Biological databases are basically used by Biomedical researchers to maintain and organize data obtain by Human Gene Expression Data Analysis, Pathway Analysis and information related to disease genes ,regulation of gene, Transcription Factor Binding Sites.

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V-raf murine sarcoma viral oncogene homolog B1, also known as BRAF, is a protein which in humans is encoded by the BRAF gene. The BRAF gene makes a protein called B-RAF, which is involved in sending signals in cells and in cell growth. This gene may be mutated (changed) in many types of cancer, which causes a change in the B-RAF protein. This can increase the growth and spread of cancer cells.

V-raf murine sarcoma viral oncogene homolog B1, also known as BRAF, is a protein which in humans is encoded by the BRAF gene. The BRAF gene makes a protein called B-RAF, which is involved in sending signals in cells and in cell growth. This gene may be mutated (changed) in many types of cancer, which causes a change in the B-RAF protein. This can increase the growth and spread of cancer cells.

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Fibroblast growth factor receptor 2 (FGFR2) is a receptor for fibroblast growth factor encoded on a gene residing on chromosome 10. The protein encoded by this gene is a member of the fibroblast growth factor receptor family

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The Epidermal Growth Factor Receptor (EGFR) activates an important pathway that leads to cell proliferation, differentiation, migration/motility, adhesion, protection from apoptosis, enhanced survival and gene transcription.

Every day a healthy immune system fights off an average of 10,000 mutant cells. Problems emerge when the immune system is not able to fight off these cells, allowing them to get a foothold and develop into a cancer. The characteristics of cancerous cells cause them to inhibit the proper regulation of the immune system.

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The presence of the V600E mutation in the BRAF gene is associated with poor prognosis and non response to anti-EGFR therapy in advanced stage colorectal cancer patients. Studies show that colorectal cancer patients with wild-type KRAS failed to respond when treated with either cetuximab or panitumumab and experienced a shorter progression-free survival and overall survival, when the BRAF mutation was present, compared to patients with wild-type BRAF tumors.1