Related Experiment Video

Updated: May 25, 2026

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays
07:42

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays

Published on: September 19, 2018

Oncogene-specific activation of tyrosine kinase networks during prostate cancer progression

Justin M Drake1, Nicholas A Graham, Tanya Stoyanova

  • 1Department of Microbiology, Immunology, and Molecular Genetics, Crump Institute for Molecular Imaging, Institute for Molecular Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

Proceedings of the National Academy of Sciences of the United States of America
|February 7, 2012
PubMed

Insights

Advanced prostate cancer shows increased tyrosine phosphorylation, even without specific mutations. This study identified key activated tyrosine kinases, suggesting new therapeutic targets for tyrosine kinase inhibitors in prostate cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Tyrosine kinase mutations are uncommon in prostate cancer.
  • Castration-resistant prostate cancer (CRPC) in humans shows elevated tyrosine phosphorylation.
  • The role of tyrosine kinase activity in prostate cancer progression, independent of specific mutations, remains unclear.

Purpose of the Study:

  • To investigate tyrosine kinase activity in prostate cancer progression.
  • To identify specific activated tyrosine kinases in the absence of dominant mutations or DNA amplification.
  • To explore potential therapeutic strategies targeting tyrosine kinases in advanced prostate cancer.

Main Methods:

  • Generation of a mouse model for prostate cancer progression using non-tyrosine kinase oncogenes.
  • Phosphotyrosine peptide enrichment and quantitative mass spectrometry.
  • Kinase:substrate relationship analysis.

Main Results:

  • Significant upregulation of tyrosine phosphorylation observed at the carcinoma stage in the mouse model.
  • Identification of activated tyrosine kinases including EGFR, EPHA2, JAK2, ABL1, and SRC.
  • Specific tyrosine kinase signatures linked to oncogene activation were detected.

Conclusions:

  • Elevated tyrosine kinase signaling is a feature of advanced prostate cancer.
  • Specific tyrosine kinase pathways are activated in genetically defined prostate cancer models.
  • Targeting these identified tyrosine kinases with inhibitors may offer novel therapeutic approaches for advanced prostate cancer.

More Related Videos

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer07:25

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

Isolation, Culture, and Characterization of Prostate Cancer-Associated Fibroblasts09:43

Isolation, Culture, and Characterization of Prostate Cancer-Associated Fibroblasts

Published on: August 1, 2025

Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...