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Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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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NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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mTOR Signaling and Cancer Progression

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An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas
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Published on: October 10, 2025

TORC1 is essential for NF1-associated malignancies.

Cory M Johannessen1, Bryan W Johnson, Sybil M Genther Williams

  • 1Genetics Division, Department of Medicine, Brigham and Women's Hospital, Ludwig Center at Dana-Farber/Harvard Cancer Center, Harvard Medical School, Boston, Massachusetts 02115, USA.

Current Biology : CB
|January 1, 2008
PubMed
Summary

Rapamycin, an mTOR inhibitor, effectively suppresses aggressive neurofibromatosis type 1 (NF1) tumors in mice. This targeted therapy shows promise for treating NF1-associated malignancies, highlighting a novel therapeutic strategy.

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Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Published on: May 17, 2024

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Neurofibromatosis type 1 (NF1) is a common familial cancer syndrome caused by inactivating mutations in the NF1 gene.
  • The NF1 protein acts as a Ras GTPase-activating protein (RasGAP), and its deficiency leads to aberrant Ras activation in tumors.
  • The specific effector pathways driving NF1-deficient tumorigenesis remain largely unknown.

Purpose of the Study:

  • To investigate the role of mammalian target of rapamycin (mTOR) signaling in NF1-associated tumor development.
  • To evaluate the efficacy of mTOR inhibitors as a targeted therapy for aggressive NF1 malignancies.
  • To elucidate the mechanisms of action for mTOR inhibitors in NF1-deficient tumors.

Main Methods:

  • Utilized a genetically engineered murine model of aggressive NF1-associated malignancies.
  • Administered the mTOR inhibitor rapamycin to assess its effect on tumor growth.
  • Analyzed downstream signaling pathways, including HIF-1alpha, AKT, and Cyclin D1, to understand rapamycin's mechanism of action.

Main Results:

  • Rapamycin significantly suppressed the growth of aggressive NF1-associated malignancies in the murine model.
  • Rapamycin's tumor suppressive effects were not mediated by the inhibition of HIF-1alpha or indirect suppression of AKT.
  • Rapamycin effectively suppressed the mTOR target Cyclin D1 in these tumors.

Conclusions:

  • mTOR pathway activity is essential for tumorigenesis in NF1-deficient cancers.
  • mTOR inhibitors represent a potential targeted therapy for NF1-associated malignancies.
  • The mechanism of action for mTOR inhibitors can vary across different cancer types, suggesting limitations for current biomarkers like HIF-1alpha suppression.