Immune escape plays an important role in tumor recurrence, metastasis, and drug resistance. Tumors evade immune response through various mechanisms, among which cancer immunoediting is widely accepted. In addition, the tumor microenvironment (TME) also plays a vital role in immune escape, including extracellular matrix, secreted molecules, immune cells, and stromal cells. Various components from TME take an active part in the modulation of the interaction between tumor cells and immune cells. For example, changes in tumor-infiltrating lymphocyte composition, such as increased accumulation of Treg cells, as well as the increased expression of CTLA-4 in T cells, potentially contribute to tumor progression and immune escape.
Despite the emergence of therapies such as chemotherapy, radiotherapy, targeted therapy, and immunotherapy that strive to achieve better efficacy, treatment outcomes in patients with malignancy are still greatly influenced by drug resistance. There are multiple potential determinants of drug resistance, among which the immune system and TME are closely related to tumor immune escape.
The importance of immune escape is proved by the success of immune checkpoint blockade, which has shown encouraging efficacy in the treatment of a variety of solid tumors, including non-small cell lung cancer and breast cancer. A study showed that the loss of ß2-microglobulin and JAK1 or JAK2 mutations contribute to the resistance to checkpoint blockade. What’s more, the new activating mutations on the target itself, pathway alterations, or histological changes caused by the selective therapeutic pressure derived from cancer therapies attenuate anti-tumor response and lead to tumor recurrence.
Breast and thoracic cancers are common malignancies around the world. Exploring potential mechanisms and therapeutic targets of immune escape is helpful to deepen the understanding of tumorigenesis and promote the research of potential treatment. The aim of this Research Topic is to elucidate the role of immune escape on breast and thoracic cancers, including its effects on tumor recurrence, metastasis, and drug resistance.
We welcome the authors to submit Original Research and Review articles that can help to shed new light on the effect of immune escape on tumor recurrence, metastasis, and drug resistance in breast and thoracic cancers. Subtopics of interest include but are not limited to:
(1) The mechanism of immune escape in breast and thoracic cancers
(2) Signaling pathways related to the immune escape in breast and thoracic cancers
(3) Potential determinants in immune escape that closely related to drug resistance in breast and thoracic cancers
(4) Potential targets and therapeutic strategies for immune escape in thoracic malignancies
(5) Mechanisms of drug resistance and strategies to overcome drug resistance
Please NOTE: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope for this section and will not be accepted as part of this Research Topic.
Immune escape plays an important role in tumor recurrence, metastasis, and drug resistance. Tumors evade immune response through various mechanisms, among which cancer immunoediting is widely accepted. In addition, the tumor microenvironment (TME) also plays a vital role in immune escape, including extracellular matrix, secreted molecules, immune cells, and stromal cells. Various components from TME take an active part in the modulation of the interaction between tumor cells and immune cells. For example, changes in tumor-infiltrating lymphocyte composition, such as increased accumulation of Treg cells, as well as the increased expression of CTLA-4 in T cells, potentially contribute to tumor progression and immune escape.
Despite the emergence of therapies such as chemotherapy, radiotherapy, targeted therapy, and immunotherapy that strive to achieve better efficacy, treatment outcomes in patients with malignancy are still greatly influenced by drug resistance. There are multiple potential determinants of drug resistance, among which the immune system and TME are closely related to tumor immune escape.
The importance of immune escape is proved by the success of immune checkpoint blockade, which has shown encouraging efficacy in the treatment of a variety of solid tumors, including non-small cell lung cancer and breast cancer. A study showed that the loss of ß2-microglobulin and JAK1 or JAK2 mutations contribute to the resistance to checkpoint blockade. What’s more, the new activating mutations on the target itself, pathway alterations, or histological changes caused by the selective therapeutic pressure derived from cancer therapies attenuate anti-tumor response and lead to tumor recurrence.
Breast and thoracic cancers are common malignancies around the world. Exploring potential mechanisms and therapeutic targets of immune escape is helpful to deepen the understanding of tumorigenesis and promote the research of potential treatment. The aim of this Research Topic is to elucidate the role of immune escape on breast and thoracic cancers, including its effects on tumor recurrence, metastasis, and drug resistance.
We welcome the authors to submit Original Research and Review articles that can help to shed new light on the effect of immune escape on tumor recurrence, metastasis, and drug resistance in breast and thoracic cancers. Subtopics of interest include but are not limited to:
(1) The mechanism of immune escape in breast and thoracic cancers
(2) Signaling pathways related to the immune escape in breast and thoracic cancers
(3) Potential determinants in immune escape that closely related to drug resistance in breast and thoracic cancers
(4) Potential targets and therapeutic strategies for immune escape in thoracic malignancies
(5) Mechanisms of drug resistance and strategies to overcome drug resistance
Please NOTE: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of the scope for this section and will not be accepted as part of this Research Topic.