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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The Ras Gene02:38

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
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Combination Therapies and Personalized Medicine02:50

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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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The Retinoblastoma Gene01:20

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Related Experiment Video

Updated: Nov 16, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Defining and Targeting BRAF Mutations in Solid Tumors.

Briana R Halle1, Douglas B Johnson2

  • 1Vanderbilt University School of Medicine, Vanderbilt University Medical Center and Vanderbilt Ingram Cancer Center, Nashville, TN, USA.

Current Treatment Options in Oncology
|February 28, 2021
PubMed
Summary

BRAF mutations are key targets in cancer therapy. Targeted drugs like vemurafenib and combination therapies show promise, improving outcomes and overcoming resistance in various BRAF-mutated solid tumors.

Keywords:
BRAFColon cancerDabrafenibEncorafenibMelanomaMutationNSCLCVemurafenib

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Employing Digital Droplet PCR to Detect BRAF V600E Mutations in Formalin-fixed Paraffin-embedded Reference Standard Cell Lines
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Author Spotlight: Integrating BRET-Based Assays and Rare Mutation Analysis to Decipher RAF Kinase Regulation in Live Cells
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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • BRAF mutations occur in up to 8% of human cancers, presenting a significant therapeutic target.
  • BRAF-targeted therapies (vemurafenib, dabrafenib, encorafenib) have improved outcomes in BRAF-mutated cancers, initially approved for metastatic melanoma.
  • Resistance to BRAF inhibitors is a common limitation, necessitating novel treatment strategies.

Purpose of the Study:

  • To review the prevalence of BRAF mutations across various human cancers.
  • To evaluate the efficacy and safety of current BRAF-targeted therapies and combination strategies.
  • To discuss future directions for treating BRAF-mutated solid tumors, including overcoming resistance.

Main Methods:

  • Literature review of studies on BRAF mutations and targeted therapies.
  • Analysis of clinical trial data for BRAF inhibitors, MEK inhibitors, and EGFR inhibitors.
  • Synthesis of evidence on treatment response, safety profiles, and resistance mechanisms.

Main Results:

  • BRAF inhibitors offer clinical benefit in BRAF-mutated cancers, with improved safety over older treatments.
  • Combination therapy with BRAF and MEK inhibitors delays resistance and enhances efficacy.
  • BRAF inhibitors combined with EGFR inhibitors show significant response in colorectal cancer.

Conclusions:

  • Targeted BRAF inhibition and combination therapies are transforming cancer treatment.
  • Addressing resistance and expanding use to less common mutations and tumor types are crucial for future progress.
  • Continued research into BRAF-mutated cancers will refine treatment strategies and improve patient outcomes.