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Related Experiment Video

Updated: Feb 26, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

BDNF: An Oncogene or Tumor Suppressor?

Daniel P Radin¹, Parth Patel²

¹Department of Pharmacology, Stony Brook University School of Medicine, Stony Brook, NY, U.S.A. danradin1@gmail.com.

Anticancer Research

|July 26, 2017

Summary

This summary is machine-generated.

Brain-derived neurotrophic factor (BDNF) and its receptor TrkB are implicated in cancer. While TrkB inhibitors show promise, new research suggests BDNF may enhance anti-tumor immunity and chemosensitivity.

Keywords:

BDNF EGFR PI3K RhoA Trkb chemotherapeutic resistance review

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Published on: August 25, 2021

Area of Science:

Neuroscience
Oncology
Molecular Biology

Background:

Neurotrophins, including brain-derived neurotrophic factor (BDNF), regulate central nervous system development via tyrosine kinase receptors like TrkB.
TrkB signaling, particularly through the PI3K/Akt pathway, is frequently upregulated in cancers, contributing to aggressive phenotypes and chemotherapy resistance.
Emerging evidence indicates hypothalamic BDNF may possess immunoaugmenting properties and reduce chemotherapy resistance.

Purpose of the Study:

To analyze the physiological consequences of TrkB receptor activation in vitro.
To discuss the dynamic effects of TrkB activation in vivo.
To propose a clinical strategy for enhancing hypothalamic BDNF to leverage its oncolytic potential.

Main Methods:

In vitro analysis of TrkB receptor activation.
In vivo studies on the dynamic consequences of TrkB activation.
Exploration of methods to increase hypothalamic BDNF expression.

Main Results:

TrkB receptor activation has significant physiological consequences both in vitro and in vivo.
Overexpression of BDNF in the hypothalamus may enhance anti-tumor immune responses.
Hypothalamic BDNF may reduce the activity of proteins conferring chemotherapy resistance.

Conclusions:

TrkB and BDNF play complex roles in cancer, with potential for both promoting resistance and enhancing anti-tumor immunity.
Targeting TrkB signaling and leveraging BDNF's immunoaugmenting properties represent potential therapeutic strategies.
Increasing hypothalamic BDNF offers a clinically feasible approach to enhance cancer treatment efficacy.