Research BRAF
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- Clinical Trials
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- Antibody-Drug Conjugates
- A brief history of ADCs
- Current research in ADCs
- Cytotoxic agent
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- Emerging therapeutic options
- HER Signaling
- How are ADCs designed to work?
- Glossary
- Monoclonal antibody
- Research ADCs
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- Targeting cancers with ADCs
- Trastuzumab Emtansine (T-DM1)
- What are ADCs?
- Antibody-Drug conjugates
- Apoptosis
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- Non-Antibody Biologics
- Targeted Small Molecules
- Apoptosis
- Apoptotic pathways
- The Bcl-2 family
- Apoptosis
- Emerging therapeutic options
- Emerging therapeutic options
- Resisting apoptosis
- Gastric Cancer
- HER1/EGFR as a therapeutic target
- MAPK Signaling
- MEK Inhibitor (GDC-0973)
- Melanoma
- Emerging therapeutic options
- PI3K Inhibitor (GDC-0941)
- Reactivating apoptosis
- PI3K/Akt/mTOR Signaling
- Therapeutic potential of HER pathways
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- Traditional Monoclonal Antibodies
- B-cell Surface Proteins
- Glossary
- Direct cell death
- Emerging therapeutic options
- Emerging therapeutic options
- Gastric Cancer
- HER Signaling
- HER1/EGFR as a therapeutic target
- HER2:HER3 dimer
- HER2 as a therapeutic target
- HER3 as a therapeutic target
- Melanoma
- Emerging therapeutic options
- Obinutuzumab (GA101)
- Angiogenic Signaling
- Inhibition of HER2 dimerization
- Therapeutic potential of HER pathways
- Slide decks and videos
- Antibody-Drug Conjugates
Oncogenic BRAF in cancer
Oncogenic BRAF can result from mutations in the BRAF gene, which may cause the protein to become overactive. The most common alteration in the BRAF gene leads to the BRAFV600E mutation. Mutations in the BRAF gene allow for BRAF to signal independently of upstream cues, and result in overactive downstream signaling via MEK and ERK. This, in turn, leads to excessive cell proliferation and survival, independent of growth factors.1,3,4
Overactivation of RAS-RAF signaling by oncogenic BRAF has been implicated in multiple malignancies, making it a potential therapeutic target in oncology. These include some melanoma tumors, papillary thyroid tumors, serous ovarian tumors, and colorectal and prostate tumors.8-11
- ~50% of melanoma tumors3
- ~40% of papillary thyroid tumors3,12
- ~30% of serous ovarian tumors12
- ~10% of colorectal tumors11
- ~10% of prostate tumors11
Since mutated BRAFV600E is prevalent in different types of cancer, including melanoma, it is a potential therapeutic target. It is important to inhibit oncogenic BRAF activity, since inhibition may result in decreased tumor cell proliferation and increased tumor cell death.13
Genentech is actively researching the potential of oncogenic BRAF as a novel therapeutic target and as a personalized approach for BRAF-driven tumors.