Molecular Cancer Biology: Genetic Mutations, Tumor Microenvironment, Cell Signaling and Immunotherapy

Molecular Cancer Biology is a sub-genomic and molecular-genetic-related topic that enriches our knowledge about the development and progression of cancer. This article primarily focus on the subtopics of Genetic mutations in cancer, Tumor microenvironment, Cell signaling pathways in cancer, and Cancer immunotherapy.

Genetic mutations in cancer: Cancer-causing mutations can arise from inherited or spontaneously induced DNA damage, such as environmental carcinogens or mutations arising from replication. These alterations confer a selective advantage to the cells, promoting tumor growth and progression. Oncogenic mutations can cause affected genes to be overexpressed or produce mutated proteins with dysregulated activity.
Tumor microenvironment: The tumor microenvironment (TME) is a crucial determinants of cancer development and progression. It consists of stromal components such as immune, inflammatory, endothelial, adipocytes, and fibroblast cells. Cancer stem cells (CSCs) or cancer stem-like cells are a small sub-set of the population within the TME, and their correlation with TME plays a vital role in shaping the differential or leading to differential survival outcomes in response to treatment regimen.
Cell signaling pathways in cancer: Cancer-causing mutations can connect with signaling pathways that control processes such as cell growth, survival, and metabolism. D dysregulated signaling is not subject to normal control mechanisms, leading to cancer progression. For example, the PI3K-Akt pathway is activated by extracellular succinate, promoting cancer cell invasion and driving epithelial-mesenchymal transformation.
Cancer immunotherapy: Immunotherapy is a potential treatment strategy for cancer that involves modulating the immune system to identify and eliminate cancer cells. For example, the tumor mutation burden (TMB) and microsatellite are evaluated as potential targets for immunotherapy. Anticancer microRNA replacement therapy has a high potential in cancer treatment, as shown by the significant decrease in tumor size for bone metastasis and colon cancer drugs.
Tumor metabolism: Tumor metabolism plays a crucial role in cancer development and progression. For example, succinate can activate the PI3K-Akt pathway via the SUCNR1-ERK1/2-STAT3-VEGF pathway, leading to extracellular succinate significantly impacts macrophages within the tumor microenvironment.
Tumor microenvironment and cancer stem cells: The tumor microenvironment enriches the stemness features of cancer stem cells (CSCs), promoting an oncogenic transformation in cancer cells. CSCs are a small sub-set of the population within the TME, and their correlation with TME plays a vital role in shaping the differential or leading to differential survival outcomes in response to treatment regimen.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor microenvironment and cancer immunotherapy: The tumor microenvironment can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the immune system, leading to a potential therapeutic strategy for cancer immunotherapy. For example, the lncRNA neighbor BRCA1 gene 2 (NBR2) promotes cell survival by upregulating GLUT1 expression, which is overexpressed in cancer.
Tumor metabolism and cancer stem cells: Tumor metabolism can regulate the expression of genes involved in cancer stem cell development, such as the lncRNA neighbor BRCA1 gene 2 (NBR2), which promotes cell survival by upregulating GLUT1 expression.
Tumor metabolism and cancer immunotherapy: Tumor metabolism can modulate the