Research BRAF
Related Resources for this page:
- Future Directions
- Antibody-Drug Conjugates
- A brief history of ADCs
- Current research in ADCs
- Cytotoxic agent
- Emerging therapeutic options
- Emerging therapeutic options
- HER Signaling
- How are ADCs designed to work?
- Glossary
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- Research ADCs
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- Trastuzumab Emtansine (T-DM1)
- What are ADCs?
- Antibody-Drug conjugates
- Apoptosis
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- Targeted Small Molecules
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- The Bcl-2 family
- Apoptosis
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- Emerging therapeutic options
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- Gastric Cancer
- HER1/EGFR as a therapeutic target
- MAPK Signaling
- MEK Inhibitor (GDC-0973)
- Melanoma
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- Reactivating apoptosis
- PI3K/Akt/mTOR Signaling
- Therapeutic potential of HER pathways
- Traditional Monoclonal Antibodies
- B-cell Surface Proteins
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- HER Signaling
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- Obinutuzumab (GA101)
- Inhibition of HER2 dimerization
- Therapeutic potential of HER pathways
- Antibody-Drug Conjugates
What is oncogenic BRAF?
Oncogenic BRAF can result from mutations in the BRAF gene. Various activating mutations (ie, somatic point mutations) in BRAF cause the protein to become overactive. This triggers a signaling cascade that can play a role in specific malignancies. Approximately 90% of known BRAF mutations are V600E mutations. These involve the substitution of glutamic acid (E) for valine (V) at position V600 of the protein chain, resulting in constitutively active BRAF. Other variants of this point mutation include lysine (K), aspartic acid (D), and arginine (R). The V600 point mutation allows BRAF to signal independently of upstream cues.3,4,6,7
As a result of constitutively active BRAF, overactive downstream signaling via MEK and ERK leads to excessive cell proliferation and survival, independent of growth factors. Oncogenic BRAF signaling may lead to increased and uncontrolled cell proliferation and resistance to apoptosis (programmed cell death).3
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BRAFV600E can activate MEK and ERK downstream, independent of upstream cues from RAS.3,4