Colorectal cancer (CRC) is a leading cause of global mortality representing the third most common cancer and responsible for over 500,000 deaths on an annual basis. There have been many developments in the field to help treatment including surgery, chemotherapy, radiotherapy and immunotherapy as well as cytotoxic and biological therapies such as anti-VEGF and anti-EGFR. However, the 5-year survival rate of metastatic CRC patients remains 35-40% and therefore, the prognosis of CRC patients remains very poor as well as reaching advanced stages of the disease. Metastasis is the key factor which impacts the survival rate as approximately half of CRC patients develop hepatic metastasis. Therefore, understanding the molecular mechanisms which influence proliferation, migration and invasion needs to be further studied to help understanding of how diagnosis and treatment can be further improved.
Molecular mechanisms of colorectal cancer remain complex due to the number of various influences including microRNAs (miRNAs) which are involved in cancer progression and metastasis with a primary role as a biomarker. There are multiple miRNAs that have been a focus in understanding the molecular mechanisms of CRC such as miR-17-5p as well as tumor suppressor miRNAs: miR-185-5p and miR-125b-5p. There have also been recent studies involving the role of long non-coding RNAs (lncRNAs) which have been found to be involved in the progression of CRC. An example of a lncRNA is DLEU1 which has had reports of influencing the molecular progression of CRC but it's underlying mechanism requires further study. DLEU1 has been found to influence cell migration, apoptosis and proliferation. Colorectal Cancer is also known to have genetic predisposition which can affect between 1-3% of CRC patients. Lynch syndrome is the most common form of inherited CRC caused by pathogenic germline mutations in several dMMR genes (MLH1, MSH2, MSH6 and PMS2) and deletions in EPCAM. Furthermore, deleterious mutations in the APC gene are known to primarily cause the autosomal dominant familial adenomatous polyposis (FAP) that commonly lead to CRC. There are studies to understand how mutations in the APC gene and BRCA1, which is a major susceptibility gene for breast and ovarian cancer, can influence the progression of CRC.
Understanding the molecular mechanism and therapies for colorectal cancer remain complex. This Research aims to provide insight into the research around understanding molecular mechanisms and targeted therapies that impact colorectal cancer. Topics of interest include:
-Role of micro-RNAs (miRNAs) in the progression of colorectal cancer
-Biomarkers as potential diagnostic markers
-Influence of genetic variations and mutations on CRC
-Novel therapies to help CRC patient survival and prognosis
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 scope for this section and will not be accepted as part of this Research Topic.
Colorectal cancer (CRC) is a leading cause of global mortality representing the third most common cancer and responsible for over 500,000 deaths on an annual basis. There have been many developments in the field to help treatment including surgery, chemotherapy, radiotherapy and immunotherapy as well as cytotoxic and biological therapies such as anti-VEGF and anti-EGFR. However, the 5-year survival rate of metastatic CRC patients remains 35-40% and therefore, the prognosis of CRC patients remains very poor as well as reaching advanced stages of the disease. Metastasis is the key factor which impacts the survival rate as approximately half of CRC patients develop hepatic metastasis. Therefore, understanding the molecular mechanisms which influence proliferation, migration and invasion needs to be further studied to help understanding of how diagnosis and treatment can be further improved.
Molecular mechanisms of colorectal cancer remain complex due to the number of various influences including microRNAs (miRNAs) which are involved in cancer progression and metastasis with a primary role as a biomarker. There are multiple miRNAs that have been a focus in understanding the molecular mechanisms of CRC such as miR-17-5p as well as tumor suppressor miRNAs: miR-185-5p and miR-125b-5p. There have also been recent studies involving the role of long non-coding RNAs (lncRNAs) which have been found to be involved in the progression of CRC. An example of a lncRNA is DLEU1 which has had reports of influencing the molecular progression of CRC but it's underlying mechanism requires further study. DLEU1 has been found to influence cell migration, apoptosis and proliferation. Colorectal Cancer is also known to have genetic predisposition which can affect between 1-3% of CRC patients. Lynch syndrome is the most common form of inherited CRC caused by pathogenic germline mutations in several dMMR genes (MLH1, MSH2, MSH6 and PMS2) and deletions in EPCAM. Furthermore, deleterious mutations in the APC gene are known to primarily cause the autosomal dominant familial adenomatous polyposis (FAP) that commonly lead to CRC. There are studies to understand how mutations in the APC gene and BRCA1, which is a major susceptibility gene for breast and ovarian cancer, can influence the progression of CRC.
Understanding the molecular mechanism and therapies for colorectal cancer remain complex. This Research aims to provide insight into the research around understanding molecular mechanisms and targeted therapies that impact colorectal cancer. Topics of interest include:
-Role of micro-RNAs (miRNAs) in the progression of colorectal cancer
-Biomarkers as potential diagnostic markers
-Influence of genetic variations and mutations on CRC
-Novel therapies to help CRC patient survival and prognosis
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 scope for this section and will not be accepted as part of this Research Topic.
