B cell Non-Hodgkin’s Lymphoma (B-NHL) represents 90% of lymphoma cases. It is a heterogeneous group of lymphoid malignancies, arising from the mature B lymphocytes compartment. Most remain incurable and current regiment therapies are associated with variable outcomes, adverse effects, and frequent relapses. Consequently, innovative therapeutic options are needed to improve the treatment of patients with B-NHL. Besides the classical genomic changes, several epigenetic modifications that cause chromatin and DNA methylation alterations are described as important mechanisms of tumorigenesis in these types of cancers. B cells lymphoma undergo additional epigenetic changes to silence or activate genes; promoting oncogenesis, metastasis, angiogenesis, and resistance to therapy.
In addition to the importance of genetic and epigenetic alteration in lymphomagenesis, tumor microenvironment (TME) also plays a crucial role in supporting tumor B cells pathogenesis. In the complex multifactorial set of cellular interactions within the TME, the continuous crosstalk between cancer B cells and healthy cells orchestrates an auspicious shelter for survival, cell evasion, immunosuppression and drug resistance. In these neoplastic conditions with a multi-scale mechanism of action, tumor B cells exhibit a range of TME dependence associated with a degree of epigenome alteration. Hence, it is important to elucidate the mechanisms by which genetic and epigenetic background within B-NHL cancers can be functionally dysregulated in the TME to influence its composition, infiltration, and information transfer.
Depending on the B-NHL group, the TME composition varies according to the non-tumor cells infiltration as well. For instance, regulatory T cells, myeloid-derived suppressor cells, tumor-associated macrophages, cancer-associated fibroblasts and stromal cells might install immunosuppression, immune cell exhaustion and chronic inflammation. In addition, TME has been intensively used as an important prognosis factor, where its composition is often correlated with a bad prognosis and poor outcome. Likewise, epigenetic plasticity represents the best opportunity for cancer cells to reach an optimal adaptation to hostile surroundings by its epigenome reprogramming. In therapy, disruption of the cancer-TME relationships is the common strategy to boost immune response and to develop drug targets as it is focused on immunosuppressive cells, immune cell checkpoints, signaling molecules, immunomodulatory agents, and chromatin remodeler proteins. Consequently, understanding epigenetic change mechanisms of cancer-TME interaction will generate substantial information to improve B-NHL diagnosis and therapy.
Our Research Topic aims to elucidate cancer B cell epigenetic reprograming capacity, and how its plasticity influences the environment in favor of tumorigenesis.
We welcomed Original Research, Review, Mini-Reviews, Brief Report papers and clinical investigation that cover, but not limited to, the following topics:
• B-NHL epigenetic programing;
• Landscape of tumor-infiltrating cells in B-NHL;
• B-NHL epigenetic plasticity related to drug resistance and cell invasion;
• Epigenetic-modulating therapies in B-NHL;
• Tumor microenvironment changes in favor of cell evasion and immunosuppression;
• Novel B-NHL epigenetic biomarkers;
• Novel B-NHL immunotherapies improving immune cell response and surveillance;
• Epigenetic plasticity related to the regulation of oncogenes expression.
B cell Non-Hodgkin’s Lymphoma (B-NHL) represents 90% of lymphoma cases. It is a heterogeneous group of lymphoid malignancies, arising from the mature B lymphocytes compartment. Most remain incurable and current regiment therapies are associated with variable outcomes, adverse effects, and frequent relapses. Consequently, innovative therapeutic options are needed to improve the treatment of patients with B-NHL. Besides the classical genomic changes, several epigenetic modifications that cause chromatin and DNA methylation alterations are described as important mechanisms of tumorigenesis in these types of cancers. B cells lymphoma undergo additional epigenetic changes to silence or activate genes; promoting oncogenesis, metastasis, angiogenesis, and resistance to therapy.
In addition to the importance of genetic and epigenetic alteration in lymphomagenesis, tumor microenvironment (TME) also plays a crucial role in supporting tumor B cells pathogenesis. In the complex multifactorial set of cellular interactions within the TME, the continuous crosstalk between cancer B cells and healthy cells orchestrates an auspicious shelter for survival, cell evasion, immunosuppression and drug resistance. In these neoplastic conditions with a multi-scale mechanism of action, tumor B cells exhibit a range of TME dependence associated with a degree of epigenome alteration. Hence, it is important to elucidate the mechanisms by which genetic and epigenetic background within B-NHL cancers can be functionally dysregulated in the TME to influence its composition, infiltration, and information transfer.
Depending on the B-NHL group, the TME composition varies according to the non-tumor cells infiltration as well. For instance, regulatory T cells, myeloid-derived suppressor cells, tumor-associated macrophages, cancer-associated fibroblasts and stromal cells might install immunosuppression, immune cell exhaustion and chronic inflammation. In addition, TME has been intensively used as an important prognosis factor, where its composition is often correlated with a bad prognosis and poor outcome. Likewise, epigenetic plasticity represents the best opportunity for cancer cells to reach an optimal adaptation to hostile surroundings by its epigenome reprogramming. In therapy, disruption of the cancer-TME relationships is the common strategy to boost immune response and to develop drug targets as it is focused on immunosuppressive cells, immune cell checkpoints, signaling molecules, immunomodulatory agents, and chromatin remodeler proteins. Consequently, understanding epigenetic change mechanisms of cancer-TME interaction will generate substantial information to improve B-NHL diagnosis and therapy.
Our Research Topic aims to elucidate cancer B cell epigenetic reprograming capacity, and how its plasticity influences the environment in favor of tumorigenesis.
We welcomed Original Research, Review, Mini-Reviews, Brief Report papers and clinical investigation that cover, but not limited to, the following topics:
• B-NHL epigenetic programing;
• Landscape of tumor-infiltrating cells in B-NHL;
• B-NHL epigenetic plasticity related to drug resistance and cell invasion;
• Epigenetic-modulating therapies in B-NHL;
• Tumor microenvironment changes in favor of cell evasion and immunosuppression;
• Novel B-NHL epigenetic biomarkers;
• Novel B-NHL immunotherapies improving immune cell response and surveillance;
• Epigenetic plasticity related to the regulation of oncogenes expression.
