures. Future efforts should prioritize multicentric and collaborative studies, as well as the establishment and maintenance of shared biobanks that integrate biological, molecular, and clinical data, thereby strengthening PCa research capacity in LAC. However, while strengthening research on biomarkers is essential, these discoveries can only translate into meaningful clinical benefit if accompanied by improvements in healthcare coverage that facilitate timely diagnosis, treatment, and follow-up for the broader population.

Among the limitations of this study, the most notable is the inability to perform a meta-analysis due to the great variability of the studies found. Furthermore, well-established biomarkers may be underrepresented in the literature reviewed because they were not the main focus of current studies in the region; an example of this is the current use of commercial panels in clinical practice in LAC countries, yet no studies evaluating them were identified. Consequently, the findings do not reflect the current utilization of biomarkers and should not be used to compare patterns of use across regions; however, they highlight prevailing research trends in biomarker investigation in the region. In addition to the disparity between the countries of origin of the articles, most commonly from Brazil, Mexico and Chile, it was observed that the studies did not always include a sample representative of the ethnic composition of their country. An example is the study by Nóbrega et al. (128) in Brazil, whose sample had 85.6% European ancestry and 14.4% African ancestry, which contrasts with the values reported by de Souza et al. (3), which reported weighted average ancestry proportions of 68.1%, 19.6%, and 11.6%, for European, African, and Native American populations, respectively. Furthermore, many studies did not include an ancestry analysis of the study population and instead limited themselves to describing ethnic origin. Future studies should ensure the inclusion of representative populations and incorporate ancestry analysis to enhance the validity and regional relevance of their findings.

5 Conclusions

The majority of studies included in this review evaluated various types of potential biomarkers in relation to PCa risk and prognosis. The most commonly studied biomarkers were those associated with AR, glutathione S-transferase enzymes, and vitamin D metabolism. Compared to studies from other regions, some of these biomarkers showed similar expression patterns, while others differed importantly, likely reflecting genetic differences associated with continental ancestry across populations. Likewise, it was noted that most studies were conducted in continental countries of LAC with a lower proportion of African ancestry, whereas island countries/territories with higher African ancestry and higher PCa mortality rates were underrepresented. Future research in the region should address these geographic gaps and prioritize collaborative studies that provide a more comprehensive understanding of the landscape of PCa in LAC. These developments, in conjunction with appropriate improvements in access to healthcare, could facilitate the development of targeted strategies for prevention, diagnosis, and treatment for the LAC population.

Data availability statement

The original contributions presented in the study are included in the article/Supplementary Material. Further inquiries can be directed to the corresponding author.

Author contributions

NP: Conceptualization, Data curation, Investigation, Writing – original draft, Writing – review & editing, Methodology. DM-G: Conceptualization, Data curation, Investigation, Methodology, Writing – original draft, Writing – review & editing. SY: Conceptualization, Data curation, Investigation, Methodology, Writing – original draft, Writing – review & editing. CC: Conceptualization, Investigation, Supervision, Writing – original draft, Writing – review & editing. RP-M: Conceptualization, Supervision, Writing – original draft, Writing – review & editing. RV: Conceptualization, Supervision, Writing – original draft, Writing – review & editing. MS: Conceptualization, Data curation, Investigation, Methodology, Supervision, Writing – original draft, Writing – review & editing.

Funding

The author(s) declared that financial support was received for this work and/or its publication. This study was supported and funded by the Instituto Nacional de Cancerología (INC) of Colombia.

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Supplementary material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fonc.2026.1740352/full#supplementary-material

References

1. Bray F, Laversanne M, Sung H, Ferlay J, Siegel RL, Soerjomataram I, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA A Cancer J Clin. (2024) 74:229–63. doi: 10.3322/caac.21834

PubMed Abstract | Crossref Full Text | Google Scholar

2. Ferlay J, Ervik M, Lam F, Laversanne M, Colombet M, Mery L, et al. Global cancer observatory. In: Global cancer observatory: cancer today (version 11). Lyon, France: International Agency for Research on Cancer (2024). Available online at: https://gco.iarc.who.int/today/ (Accessed April 1, 2025).

Google Scholar

3. Souza AM, de, Resende SS, Sousa TN, and de, Brito CFA. A systematic scoping review of the genetic ancestry of the Brazilian population. Genet Mol Biol. (2019) 42:495–508. doi: 10.1590/1678-4685-GMB-2018-0076

PubMed Abstract | Crossref Full Text | Google Scholar

4. Mathias RA, Taub MA, Gignoux CR, Fu W, Musharoff S, O’Connor TD, et al. A continuum of admixture in the Western Hemisphere revealed by the African Diaspora genome. Nat Commun. (2016) 7:12522. doi: 10.1038/ncomms12522

PubMed Abstract | Crossref Full Text | Google Scholar

5. Benn-Torres J, Bonilla C, Robbins CM, Waterman L, Moses TY, Hernandez W, et al. Admixture and population stratification in african caribbean populations. Ann Hum Genet. (2008) 72:90–8. doi: 10.1111/j.1469-1809.2007.00398.x

PubMed Abstract | Crossref Full Text | Google Scholar

6. Martínez-Cortés G, Salazar-Flores J, Gabriela Fernández-Rodríguez L, Rubi-Castellanos R, Rodríguez-Loya C, Velarde-Félix JS, et al. Admixture and population structure in Mexican-Mestizos based on paternal lineages. J Hum Genet. (2012) 57:568–74. doi: 10.1038/jhg.2012.67

PubMed Abstract | Crossref Full Text | Google Scholar

7. Murray T, Beaty TH, Mathias RA, Rafaels N, Grant AV, Faruque MU, et al. African and non-African admixture components in African Americans and an African Caribbean population. Genet Epidemiol. (2010) 34:561–8. doi: 10.1002/gepi.20512

PubMed Abstract | Crossref Full Text | Google Scholar

8. Torres JB, Stone AC, and Kittles R. An anthropological genetic perspective on Creolization in the Anglophone Caribbean. Am J Phys Anthropol. (2013) 151:135–43. doi: 10.1002/ajpa.22261

PubMed Abstract | Crossref Full Text | Google Scholar

9. Campos-Sánchez R, Raventós H, and Barrantes R. Ancestry informative markers clarify the regional admixture variation in the Costa Rican population. hub. (2013) 85:721–40. doi: 10.1353/hub.2013.a541098

PubMed Abstract | Crossref Full Text | Google Scholar

10. Marcheco-Teruel B, Parra EJ, Fuentes-Smith E, Salas A, Buttenschøn HN, Demontis D, et al. Cuba: exploring the history of admixture and the genetic basis of pigmentation using autosomal and uniparental markers. PloS Genet. (2014) 10:e1004488. doi: 10.1371/journal.pgen.1004488

PubMed Abstract | Crossref Full Text | Google Scholar

11. Miljkovic-Gacic I, Ferrell RE, Patrick AL, Kammerer CM, and Bunker CH. Estimates of african, european and native american ancestry in afro-caribbean men on the island of tobago. Hum Heredity. (2006) 60:129–33. doi: 10.1159/000089553

PubMed Abstract | Crossref Full Text | Google Scholar

12. Nagar SD, Conley AB, Chande AT, Rishishwar L, Sharma S, Mariño-Ramírez L, et al. Genetic ancestry and ethnic identity in Ecuador. HGG Adv. (2021) 2:100050. doi: 10.1016/j.xhgg.2021.100050

PubMed Abstract | Crossref Full Text | Google Scholar

13. Castro Pérez E, Sanchez de Chial M, Chen O, Ramos C, and Mayorga B. Estructura Genética de la Población Panameñagenes ancestrales e implicaciones Biométricas. Zenodo. (2025) 23. doi: 10.5281/ZENODO.15121745

Crossref Full Text | Google Scholar

14. Eyheramendy S, Martinez FI, Manevy F, Vial C, and Repetto GM. Genetic structure characterization of Chileans reflects historical immigration patterns. Nat Commun. (2015) 6:6472. doi: 10.1038/ncomms7472

PubMed Abstract | Crossref Full Text | Google Scholar

15. Homburger JR, Moreno-Estrada A, Gignoux CR, Nelson D, Sanchez E, Ortiz-Tello P, et al. Genomic insights into the ancestry and demographic history of south america. PloS Genet. (2015) 11:e1005602. doi: 10.1371/journal.pgen.1005602

PubMed Abstract | Crossref Full Text | Google Scholar

16. Wang S, Ray N, Rojas W, Parra MV, Bedoya G, Gallo C, et al. Geographic patterns of genome admixture in latin american mestizos. PloS Genet. (2008) 4:e1000037. doi: 10.1371/journal.pgen.1000037

PubMed Abstract | Crossref Full Text | Google Scholar

17. Via M, Gignoux CR, Roth LA, Fejerman L, Galanter J, Choudhry S, et al. History shaped the geographic distribution of genomic admixture on the island of Puerto Rico. PloS One. (2011) 6:e16513. doi: 10.1371/journal.pone.0016513

PubMed Abstract | Crossref Full Text | Google Scholar

18. Moura RR, Coelho AVC, Balbino V de Q, Crovella S, and Brandão LAC. Meta-analysis of Brazilian genetic admixture and comparison with other Latin America countries. Am J Hum Biol. (2015) 27:674–80. doi: 10.1002/ajhb.22714

PubMed Abstract | Crossref Full Text | Google Scholar

19. Sans M, Merriwether DA, Hidalgo PC, Bentancor N, Weimer TA, Franco MHLP, et al. Population structure and admixture in Cerro Largo, Uruguay, based on blood markers and mitochondrial DNA polymorphisms. Am J Hum Biol. (2006) 18:513–24. doi: 10.1002/ajhb.20520

PubMed Abstract | Crossref Full Text | Google Scholar

20. Horimoto A, Cai J, Thornton T, and Franceschini N. POS-424 genetic admixture of U.S. Hispanics from central america. Kidney Int Rep. (2021) 6:S183. doi: 10.1016/j.ekir.2021.03.447

Crossref Full Text | Google Scholar

21. Nuñez C, Baeta M, Sosa C, Casalod Y, Ge J, Budowle B, et al. Reconstructing the population history of Nicaragua by means of mtDNA, Y-chromosome STRs, and autosomal STR markers. Am J Phys Anthropol. (2010) 143:591–600. doi: 10.1002/ajpa.21355

PubMed Abstract | Crossref Full Text | Google Scholar

22. Simão F, Ribeiro J, Vullo C, Catelli L, Gomes V, Xavier C, et al. The ancestry of eastern Paraguay: A typical south american profile with a unique pattern of admixture. Genes (Basel). (2021) 12:1788. doi: 10.3390/genes12111788

PubMed Abstract | Crossref Full Text | Google Scholar

23. Taboada-Echalar P, Álvarez-Iglesias V, Heinz T, Vidal-Bralo L, Gómez-Carballa A, Catelli L, et al. The genetic legacy of the pre-colonial period in contemporary Bolivians. PloS One. (2013) 8:e58980. doi: 10.1371/journal.pone.0058980

PubMed Abstract | Crossref Full Text | Google Scholar

24. Simms TM, Rodriguez CE, Rodriguez R, and Herrera RJ. The genetic structure of populations from Haiti and Jamaica reflect divergent demographic histories. Am J Phys Anthropol. (2010) 142:49–66. doi: 10.1002/ajpa.21194

PubMed Abstract | Crossref Full Text | Google Scholar

25. Chande AT, Nagar SD, Rishishwar L, Mariño-Ramírez L, Medina-Rivas MA, Valderrama-Aguirre AE, et al. The impact of ethnicity and genetic ancestry on disease prevalence and risk in Colombia. Front Genet. (2021) 12:690366. doi: 10.3389/fgene.2021.690366

PubMed Abstract | Crossref Full Text | Google Scholar

26. Mendisco F, Pemonge M-H, Romon T, Lafleur G, Richard G, Courtaud P, et al. Tracing the genetic legacy in the French Caribbean islands: A study of mitochondrial and Y-chromosome lineages in the Guadeloupe archipelago. Am J Phys Anthropology. (2019) 170:507–18. doi: 10.1002/ajpa.23931

PubMed Abstract | Crossref Full Text | Google Scholar

27. Rebbeck TR, Devesa SS, Chang B-L, Bunker CH, Cheng I, Cooney K, et al. Global patterns of prostate cancer incidence, aggressiveness, and mortality in men of african descent. Prostate Cancer. (2013) 2013:1–12. doi: 10.1155/2013/560857

PubMed Abstract | Crossref Full Text | Google Scholar

28. McHugh J, Saunders EJ, Dadaev T, McGrowder E, Bancroft E, Kote-Jarai Z, et al. Prostate cancer risk in men of differing genetic ancestry and approaches to disease screening and management in these groups. Br J Cancer. (2022) 126:1366–73. doi: 10.1038/s41416-021-01669-3

PubMed Abstract | Crossref Full Text | Google Scholar

29. Odedina FT, Akinremi TO, Chinegwundoh F, Roberts R, Yu D, Reams RR, et al. Prostate cancer disparities in Black men of African descent: a comparative literature review of prostate cancer burden among Black men in the United States, Caribbean, United Kingdom, and West Africa. Infect Agent Cancer. (2009) 4 Suppl 1:S2. doi: 10.1186/1750-9378-4-S1-S2

PubMed Abstract | Crossref Full Text | Google Scholar

30. Pichardo CM, Ezeani A, Acevedo AM, Agurs-Collins T, Bailey-Whyte M, Dorsey TH, et al. West african genetic ancestry, neighborhood deprivation, and prostate cancer. JAMA Netw Open. (2024) 7:e2433546. doi: 10.1001/jamanetworkopen.2024.33546

PubMed Abstract | Crossref Full Text | Google Scholar

31. Gu J, Chery L, González GMN, Huff C, Strom S, Jones JA, et al. A west African ancestry-associated SNP on 8q24 predicts a positive biopsy in African American men with suspected prostate cancer following PSA screening. Prostate. (2024) 84:694–705. doi: 10.1002/pros.24686

PubMed Abstract | Crossref Full Text | Google Scholar

32. FDA-NIH Biomarker Working Group. BEST (Biomarkers, EndpointS, and other Tools) Resource. Silver Spring (MD: Food and Drug Administration (US (2016). Available online at: http://www.ncbi.nlm.nih.gov/books/NBK326791/ (Accessed May 27, 2025).

Google Scholar

33. Shah A, Grimberg DC, and Inman BA. Classification of molecular biomarkers. Société Internationale d’Urologie J. (2020) 1:8–15. doi: 10.48083/AKUI6936

Crossref Full Text | Google Scholar

34. Wilson TK and Zishiri OT. Prostate cancer: A review of genetics, current biomarkers and personalised treatments. Cancer Rep (Hoboken). (2024) 7:e70016. doi: 10.1002/cnr2.70016

PubMed Abstract | Crossref Full Text | Google Scholar

35. Chen J-Y, Wang P-Y, Liu M-Z, Lyu F, Ma M-W, Ren X-Y, et al. Biomarkers for prostate cancer: from diagnosis to treatment. Diagnostics. (2023) 13:3350. doi: 10.3390/diagnostics13213350

PubMed Abstract | Crossref Full Text | Google Scholar

36. Tricco AC, Lillie E, Zarin W, O’Brien KK, Colquhoun H, Levac D, et al. PRISMA extension for scoping reviews (PRISMA-scR): checklist and explanation. Ann Intern Med. (2018) 169:467–73. doi: 10.7326/M18-0850

PubMed Abstract | Crossref Full Text | Google Scholar

37. Kidd LR, Jones DZ, Rogers EN, Kidd NC, Beache S, Rudd JE, et al. Chemokine Ligand 5 (CCL5) and chemokine receptor (CCR5) genetic variants and prostate cancer risk among men of African Descent:a case-control study. Hered Cancer Clin Pract. (2012) 10:16. doi: 10.1186/1897-4287-10-16

PubMed Abstract | Crossref Full Text | Google Scholar

38. Dubey B, Jackson MD, Zeigler-Johnson C, Devarajan K, Flores-Obando RE, McFarlane-Anderson N, et al. Inflammation polymorphisms and prostate cancer risk in Jamaican men: Role of obesity/body size. Gene. (2017) 636:96–102. doi: 10.1016/j.gene.2017.09.016

PubMed Abstract | Crossref Full Text | Google Scholar

39. Dubey B, Jackson M, Zeigler-Johnson C, Devarajan K, Flores-Obando RE, McFarlane-Anderson N, et al. Interactive effect of TLR SNPs and exposure to sexually transmitted infections on prostate cancer risk in Jamaican men. Prostate. (2020) 80:1365–72. doi: 10.1002/pros.24067

PubMed Abstract | Crossref Full Text | Google Scholar

40. Jones DZ, Ragin C, Kidd NC, Flores-Obando RE, Jackson M, McFarlane-Anderson N, et al. The impact of genetic variants in inflammatory-related genes on prostate cancer risk among men of African Descent: a case control study. Hered Cancer Clin Pract. (2013) 11:19. doi: 10.1186/1897-4287-11-19

PubMed Abstract | Crossref Full Text | Google Scholar

41. Zambra FMB, Biolchi V, De Cerqueira CCS, Brum IS, Castelli EC, and Chies JAB. Immunogenetics of prostate cancer and benign hyperplasia – the potential use of an HLA-G variant as a tag SNP for prostate cancer risk. HLA. (2016) 87:79–88. doi: 10.1111/tan.12741

PubMed Abstract | Crossref Full Text | Google Scholar

42. Da Silva Lawisch GK, Biolchi V, Kaufmann G, Nicolai G, Capitaneo E, Rosembach TR, et al. The role of FASL, BCL-2 and BAX polymorphisms in Brazilian patients with prostate cancer and benign prostatic hyperplasia. Mol Biol Rep. (2022) 49:9445–51. doi: 10.1007/s11033-022-07805-3

PubMed Abstract | Crossref Full Text | Google Scholar

43. Henning JD, Bunker CH, Shea P, Ferrell RE, Patrick AL, and Jenkins FJ. Abstract 5726: Association between human herpesvirus 8 infection, inflammation and a polymorphism in the IL-6 signaling receptor in increased prostate cancer risk among men of African descent. Cancer Res. (2010) 70:5726–6. doi: 10.1158/1538-7445.AM10-5726

Crossref Full Text | Google Scholar

44. De Lima Junior MM, Reis LO, Guilhen ACT, Granja F, De Lima Oliveira MN, Ferreira U, et al. N-acetyltransferase-2 gene polymorphisms and prostate cancer susceptibility in Latin American patients. Med Oncol. (2012) 29:2889–94. doi: 10.1007/s12032-012-0157-4

PubMed Abstract | Crossref Full Text | Google Scholar

45. Sá RAD, Moreira ADS, Cabello PH, Ornellas AA, Costa EB, Matos CDS, et al. Human glutathione S-transferase polymorphisms associated with prostate cancer in the Brazilian population. Int Braz J urol. (2014) 40:463–73. doi: 10.1590/S1677-5538.IBJU.2014.04.04

PubMed Abstract | Crossref Full Text | Google Scholar

46. Acevedo C, Opazo JL, Huidobro C, Cabezas J, Iturrieta J, and Quiñones Sepúlveda L. Positive correlation between single or combined genotypes of CYP1A1 and GSTM1 in relation to prostate cancer in Chilean people. Prostate. (2003) 57:111–7. doi: 10.1002/pros.10274

PubMed Abstract | Crossref Full Text | Google Scholar

47. Mallick S, Romana M, Blanchet P, and Multigner L. GSTM1 and GSTT1 polymorphisms and the risk of prostate cancer in a caribbean population of african descent. Urology. (2007) 69:1165–9. doi: 10.1016/j.urology.2007.02.039

PubMed Abstract | Crossref Full Text | Google Scholar

48. Emeville E, Broquère C, Brureau L, Ferdinand S, Blanchet P, Multigner L, et al. Copy number variation of GSTT1 and GSTM1 and the risk of prostate cancer in a caribbean population of african descent. PloS One. (2014) 9:e107275. doi: 10.1371/journal.pone.0107275

PubMed Abstract | Crossref Full Text | Google Scholar

49. Kuasne H, Rodrigues IS, Fuganti PE, Losi-Guembarovski R, Ito K, Kishima MO, et al. Polymorphisms in the AR and PSA genes as markers of susceptibility and aggressiveness in prostate cancer. Cancer Invest. (2010) 28:917–24. doi: 10.3109/07357907.2010.483509

PubMed Abstract | Crossref Full Text | Google Scholar

50. Correa LL, Vieira Neto L, Lima GAB, Gabrich R, Miranda LCDD, and Gadelha MR. Insulin-like growth factor (IgF)-I, IgF binding protein-3, and prostate cancer: correlation with gleason score. Int Braz J Urol febrero. (2015) 41:110–5. doi: 10.1590/S1677-5538.IBJU.2015.01.15

PubMed Abstract | Crossref Full Text | Google Scholar

51. De Souza MR, De Souza MF, De Nóbrega M, Cilião HL, Dos Reis MB, Fuganti PE, et al. Polymorphic variants of the CASP3, CASP9, BCL-2 and NKX3–1 genes as candidate markers for prostate cancer susceptibility and poor prognosis. Mol Biol Rep. (2022) 49:9079–87. doi: 10.1007/s11033-022-07654-0

PubMed Abstract | Crossref Full Text | Google Scholar

52. Meola J, Goulart LR, Oliveira JDD, Neves AF, Oliveira WP, Saraiva ACM, et al. Differential expression of the KLK2 and KLK3 genes in peripheral blood and tissues of patients with prostate cancer. Genet Mol Biol. (2006) 29:193–9. doi: 10.1590/S1415-47572006000200001

Crossref Full Text | Google Scholar

53. Alonso V, Neves AF, Marangoni K, de Faria PC, Batista C, Freschi ER, et al. Gene expression profile of prostate cancer patients by chemiluminescent analysis. Analytical Lett. (2009) 42:166–77. doi: 10.1080/00032710802568655

Crossref Full Text | Google Scholar

54. Trujillo-Cáceres SJ, Torres-Sánchez L, Burguete-García AI, Orbe Orihuela YC, Vázquez-Salas RA, Álvarez-Topete E, et al. Contribution of MSMB promoter region gene polymorphism to early-onset prostate cancer risk in Mexican males. Oncotarget. (2019) 10:738–48. doi: 10.18632/oncotarget.26592

PubMed Abstract | Crossref Full Text | Google Scholar

55. Kuasne H, Rodrigues IS, Losi-Guembarovski R, Reis MB, Fuganti PE, Gregório EP, et al. Base excision repair genes XRCC1 and APEX1 and the risk for prostate cancer. Mol Biol Rep. (2011) 38:1585–91. doi: 10.1007/s11033-010-0267-z

PubMed Abstract | Crossref Full Text | Google Scholar

56. Cypriano AS, Alves G, Ornellas AA, Scheinkman J, Almeida R, Scherrer L, et al. RAD51, and APEX1 DNA repair genotypes and prostate cancer risk in the male population of Rio de Janeiro, Brazil. Genet Mol Biol. (2017) 40:751–8. doi: 10.1590/1678-4685-gmb-2017-0039

PubMed Abstract | Crossref Full Text | Google Scholar

57. Martínez-Nava GA, Gómez R, Burguete-García AI, Vázquez-Salas RA, Ventura-Bahena A, and Torres-Sánchez L. BRCA1 and VDR gene polymorphisms are associated with prostate cancer risk in Mexican men. Mol Carcinogenesis. (2020) 59:629–39. doi: 10.1002/mc.23187

PubMed Abstract | Crossref Full Text | Google Scholar

58. Ortiz-Sánchez C, Encarnación-Medina J, Park JY, Moreno N, Ruiz-Deya G, and Matta J. Reduced DNA repair capacity in prostate cancer patients: A phenotypic approach using the cometChip. Cancers (Basel). (2022) 14:3117. doi: 10.3390/cancers14133117

PubMed Abstract | Crossref Full Text | Google Scholar

59. Matta J, Ortiz-Sánchez C, Encarnación-Medina J, Torres-Caraballo S, Oliveras J, Park J, et al. DNA repair capacity and clinicopathological characteristics in puerto rican hispanic/latino patients with metastatic castration-resistant prostate cancer. Cancers. (2025) 17:279. doi: 10.3390/cancers17020279

PubMed Abstract | Crossref Full Text | Google Scholar

60. El-Chaer WK, Tonet-Furioso AC, Morais Junior GS, Souza VC, Avelar GG, Henriques AD, et al. Serum levels of matrix metalloproteinase-1 in Brazilian patients with benign prostatic hyperplasia or prostate cancer. Curr Gerontology Geriatrics Res. (2020) 2020:1–7. doi: 10.1155/2020/6012102

PubMed Abstract | Crossref Full Text | Google Scholar

61. dos Reis ST, Pontes J, Villanova FE, Borra PM de A, Antunes AA, Dall’oglio MF, et al. Genetic polymorphisms of matrix metalloproteinases: susceptibility and prognostic implications for prostate cancer. J Urol. (2009) 181:2320–5. doi: 10.1016/j.juro.2009.01.012

PubMed Abstract | Crossref Full Text | Google Scholar

62. Silva RLD, Paes FLA, Silva SMSD, Santos F, Santana ESD, and Silva Neto JDC. Specific immunohistochemical expression of Mmp-26 in prostatic adenocarcinoma. Acad Bras Ciênc. (2025) 97:e20231380. doi: 10.1590/0001-3765202520231380

PubMed Abstract | Crossref Full Text | Google Scholar

63. Tilli TM, Thuler LC, Matos AR, Coutinho-Camillo CM, Soares FA, da Silva EA, et al. Expression analysis of osteopontin mRNA splice variants in prostate cancer and benign prostatic hyperplasia. Exp Mol Pathol. (2012) 92:13–9. doi: 10.1016/j.yexmp.2011.09.014

PubMed Abstract | Crossref Full Text | Google Scholar

64. Matos AR, Coutinho-Camillo CM, Thuler LCS, Fonseca FP, Soares FA, Silva EA, et al. Expression analysis of thrombospondin 2 in prostate cancer and benign prostatic hyperplasia. Exp Mol Pathol. (2013) 94:438–44. doi: 10.1016/j.yexmp.2013.02.002

PubMed Abstract | Crossref Full Text | Google Scholar

65. Bonilla C, Mason T, Long L, Ahaghotu C, Chen W, Zhao A, et al. E-cadherin polymorphisms and haplotypes influence risk for prostate cancer. Prostate. (2006) 66:546–56. doi: 10.1002/pros.20374

PubMed Abstract | Crossref Full Text | Google Scholar

66. Neto BS, Koff WJ, Biolchi V, Brenner C, Biolo KD, Spritzer PM, et al. Polymorphic CAG and GGC repeat lengths in the androgen receptor gene and prostate cancer risk: analysis of a Brazilian population. Cancer Invest. (2008) 26:74–80. doi: 10.1080/07357900701638251

PubMed Abstract | Crossref Full Text | Google Scholar

67. Paz−y−Miño C, Robles P, Salazar C, Leone PE, García−Cárdenas JM, Naranjo M, et al. Positive association of the androgen receptor CAG repeat length polymorphism with the risk of prostate cancer. Mol Med Rep. (2016) 14:1791–8. doi: 10.3892/mmr.2016.5414

PubMed Abstract | Crossref Full Text | Google Scholar

68. Biolchi V, Neto BS, Pianta DB, Koff WJ, Berger M, and Brum IS. Androgen receptor GGC polymorphism and testosterone levels associated with high risk of prostate cancer and benign prostatic hyperplasia. Mol Biol Rep. (2013) 40:2749–56. doi: 10.1007/s11033-012-2293-5

PubMed Abstract | Crossref Full Text | Google Scholar

69. Gómez R, Torres-Sánchez L, Camacho-Mejorado R, Burguete-García AI, Vázquez-Salas RA, Martínez-Nava GA, et al. Androgen receptor CAG polymorphism and sporadic and early-onset prostate cancer among Mexican men. J Hum Genet. (2016) 61:781–6. doi: 10.1038/jhg.2016.49

PubMed Abstract | Crossref Full Text | Google Scholar

70. Paz-y-Miño C, Witte T, Robles P, Llumipanta W, Díaz M, Arévalo M, et al. Association among polymorphisms in the steroid 5α-reductase type II (SRD5A2) gene, prostate cancer risk, and pathologic characteristics of prostate tumors in an Ecuadorian population. Cancer Genet Cytogenetics. (2009) 189:71–6. doi: 10.1016/j.cancergencyto.2008.09.012

PubMed Abstract | Crossref Full Text | Google Scholar

71. Brureau L, Moningo D, Emeville E, Ferdinand S, Punga A, Lufuma S, et al. Polymorphisms of estrogen metabolism-related genes and prostate cancer risk in two populations of african ancestry. PloS One. (2016) 11:e0153609. doi: 10.1371/journal.pone.0153609

PubMed Abstract | Crossref Full Text | Google Scholar

72. Laurent B, Marc R, Pascal B, and Luc M. 349 Polymorphisms Of The Enzymes Of The Metabolism Of Oestrogens And Prostate Cancer. J Urol. (2012) 187:e142. doi: 10.1016/j.juro.2012.02.410

Crossref Full Text | Google Scholar

73. López-Cortés A, Jaramillo-Koupermann G, Muñoz MJ, Cabrera A, Echeverría C, Paz-y-Miño C, et al. Genetic polymorphisms in MTHFR (C677T, A1298C), MTR (A2756G) and MTRR (A66G) genes associated with pathological characteristics of prostate cancer in the Ecuadorian population. Am J Med Sci. (2013) 346:447–54. doi: 10.1097/MAJ.0b013e3182882578

PubMed Abstract | Crossref Full Text | Google Scholar

74. Veronique-Baudin J, Dieye M, Kouyoumdjian J-C, Vacheron F, Draganescu C, and Azaloux H. Case-control study of the genes of receptors of the androgens of vitamin-D and of 5-alphareductase in a population of Afro-Caribbean population with prostate cancer. Prog Urol. (2006) 16:303–10.

PubMed Abstract | Google Scholar

75. Faucz FR, Horvath A, Rothenbuhler A, Almeida MQ, Libé R, Raffin-Sanson M-L, et al. Phosphodiesterase 11A (PDE11A) genetic variants may increase susceptibility to prostatic cancer. J Clin Endocrinol Metab. (2011) 96:E135–140. doi: 10.1210/jc.2010-1655

PubMed Abstract | Crossref Full Text | Google Scholar

76. Jackson MD, Tulloch-Reid MK, Lindsay CM, Smith G, Bennett FI, McFarlane-Anderson N, et al. Both serum 25-hydroxyvitamin D and calcium levels may increase the risk of incident prostate cancer in Caribbean men of African ancestry. Cancer Med. (2015) 4:925–35. doi: 10.1002/cam4.457

PubMed Abstract | Crossref Full Text | Google Scholar

77. Salgado Montilla JL, Rodriguez Caban JL, Sanchez Garcia J, Sanchez Orti R, and Irizarry Ramirez M. Impact of FTO SNPs rs9930506 and rs9939609 in Prostate Cancer Severity in a Cohort of Puerto Rican Men. Arch Cancer Res. (2017) 5:148. doi: 10.21767/2254-6081.1000148

PubMed Abstract | Crossref Full Text | Google Scholar

78. Okobia MN, Zmuda JM, Ferrell RE, Patrick AL, and Bunker CH. Chromosome 8q24 variants are associated with prostate cancer risk in a high risk population of African ancestry. Prostate. (2011) 71:1054–63. doi: 10.1002/pros.21320

PubMed Abstract | Crossref Full Text | Google Scholar

79. Irizarry-Ramirez M, Kittles R, Wang X, Nogueras-Gonzalez GM, Salgado-Montilla J, Roberson P, et al. Ancestry and prostate cancer genetic risk loci in Hispanic Puerto Rican men: Comparative study with African American men. JCO. (2015) 33:e16033–3. doi: 10.1200/jco.2015.33.15_suppl.e16033

Crossref Full Text | Google Scholar

80. San Francisco IF, Rojas PA, Torres-Estay V, Smalley S, Cerda-Infante J, Montecinos VP, et al. Association of RNASEL and 8q24 variants with the presence and aggressiveness of hereditary and sporadic prostate cancer in a hispanic population. J Cell Mol Medi. (2014) 18:125–33. doi: 10.1111/jcmm.12171

PubMed Abstract | Crossref Full Text | Google Scholar

81. Kidd LR, Coulibaly A, Templeton TM, Chen W, Long LO, Mason T, et al. Germline BCL-2 sequence variants and inherited predisposition to prostate cancer. Prostate Cancer Prostatic Dis. (2006) 9:284–92. doi: 10.1038/sj.pcan.4500884

PubMed Abstract | Crossref Full Text | Google Scholar

82. Sierra Díaz E, Sánchez Corona J, Rosales Gómez RC, Gutierrez Rubio SA, Vázquez Camacho JG, Solano Moreno H, et al. Angiotensin-converting enzyme insertion/deletion and angiotensin type 1 receptor A1166C polymorphisms as genetic risk factors in benign prostatic hyperplasia and prostate cancer. J Renin Angiotensin Aldosterone Syst. (2009) 10:241–6. doi: 10.1177/1470320309352800

PubMed Abstract | Crossref Full Text | Google Scholar

83. Martinez-Fierro ML, Leach RJ, Gomez-Guerra LS, Garza-Guajardo R, Johnson-Pais T, Beuten J, et al. Identification of viral infections in the prostate and evaluation of their association with cancer. BMC Cancer. (2010) 10:326. doi: 10.1186/1471-2407-10-326

PubMed Abstract | Crossref Full Text | Google Scholar

84. Álvarez-Topete E, Torres-Sánchez LE, Hernández-Tobías EA, Véliz D, Hernández-Pérez JG, López-González M de L, et al. Circum-Mediterranean influence in the Y-chromosome lineages associated with prostate cancer in Mexican men: A Converso heritage founder effect? PloS One. (2024) 19:e0308092. doi: 10.1371/journal.pone.0308092

PubMed Abstract | Crossref Full Text | Google Scholar

85. Martinez-Fierro ML, Garza-Veloz I, Rojas-Martinez A, Ortiz-Lopez R, Castruita-de La Rosa C, Ortiz-Castro Y, et al. Positive association between vascular endothelial growth factor (VEGF) -2578 C/A variant and prostate cancer. CBM. (2013) 13:235–41. doi: 10.3233/CBM-130348

PubMed Abstract | Crossref Full Text | Google Scholar

86. Arámbula-Meraz E, Irigoyen-Arredondo M, Cedano-Prieto D, Romo-Martínez E, Luque-Ortega F, Picos-Cárdenas V, et al. Promoter polymorphisms of the PCA3 gene are not associated with its overexpression in prostate cancer patients. J Genet. (2020) 99:51. doi: 10.1007/s12041-020-01202-0

PubMed Abstract | Crossref Full Text | Google Scholar

87. Bica CG, de Moura da Silva LL, Toscani NV, da Cruz IBM, Sá G, Graudenz MS, et al. MnSOD gene polymorphism association with steroid-dependent cancer. Pathol Oncol Res. (2009) 15:19–24. doi: 10.1007/s12253-008-9064-6

PubMed Abstract | Crossref Full Text | Google Scholar

88. Acuña P, Ellwanger A, Ramírez A, Cardemil F, Vega J, and Casalino R. Identificación de factor de crecimiento vascular endotelial en células glandulares de tejido prostético Maligno y benigno: Relación con la recidiva tumoral al año de la prostatectomía. Rev Médica Chile febrero. (2013) 141:153–9.

Google Scholar

89. Irizarry-Ramírez M, Kittles RA, Wang X, Salgado-Montilla J, Nogueras-González GM, Sánchez-Ortiz R, et al. Genetic ancestry and prostate cancer susceptibility SNPs in puerto rican and african american men. Prostate. (2017) 77:1118. doi: 10.1002/pros.23368

PubMed Abstract | Crossref Full Text | Google Scholar

90. Pereira NM, Martins EAC, Quintela MG, Cunha AA, da, Santos Netto MMD, and Waisberg J. Presence of HPV in prostate tissue from patients submitted to prostate biopsy. Acta Cir Bras. (2023) 37:e371205. doi: 10.1590/acb371205

PubMed Abstract | Crossref Full Text | Google Scholar

91. Rogers EN, Jones DZ, Kidd NC, Yeyeodu S, Brock G, Ragin C, et al. Toll-like receptor-associated sequence variants and prostate cancer risk among men of African descent. Genes Immun. (2013) 14:347–55. doi: 10.1038/gene.2013.22

PubMed Abstract | Crossref Full Text | Google Scholar

92. Portela P, Jobim LF, Salim PH, Koff WJ, Wilson TJ, Jobim MR, et al. Analysis of KIR gene frequencies and HLA class I genotypes in prostate cancer and control group. Int J Immunogenetics. (2012) 39:423–8. doi: 10.1111/j.1744-313X.2012.01115.x

PubMed Abstract | Crossref Full Text | Google Scholar

93. Shea PR, Ishwad CS, Bunker CH, Patrick AL, Kuller LH, and Ferrell RE. RNASEL and RNASEL-inhibitor variation and prostate cancer risk in Afro-Caribbeans. Prostate. (2008) 68:354–9. doi: 10.1002/pros.20687

PubMed Abstract | Crossref Full Text | Google Scholar

94. Zabala W, Delgado C, Pardo T, Borjas L, Rojas-Atencio A, Reyes F, et al. Polimorfismo G1385A del gen RNASEL y su asociación con el desarrollo de cáncer de próstata. Estudio preliminar. Investigación Clínica. (2009) 50:295–301.

Google Scholar

95. Pardo T, Salcedo P, Quintero JM, Borjas L, Fernández-Mestre M, Sánchez Y, et al. Study of the association between the polymorphism of the TNF-α gene and prostate cáncer. Rev Alerg Mex. (2019) 66:154–62. doi: 10.29262/ram.v66i2.517

PubMed Abstract | Crossref Full Text | Google Scholar

96. De Souza LCF, Brito TLS, Almeida AT, Muniz YP, Nishiyama PB, Souza CL, et al. Association study between GSTM1 and GSTT1 genotypes and other possible risk factors in prostate cancer patients in a population from southwest Bahia, Brazil. Genet Mol Res. (2019) 18:GMR18296. doi: 10.4238/gmr18296

Crossref Full Text | Google Scholar

97. Lima MM, Oliveira MNL, Granja F, Trindade ACG, De Castro Santos LEM, and Ward LS. Lack of association of GSTT1, GSTM1, GSTO1, GSTP1 and CYP1A1 polymorphisms for susceptibility and outcome in Brazilian prostate cancer patients. Folia Biol (Praha). (2008) 54:102–8. doi: 10.14712/fb2008054030102

PubMed Abstract | Crossref Full Text | Google Scholar

98. Angeli Greaves M, Garate J, Pérez Pereda MG, Viera E, Yibirin M, Harrisson S, et al. Cáncer de próstata y polimorfismos de la glutation s-transferasa en una población venezolana. Rev Digital Postgrado. (2019) 8:2.

Google Scholar

99. Santos ML, Sarkis ÁS, Nishimoto IN, and Nagai MA. Androgen receptor CAG repeat polymorphism in prostate cancer from a Brazilian population. Cancer Detection Prev. (2003) 27:321–6. doi: 10.1016/S0361-090X(03)00106-5

PubMed Abstract | Crossref Full Text | Google Scholar

100. dos Santos A, Ribeiro ML, Mesquita JC, Carvalho-Salles AB, and Hackel C. No association of the 5’ promoter region polymorphism of CYP17 gene with prostate cancer risk. Prostate Cancer Prostatic Dis. (2002) 5:28–31. doi: 10.1038/sj.pcan.4500550

PubMed Abstract | Crossref Full Text | Google Scholar

101. Maistro S, Snitcovsky I, Sarkis AS, da Silva IA, and Brentani MM. Vitamin D receptor polymorphisms and prostate cancer risk in Brazilian men. Int J Biol Markers. (2004) 19:245–9. doi: 10.1177/172460080401900311

PubMed Abstract | Crossref Full Text | Google Scholar

102. Murphy AB, Ukoli F, Freeman V, Bennett F, Aiken W, Tullock T, et al. 8q24 risk alleles in West African and Caribbean men. Prostate. (2012) 72:1366–73. doi: 10.1002/pros.22486

PubMed Abstract | Crossref Full Text | Google Scholar

103. Nemesure B, Wu S-Y, Hennis A, and Leske MC. Distribution of duffy antigen receptor for chemokines (DARC) and risk of prostate cancer in Barbados, west indies. J Immigrant Minority Health. (2015) 17:679–83. doi: 10.1007/s10903-013-9970-x

PubMed Abstract | Crossref Full Text | Google Scholar

104. Basulto-Martínez M, Flores-Tapia JP, Conde-Ferráez L, Esuqeda-Mendoza A, Kantun Moreno N, Gómez-Carballo J, et al. Molecular detection of human papillomavirus among patients with benign prostatic hyperplasia and prostate cáncer. Arch Esp Urol. (2022) 75:27–33.

PubMed Abstract | Google Scholar

105. Cano D, Gomez CF, Ospina N, Cajigas JA, Groot H, Andrade RE, et al. Mitochondrial DNA haplogroups and susceptibility to prostate cancer in a Colombian population. ISRN Oncol. (2014) 2014:1–11. doi: 10.1155/2014/530675

PubMed Abstract | Crossref Full Text | Google Scholar

106. Shea PR, Ferrell RE, Patrick AL, Kuller LH, and Bunker CH. ELAC2 and prostate cancer risk in Afro-Caribbeans of Tobago. Hum Genet. (2002) 111:398–400. doi: 10.1007/s00439-002-0816-1

PubMed Abstract | Crossref Full Text | Google Scholar

107. Martínez-Rizo A, Casillas-Rangel X, Cuerpo Académico Investigación Bioquímica (UAN-CA-266), Andrade-Madrid H, Benites-Godinez V, and Rodríguez-Ocampo N. Abstract 1279: A polymorphism of VEGF -2489C/T is associated with prostate cancer susceptibility in Mexicans. Cancer Res. (2017) 77:1279–9. doi: 10.1158/1538-7445.AM2017-1279

Crossref Full Text | Google Scholar

108. Martínez-Rizo A, González-Cordova B, Peña-George C, (CA-UAN-266) CA de IB, Navarro-Partida J, González-Carrillo M, et al. Abstract 1222: Functional single-nucleotide polymorphisms in the TGFb and TGFbRI gene and their association with prostate cancer in Western Mexicans. Cancer Res. (2018) 78:1222. doi: 10.1158/1538-7445.AM2018-1222

Crossref Full Text | Google Scholar

109. Patiño-García B, Arroyo C, Rangel-Villalobos H, Soto-Vega E, Velarde-Félix JS, Gabilondo F, et al. Association between polymorphisms of the androgen and vitamin D receptor genes with prostate cancer risk in a Mexican population. Rev Invest Clin. (2007) 59:25–31.

PubMed Abstract | Google Scholar

110. Elson JK, Beebe-Dimmer JL, Morgenstern H, Chilkuri M, Blanchard J, and Lentsch AB. The Duffy Antigen/Receptor for Chemokines (DARC) and prostate-cancer risk among Jamaican men. J Immigr Minor Health. (2011) 13:36–41. doi: 10.1007/s10903-010-9330-z

PubMed Abstract | Crossref Full Text | Google Scholar

111. Bernardes JGB, Fernandes MR, Rodrigues JCG, Vinagre LWMS, Pastana LF, Dobbin EAF, et al. Association of androgenic regulation and microRNAs in acinar adenocarcinoma of prostate. Genes. (2022) 13:622. doi: 10.3390/genes13040622

PubMed Abstract | Crossref Full Text | Google Scholar

112. Sánchez BE, Aguayo A, Martínez B, Rodríguez F, Marmolejo M, Svyryd Y, et al. Using genetic and epigenetic markers to improve differential diagnosis of prostate cancer and benign prostatic hyperplasia by noninvasive methods in mexican patients. Clin Genitourin Cancer. (2018) 16:e867–77. doi: 10.1016/j.clgc.2018.02.004

PubMed Abstract | Crossref Full Text | Google Scholar

113. Nobrega M, dos RMB, de SMF, HH F, Costa Brandão Berti F, Souza ILM, et al. Comparative analysis of extracellular vesicles miRNAs (EV-miRNAs) and cell-free microRNAs (cf-miRNAs) reveals that EV-miRNAs are more promising as diagnostic and prognostic biomarkers for prostate cancer. Gene. (2025) 939:149186. doi: 10.1016/j.gene.2024.149186

PubMed Abstract | Crossref Full Text | Google Scholar

114. Pereira VS, Alves BDCA, Waisberg J, Fonseca F, and Gehrke F. Detection of COX-2 in liquid biopsy of patients with prostate cancer. J Clin Pathol. (2023) 76:189–93. doi: 10.1136/jclinpath-2021-207755

PubMed Abstract | Crossref Full Text | Google Scholar

115. Floriano-Sánchez E, Castro-Marín M, and Cárdenas-Rodríguez N. Marcadores moleculares relacionados con cáncer de próstata: 3-nitrotirosina y expresión génica y protéica de la Mn-superóxido dismutasa (Mn-SOD). Arch Esp Urol. (2009) 62:702–11. doi: 10.4321/S0004-06142009000900003

PubMed Abstract | Crossref Full Text | Google Scholar

116. Murray NP, Reyes E, Fuentealba C, Jacob O, and Orellana N. Extended use of P504S positive primary circulating prostate cell detection to determine the need for initial prostate biopsy in a prostate cancer screening program in Chile. Asian Pacific J Cancer Prev. (2014) 15:9335–9. doi: 10.7314/APJCP.2014.15.21.9335

PubMed Abstract | Crossref Full Text | Google Scholar

117. Murray NP, Reyes E, Fuentealba C, Orellana N, Morales F, and Jacob O. Comparison of the formula of PSA, age, prostate volume and race versus PSA density and the detection of primary Malignant circulating prostate cells in predicting a positive initial prostate biopsy in Chilean men with suspicion of prostate cancer. Asian Pacific J Cancer Prev. (2015) 16:5365–70. doi: 10.7314/APJCP.2015.16.13.5365

PubMed Abstract | Crossref Full Text | Google Scholar

118. Murray NP, Reyes E, Orellana N, Fuentealba C, and Jacob O. Prostate Cancer Screening in the Fit Chilean Elderly: a Head to Head Comparison of Total Serum PSA versus Age Adjusted PSA versus Primary Circulating Prostate Cells to Detect Prostate Cancer at Initial Biopsy. Asian Pacific J Cancer Prev. (2015) 16:601–6. doi: 10.7314/APJCP.2015.16.2.601

PubMed Abstract | Crossref Full Text | Google Scholar

119. Murray NP, Reyes E, Fuentealba C, Orellana N, Jacob O, and Badilla S. Head-to-head comparison of the Montreal nomogram with the detection of primary Malignant circulating prostate cells to predict prostate cancer at initial biopsy in Chilean men with suspicion of prostate cancer. Urologic Oncol Semin Original Investigations. (2015) 33:203.e19–203.e25. doi: 10.1016/j.urolonc.2015.01.021

PubMed Abstract | Crossref Full Text | Google Scholar

120. Murray NP, Murray N, Reyes E, Orellana N, Fuentealba C, and Jacob O. Head to head comparison of the chun nomogram, percentage free PSA and primary circulating prostate cells to predict the presence of prostate cancer at repeat biopsy. Asian Pacific J Cancer Prev. (2016) 17:2941–6.

PubMed Abstract | Google Scholar

121. Ramos CG, Valdevenito R, Vergara I, Anabalon P, Sanchez C, and Fulla J. PCA3 sensitivity and specificity for prostate cancer detection in patients with abnormal PSA and/or suspicious digital rectal examination. First Latin American experience. . Urol Oncol. (2013) 31:1522–6. doi: 10.1016/j.urolonc.2012.05.002

PubMed Abstract | Crossref Full Text | Google Scholar

122. Rosin RD, Haynes A, Kidd M, Drozdov I, Modlin I, and Halim A. Evaluation of a multigenomic liquid biopsy (PROSTest) for prostate cancer detection and follow-up in a Caribbean population. Cancer Epidemiol. (2024) 92:102642. doi: 10.1016/j.canep.2024.102642

PubMed Abstract | Crossref Full Text | Google Scholar

123. Gotardelo DR, Courrol LC, Bellini MH, De Oliveira Silva FR, and Soares CRJ. Porphyrins are increased in the faeces of patients with prostate cancer: a case-control study. BMC Cancer. (2018) 18:1090. doi: 10.1186/s12885-018-5030-1

PubMed Abstract | Crossref Full Text | Google Scholar

124. Pinheiro LCL, Pereira ÉR, Francelino AL, Guembarovski AFML, Fuganti PE, de Oliveira KB, et al. Metalloproteinase 9 immunostaining profile is positively correlated with tumor grade, extraprostatic extension and biochemical recurrence in prostate cancer. Pathol Res Pract. (2024) 253:155024. doi: 10.1016/j.prp.2023.155024

PubMed Abstract | Crossref Full Text | Google Scholar

125. Góes IA, Pereira MRM, Crotti E, Pereira GP, Yoshitani MM, Castro MA, et al. Content and tissue expression of Collagen I, Collagen IV, and Laminin in the Extracellular Matrix in Prostate Adenocarcinoma. J Mol Histol junio. (2024) 55:371–8. doi: 10.1007/s10735-024-10196-3

PubMed Abstract | Crossref Full Text | Google Scholar

126. Pinheiro LCL, Pupim ACE, Pereira ÉR, Ahrens TM, Mendonça AC, Francelino AL, et al. Deposition of collagen III and alterations in basement membrane integrity as candidate prognostic markers in prostate cancer. Exp Cell Res. (2024) 439:114077. doi: 10.1016/j.yexcr.2024.114077

PubMed Abstract | Crossref Full Text | Google Scholar

127. Contreras HR, Ledezma RA, Vergara J, Cifuentes F, Barra C, Cabello P, et al. The expression of syndecan-1 and -2 is associated with Gleason score and epithelial-mesenchymal transition markers, E-cadherin and beta-catenin, in prostate cancer. Urol Oncol. (2010) 28:534–40. doi: 10.1016/j.urolonc.2009.03.018

PubMed Abstract | Crossref Full Text | Google Scholar

128. Nóbrega M, de, Cilião HL, Souza MF, de, Souza MR, de, Serpeloni JM, Fuganti PE, et al. Association of polymorphisms of PTEN, AKT1, PI3K, AR, and AMACR genes in patients with prostate cancer. Genet Mol Biol. (2020) 43:e20180329. doi: 10.1590/1678-4685-GMB-2018-0329

PubMed Abstract | Crossref Full Text | Google Scholar

129. Melão BVLA, Faria STDR, Leite KRM, Pimenta RCA, Srougi M, and Antunes AA. Is there a relationship between testosterone and androgen receptor with prostatectomy outcomes? Can J Urol. (2024) 31:11931–40.

PubMed Abstract | Google Scholar

130. Souza MFD, Kuasne H, Barros-Filho MDC, Cilião HL, Marchi FA, Fuganti PE, et al. Circulating mRNA signature as a marker for high-risk prostate cancer. Carcinogenesis. (2020) 41:139–45. doi: 10.1093/carcin/bgz129

PubMed Abstract | Crossref Full Text | Google Scholar

131. Morais CE, Gurgel DC, Teixeira AC, Mattos TVA, Silva AVAD, and Tavora F. Prevalence of ERG expression and PTEN loss in a Brazilian prostate cancer cohort. Braz J Med Biol Res. (2019) 52:e8483. doi: 10.1590/1414-431x20198483

PubMed Abstract | Crossref Full Text | Google Scholar

132. Acosta-Vega NL, Varela R, Mesa JA, Garai J, Baddoo MC, Gómez-Gutiérrez A, et al. Metabolic pathways enriched according to ERG status are associated with biochemical recurrence in Hispanic/Latino patients with prostate cancer. Cancer Med. (2023) 12:4306–20. doi: 10.1002/cam4.5301

PubMed Abstract | Crossref Full Text | Google Scholar

133. Recuero S da C, Viana NI, Reis ST, Mendes KT, Talib LL, Gattaz WF, et al. Phospholipase A2 expression in prostate cancer as a biomarker of good prognosis: A comprehensive study in patients with long follow-up. Urologia. (2024) 91:720–6. doi: 10.1177/03915603241257362

PubMed Abstract | Crossref Full Text | Google Scholar

134. Canto P, Granados JB, Feria-Bernal G, Coral-Vázquez RM, García-García E, Tejeda ME, et al. PPARGC1A and ADIPOQ polymorphisms are associated with aggressive prostate cancer in Mexican-Mestizo men with overweight or obesity. Cancer Biomarkers. (2017) 19:297–303. doi: 10.3233/CBM-160467

PubMed Abstract | Crossref Full Text | Google Scholar

135. Acevedo CA, Quiñones LA, Catalán J, Cáceres DD, Fullá JA, and Roco AM. Impact of CYP1A1, GSTM1, and GSTT1 polymorphisms in overall and specific prostate cancer survival. Urol Oncol. (2014) 32:280–90. doi: 10.1016/j.urolonc.2013.05.010

PubMed Abstract | Crossref Full Text | Google Scholar

136. Cotignola J, Leonardi DB, Shahabi A, Acuña AD, Stern MC, Navone N, et al. Glutathione-S-transferase (GST) polymorphisms are associated with relapse after radical prostatectomy. Prostate Cancer Prostatic Dis. (2013) 16:28–34. doi: 10.1038/pcan.2012.45

PubMed Abstract | Crossref Full Text | Google Scholar

137. Granados JB, Méndez JP, Feria-Bernal G, García-García E, Tejeda ME, Rojano-Mejía D, et al. Association of a TFAM haplotype with aggressive prostate cancer in overweight or obese Mexican Mestizo men. Urologic Oncol Semin Original Investigations. (2017) 35:111. doi: 10.1016/j.urolonc.2016.10.011

PubMed Abstract | Crossref Full Text | Google Scholar

138. Freitas CSM, Silva FR, Silva TAM, and da, Soares AN. Genetic investigation of prostate cancer: Evaluation of markers and relationship with Gleason score and metastasis. JCO. (2024) 42:e17066–6. doi: 10.1200/JCO.2024.42.16_suppl.e17066

Crossref Full Text | Google Scholar

139. Rodríguez H, Rodríguez N, Gallegos I, Arriaza C, and Espinoza-Navarro O. Humoral and cellular immunology in human prostate cancer: plasma cells and T and B lymphocytes. Int J Morphol octubre. (2023) 41:1558–63. doi: 10.4067/S0717-95022023000501558

Crossref Full Text | Google Scholar

140. Franz JM, Portela P, Salim PH, Berger M, Fernando Jobim L, Roesler R, et al. CXCR2 + 1208 CT genotype may predict earlier clinical stage at diagnosis in patients with prostate cancer. Cytokine. (2017) 97:193–200. doi: 10.1016/j.cyto.2017.06.001

PubMed Abstract | Crossref Full Text | Google Scholar

141. Alves S, Junior CS, Muniz G, Silva L, Zortea R, Lima V, et al. Application of Z-scan technique in detecting circulating free DNA for prostate cancer diagnosis and monitoring. Lasers Med Sci. (2025) 40:1–7. doi: 10.1007/s10103-025-04357-3

PubMed Abstract | Crossref Full Text | Google Scholar

142. Febronio EM, Secaf A de F, Chahud F, Elias J, Reis RB, and Muglia VF. Pilot study examining the use of DCE MRI with pharmacokinetic analysis to evaluate hypoxia in prostate cancer. J Comput Assist Tomogr. (2025) 49(5):571–6. doi: 10.1097/RCT.0000000000001707

PubMed Abstract | Crossref Full Text | Google Scholar

143. Cavalcante SLCDA, Barros Silva PGD, Hirth CG, Frederico IKS, Furtado CLM, Ó Pessoa CD, et al. The p16 immunostaining predicts the risk of recurrence in prostate cancer. Asian Pac J Cancer Prev. (2025) 26:77–83. doi: 10.31557/APJCP.2025.26.1.77

PubMed Abstract | Crossref Full Text | Google Scholar

144. dos Santos GA, Viana NI, Pimenta R, de Camargo JA, Guimaraes VR, Romão P, et al. Upregulation of shelterin and CST genes and longer telomeres are associated with unfavorable prognostic characteristics in prostate cancer. Cancer Genet. (2024) 284–285:20–9. doi: 10.1016/j.cancergen.2024.03.006

PubMed Abstract | Crossref Full Text | Google Scholar

145. Barros ÉAF, de, Pontes-Junior J, Reis ST, Lima AER, Souza IC, Salgueiro JL, et al. Correlation between chromosome 9p21 locus deletion and prognosis in clinically localized prostate cancer. Int J Biol Markers. (2017) 32:e248–54. doi: 10.5301/jbm.5000242

PubMed Abstract | Crossref Full Text | Google Scholar

146. Patel MS, Almubarak M, Matta J, Ortiz-Sanchez C, Encarnacion J, Ruiz-Deya G, et al. 5hmC-profiles in Puerto Rican Hispanic/Latino men with aggressive prostate cancer. Front Oncol. (2025) 15:1541878. doi: 10.3389/fonc.2025.1541878

PubMed Abstract | Crossref Full Text | Google Scholar

147. Eguchi FC, Faria EF, Neto CS, Longatto-Filho A, Zanardo-Oliveira C, Taboga SR, et al. The role of TMPRSS2:ERG in molecular stratification of PCa and its association with tumor aggressiveness: a study in Brazilian patients. Sci Rep. (2014) 4:5640. doi: 10.1038/srep05640

PubMed Abstract | Crossref Full Text | Google Scholar

148. Segura-Moreno YY, Sanabria-Salas MC, Mesa JAM-LD, Varela-Ramirez R, Acosta-Vega NL, and Serrano ML. Determination of ERG(+), EZH2, NKX3.1, and SPINK-1 subtypes to evaluate their association with clonal origin and disease progression in multifocal prostate cancer. Cancer Rep. (2022) 6:e1728. doi: 10.1002/cnr2.1728

PubMed Abstract | Crossref Full Text | Google Scholar

149. Montero-Ovalle W, Sanabria-Salas MC, Mesa-López de Mesa J, Varela-Ramírez R, Segura-Moreno YY, Sánchez-Villalobos SA, et al. Determination of TMPRSS2-ERG, SPOP, FOXA1, and IDH1 prostate cancer molecular subtypes in Colombian patients and their possible implications for prognosis. Cell Biol Int. (2023) 47:1017–30. doi: 10.1002/cbin.12000

PubMed Abstract | Crossref Full Text | Google Scholar

150. Ruiz-Deya G, Matta J, Encarnación-Medina J, Ortiz-Sanchéz C, Dutil J, Putney R, et al. Differential DNA methylation in prostate tumors from puerto rican men. Int J Mol Sci. (2021) 22:733. doi: 10.3390/ijms22020733

PubMed Abstract | Crossref Full Text | Google Scholar

151. Parra-Medina R, Payán-Gómez C, Acosta-Vega NL, and Ramírez-Clavijo S. Expression of chemokine (C-C motif) receptor 7 in prostate cancer tissue of young patients and in metastatic cancer cells. Exp Oncol. (2024) 46:137–41. doi: 10.32471/exp-oncology.2312-8852.vol-44-no-2.18025

PubMed Abstract | Crossref Full Text | Google Scholar

152. Gaston SM, Griswold AJ, Kryvenko ON, Gu T, Zhang G-N, Prakash NS, et al. Abstract 2149: West African genetic ancestry and origin of the BRCA1 locus in Jamaican men with high grade prostate cancer. Cancer Res. (2024) 84:2149. doi: 10.1158/1538-7445.AM2024-2149

Crossref Full Text | Google Scholar

153. Yorioka MAW, Murta CB, Leite KRM, Cardili L, de Mello ES, de Carvalho Fazoli AJ, et al. ERG and PTEN role on active surveillance for low-risk prostate cancer in the multiparametric MRI era. Prostate. (2025) 85:364–73. doi: 10.1002/pros.24835

PubMed Abstract | Crossref Full Text | Google Scholar

154. Acosta-Vega NL, Varela R, Mesa JA, Garai J, Gómez-Gutiérrez A, Serrano-Gómez SJ, et al. Genetic ancestry and radical prostatectomy findings in Hispanic/Latino patients. Front Oncol. (2024) 14:1338250. doi: 10.3389/fonc.2024.1338250

PubMed Abstract | Crossref Full Text | Google Scholar

155. Angel M, Freile B, Rodriguez A, Cayol F, Manneh Kopp R, Rioja P, et al. Genomic landscape in prostate cancer in a latin american population. JCO Glob Oncol. (2024) 10:e2400072. doi: 10.1200/GO.24.00072

PubMed Abstract | Crossref Full Text | Google Scholar

156. Magnani M, Castro-Gomez RH, Aoki MN, Gregório EP, Libos F, Morimoto HK, et al. Analysis of peripheral T cells and the CC chemokine receptor (CCR5) delta32 polymorphism in prostate cancer patients treated with carboxymethyl-glucan (CM-G). Natural Product Res. (2012) 26:945–51. doi: 10.1080/14786419.2010.535159

PubMed Abstract | Crossref Full Text | Google Scholar

157. Magnani M, Castro-Gomez RJH, Mori MP, Kuasne H, Gregório EP, Libos F, et al. Protective effect of carboxymethyl-glucan (CM-G) against DNA damage in patients with advanced prostate cancer. Genet Mol Biol. (2010) 34:131–5. doi: 10.1590/S1415-47572010005000103

PubMed Abstract | Crossref Full Text | Google Scholar

158. Berger M, Kreutz FT, Horst JL, Baldi AC, and Koff WJ. Phase I study with an autologous tumor cell vaccine for locally advanced or metastatic prostate cancer. J Pharm Pharm Sci. (2007) 10:144–52.

Google Scholar

159. Gongora ABL, Marshall CH, Velho PI, Lopes CDH, Marin JF, Camargo AA, et al. Extreme responses to a combination of DNA-damaging therapy and immunotherapy in CDK12-altered metastatic castration-resistant prostate cancer: A potential therapeutic vulnerability. Clin Genitourin Cancer. (2022) 20:183–8. doi: 10.1016/j.clgc.2021.11.015

PubMed Abstract | Crossref Full Text | Google Scholar

160. Rojas-Martínez A, Manzanera AG, Sukin SW, Esteban-María J, González-Guerrero JF, Gomez-Guerra L, et al. Intraprostatic distribution and long-term follow-up after AdV-tk immunotherapy as neoadjuvant to surgery in patients with prostate cancer. Cancer Gene Ther. (2013) 20:642–9. doi: 10.1038/cgt.2013.56

PubMed Abstract | Crossref Full Text | Google Scholar

161. Pacheco-Orozco RA, Montealegre-Páez L, Cayol F, Martínez-Gregorio H, Oliver J, Frecha C, et al. AR-V7 as a biomarker for resistance to treatment with abiraterone/enzalutamide in three latin american countries: A hypothetical cost-saving analysis. Oncologist. (2020) 25:e1990–5. doi: 10.1634/theoncologist.2020-0043

PubMed Abstract | Crossref Full Text | Google Scholar

162. Reyes D, Salazar L, Espinoza E, Pereda C, Castellón E, Valdevenito R, et al. Tumour cell lysate-loaded dendritic cell vaccine induces biochemical and memory immune response in castration-resistant prostate cancer patients. Br J Cancer. (2013) 109:1488–97. doi: 10.1038/bjc.2013.494

PubMed Abstract | Crossref Full Text | Google Scholar

163. Campal-Espinosa AC, Junco-Barranco JA, Fuentes-Aguilar F, Calzada-Aguilera L, Rivacoba-Betancourt A, Rodríguez-Bueno RH, et al. Influence of humoral response against gnRH, generated by immunization with a therapeutic vaccine candidate on the evolution of patients with castration-sensitive prostate adenocarcinoma. Technol Cancer Res Treat. (2023) 22:15330338231207318. doi: 10.1177/15330338231207318

PubMed Abstract | Crossref Full Text | Google Scholar

164. Ferreira Bruzzi Porto H, Lopes GCK, Bekierman HBV, Altino De Almeida S, Da Matta Andreiuolo F, Lucena E, et al. A complete response to combined immunotherapy in a patient with an ATM plus SF3B1 mutation and a moderate tumor mutational burden with a high-grade treatment-emergent neuroendocrine prostate cancer: case report and review of the literature. Case Rep Oncol. (2024) 17:950–9. doi: 10.1159/000540573

PubMed Abstract | Crossref Full Text | Google Scholar

165. Isaacsson Velho P, Bastos DA, Saint’ana PT, Rigatti B, da Costa ET, Muniz DQB, et al. Nivolumab in patients with metastatic castration-resistant prostate cancer with and without DNA repair defects. Clin Cancer Res. (2024) 30:5342–52. doi: 10.1158/1078-0432.CCR-24-1595

PubMed Abstract | Crossref Full Text | Google Scholar

166. De Bono JS, Mehra N, Scagliotti GV, Castro E, Dorff T, Stirling A, et al. Talazoparib monotherapy in metastatic castration-resistant prostate cancer with DNA repair alterations (TALAPRO-1): an open-label, phase 2 trial. Lancet Oncol. (2021) 22:1250–64. doi: 10.1016/S1470-2045(21)00376-4

PubMed Abstract | Crossref Full Text | Google Scholar

167. Smith MR, Scher HI, Sandhu S, Efstathiou E, Lara PN, Yu EY, et al. Niraparib in patients with metastatic castration-resistant prostate cancer and DNA repair gene defects (GALAHAD): a multicentre, open-label, phase 2 trial. Lancet Oncol. (2022) 23:362–73. doi: 10.1016/S1470-2045(21)00757-9

PubMed Abstract | Crossref Full Text | Google Scholar

168. Campos-Fernández E, Alqualo NO, Vaz ER, Rodrigues CM, and Alonso-Goulart V. Unveiling the characteristics of D4 and R4 aptamers for their future use in prostate cancer clinical practice. Biophys Chem. (2024) 311:107259. doi: 10.1016/j.bpc.2024.107259

PubMed Abstract | Crossref Full Text | Google Scholar

169. Ariffen NA, Ornellas AA, Alves G, Shana’ah AM, Sharma S, Kankel S, et al. Amplification of different satellite-DNAs in prostate cancer. Pathol - Res Pract. (2024) 256:155269. doi: 10.1016/j.prp.2024.155269

PubMed Abstract | Crossref Full Text | Google Scholar

170. Ribeiro ML, Santos A, Carvalho-Salles AB, and Hackel C. Allelic frequencies of six polymorphic markers for risk of prostate cancer. Braz J Med Biol Res. (2002) 35:205–13. doi: 10.1590/s0100-879x2002000200009

PubMed Abstract | Crossref Full Text | Google Scholar

171. Marlin R, Créoff M, Merle S, Jean-Marie-Flore M, Rose M, Malsa S, et al. Mutation HOXB13 c.853delT in Martinican prostate cancer patients. Prostate. (2020) 80:463–70. doi: 10.1002/pros.23960

PubMed Abstract | Crossref Full Text | Google Scholar

172. Coelho KBCA, Squire JA, Duarte KG, Sares CTG, Moreda NA, Pereira JL, et al. Germline variants in early and late-onset Brazilian prostate cancer patients. Urol Oncol. (2024) 42:68.e11–9. doi: 10.1016/j.urolonc.2024.01.015

PubMed Abstract | Crossref Full Text | Google Scholar

173. Lautert-Dutra W, Melo C M, Chaves LP, Crozier C, P Saggioro F, B Dos Reis R, et al. Loss of heterozygosity impacts MHC expression on the immune microenvironment in CDK12-mutated prostate cancer. Mol Cytogenet. (2024) 17:11. doi: 10.1186/s13039-024-00680-6

PubMed Abstract | Crossref Full Text | Google Scholar

174. Manneh R, Verson CA, Martin A, Delgado A, Isaacsson Velho PH, Manduley A, et al. Prospective study of homologous recombination repair gene mutation prevalence in patients with advanced prostate cancer from latin america: challenges and future approaches. JCO Precis Oncol. (2024) 8:e2300628. doi: 10.1200/PO.23.00628

PubMed Abstract | Crossref Full Text | Google Scholar

175. Gajardo JRC, Tobias-MaChado M, Simardi LH, Corrêa TD, and Wroclawski ER. Incidência de mutação no códon 12 do protoncogene K-ras em carcinoma de próstata humana em uma amostra da população brasileira. J Bras Patol Med Lab. (2004) 40:161–7. doi: 10.1590/S1676-24442004000300006

Crossref Full Text | Google Scholar

176. Chávarri-Guerra Y, Bourlon MT, Rodríguez-Olivares JL, Orozco L, Bazua D, Rodríguez-Faure A, et al. Germline DNA repair genes pathogenic variants among mexican patients with prostate cancer. Clin Genitourin Cancer. (2023) 21:569–73. doi: 10.1016/j.clgc.2023.05.012

PubMed Abstract | Crossref Full Text | Google Scholar

177. Qin Z, Li X, Han P, Zheng Y, Liu H, Tang J, et al. Association between polymorphic CAG repeat lengths in the androgen receptor gene and susceptibility to prostate cancer: A systematic review and meta-analysis. Medicine. (2017) 96:e7258. doi: 10.1097/MD.0000000000007258

PubMed Abstract | Crossref Full Text | Google Scholar

178. Gong M, Dong W, Shi Z, Xu Y, Ni W, and An R. Genetic polymorphisms of GSTM1, GSTT1, and GSTP1 with prostate cancer risk: a meta-analysis of 57 studies. PloS One. (2012) 7:e50587. doi: 10.1371/journal.pone.0050587

PubMed Abstract | Crossref Full Text | Google Scholar

179. Malik SS, Kazmi Z, Fatima I, Shabbir R, Perveen S, and Masood N. Genetic polymorphism of GSTM1 and GSTT1 and risk of prostatic carcinoma - a meta-analysis of 7,281 prostate cancer cases and 9,082 healthy controls. Asian Pacific J Cancer Prev. (2016) 17:2629–35.

PubMed Abstract | Google Scholar

180. Nock NL, Bock C, Neslund-Dudas C, Beebe-Dimmer J, Rundle A, Tang D, et al. Polymorphisms in glutathione S-transferase genes increase risk of prostate cancer biochemical recurrence differentially by ethnicity and disease severity. Cancer Causes Control. (2009) 20:1915–26. doi: 10.1007/s10552-009-9385-0

PubMed Abstract | Crossref Full Text | Google Scholar

181. Holt SK, Kwon EM, Peters U, Ostrander EA, and Stanford JL. Vitamin D pathway gene variants and prostate cancer risk. Cancer Epidemiol Biomarkers Prev. (2009) 18:1929–33. doi: 10.1158/1055-9965.EPI-09-0113

PubMed Abstract | Crossref Full Text | Google Scholar

182. Ingles SA, Ross RK, Yu MC, Irvine RA, La Pera G, Haile RW, et al. Association of prostate cancer risk with genetic polymorphisms in vitamin D receptor and androgen receptor. J Natl Cancer Inst. (1997) 89:166–70. doi: 10.1093/jnci/89.2.166

PubMed Abstract | Crossref Full Text | Google Scholar

183. Xu Y, Shao X, Yao Y, Xu L, Chang L, Jiang Z, et al. Positive association between circulating 25-hydroxyvitamin D levels and prostate cancer risk: new findings from an updated meta-analysis. J Cancer Res Clin Oncol. (2014) 140:1465–77. doi: 10.1007/s00432-014-1706-3

PubMed Abstract | Crossref Full Text | Google Scholar

184. Li W and Yu T. Relationship between 25-hydroxyvitamin D and IGF1: a cross-sectional study of the Third National Health and Nutrition Examination Survey participants. J Health Popul Nutr. (2023) 42:35. doi: 10.1186/s41043-023-00374-6

PubMed Abstract | Crossref Full Text | Google Scholar

185. Matsushita M, Fujita K, Hayashi T, Kayama H, Motooka D, Hase H, et al. Gut microbiota–derived short-chain fatty acids promote prostate cancer growth via IGF1 signaling. Cancer Res. (2021) 81:4014–26. doi: 10.1158/0008-5472.CAN-20-4090

PubMed Abstract | Crossref Full Text | Google Scholar

186. Cornford P, Tilki D, and van den Bergh R. EAU-EANM-ESTRO-ESUR-ISUP-SIOG guidelines on prostate cancer. Arnhem, The Netherlands: EAU Guidelines Office (2025). Available online at: https://uroweb.org/guidelines/prostate-cancer (Accessed June 1, 2025).

Google Scholar

187. Wei JT, Barocas D, Carlsson S, Coakley F, Eggener S, Etzioni R, et al. Early detection of prostate cancer: AUA/SUO guideline part II: considerations for a prostate biopsy. J Urol. (2023) 210:54–63. doi: 10.1097/JU.0000000000003492

PubMed Abstract | Crossref Full Text | Google Scholar

188. Merriel SWD, Pocock L, Gilbert E, Creavin S, Walter FM, Spencer A, et al. Systematic review and meta-analysis of the diagnostic accuracy of prostate-specific antigen (PSA) for the detection of prostate cancer in symptomatic patients. BMC Med. (2022) 20:54. doi: 10.1186/s12916-021-02230-y

PubMed Abstract | Crossref Full Text | Google Scholar

189. Balakrishnan AS, Palmer NR, Fergus KB, Gaither TW, Baradaran N, Ndoye M, et al. Minority recruitment trends in phase III prostate cancer clinical trials (2003 to 2014): progress and critical areas for improvement. J Urol. (2019) 201:259–67. doi: 10.1016/j.juro.2018.09.029

PubMed Abstract | Crossref Full Text | Google Scholar

190. Hawlina S, Chowdhury HH, Smrkolj T, and Zorec R. Dendritic cell-based vaccine prolongs survival and time to next therapy independently of the vaccine cell number. Biol Direct. (2022) 17:5. doi: 10.1186/s13062-022-00318-w

PubMed Abstract | Crossref Full Text | Google Scholar

191. Tryggestad AMA, Axcrona K, Axcrona U, Bigalke I, Brennhovd B, Inderberg EM, et al. Long-term first-in-man Phase I/II study of an adjuvant dendritic cell vaccine in patients with high-risk prostate cancer after radical prostatectomy. Prostate. (2022) 82:245–53. doi: 10.1002/pros.24267

PubMed Abstract | Crossref Full Text | Google Scholar

192. UNESCO Institute for Statistics (UIS). Research and development expenditure (% of GDP) (2025). Available online at: https://databank.worldbank.org/source/world-development-indicators/Series/GB.XPD.RSDV.GD.ZS (Accessed April 1, 2025).

Google Scholar

Keywords: biomarkers, Caribbean region, diagnosis, disease susceptibility, Latin America, prognosis, prostatic neoplasms, therapeutics

Citation: Prada NJ, Mendivelso-González D, Yepes S, Corredor C, Parra-Medina R, Varela R and Serrano ML (2026) Research on potential biomarkers of prostate cancer in Latin America and the Caribbean: a scoping review. Front. Oncol. 16:1740352. doi: 10.3389/fonc.2026.1740352

Received: 05 November 2025; Accepted: 13 January 2026; Revised: 28 December 2025;
Published: 30 January 2026.

Edited by:

Felipe D’Almeida Costa, A. C. Camargo Cancer Center, Brazil

Reviewed by:

Sruthi Ranganathan, University of Cambridge, United Kingdom
Pablo Rojas, Las Condes Clinic, Chile

Copyright © 2026 Prada, Mendivelso-González, Yepes, Corredor, Parra-Medina, Varela and Serrano. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Martha Lucía Serrano, bWxzZXJyYW5vbEB1bmFsLmVkdS5jbw==

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