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Related Concept Videos

Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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 specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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 specific...

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Related Experiment Video

Updated: May 9, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

A STATement on vemurafenib-resistant melanoma.

Edward J Hartsough1, Andrew E Aplin

  • 1Department of Cancer Biology and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. ejh004@Jefferson.edu

The Journal of Investigative Dermatology
|July 17, 2013
PubMed
Summary

Acquired resistance to BRAF inhibitors in melanoma can be overcome by targeting signal transducer and activator of transcription 3 (STAT3) and paired box 3 (PAX3) signaling pathways, offering new therapeutic strategies.

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Last Updated: May 9, 2026

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Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma
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Published on: September 8, 2021

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Late-stage melanomas with mutant BRAF (V600E/K) have advanced treatment options.
  • Acquired resistance to BRAF inhibitors like vemurafenib remains a significant challenge in melanoma treatment.
  • Resistance mechanisms are diverse, necessitating broad therapeutic strategies.

Purpose of the Study:

  • To investigate the role of signal transducer and activator of transcription 3 (STAT3)-paired box 3 (PAX3) signaling in acquired resistance to BRAF inhibitors.
  • To explore STAT3-targeted therapies as a potential strategy to overcome vemurafenib resistance in melanomas.

Main Methods:

  • Analysis of melanoma cell lines exhibiting acquired resistance to vemurafenib.
  • Investigating the involvement of STAT3 and PAX3 signaling pathways.
  • Evaluating the efficacy of STAT3-targeted therapies.

Main Results:

  • The study identifies STAT3-PAX3 signaling as a potential mechanism driving acquired resistance to vemurafenib in melanomas.
  • Targeting STAT3 demonstrates potential in overcoming this resistance.

Conclusions:

  • STAT3-PAX3 signaling is implicated in vemurafenib resistance in melanoma.
  • STAT3-targeted therapies represent a promising approach to overcome acquired resistance and improve treatment outcomes for melanoma patients.