Clinical and Biological Insight into MAPK Signaling and Tumor Heterogeneity Using Circulating Tumor Biomarkers

Abstract

Prostate cancer is a leading cause of cancer-related mortality in men. Although therapies that inhibit androgen receptor (AR) activity are initially effective, patients ultimately succumb to metastatic castration resistant prostate cancer (mCRPC). The molecular events leading to this are incompletely understood. There is a need for minimally invasive means to obtain tumor information to overcome these knowledge gaps. Circulating tumor cells (CTCs) are cells that break away from either the primary tumor or metastatic sites. Moreover, serial CTC analyses performed in the context of treatment changes can characterize the mutational landscape of tumors as they evolve, particularly for novel agents such as MEK inhibitors. However, the profiles of sensitivity or resistance to MEK inhibition are unknown, particularly as the tumor may evolve in response to treatment. We have begun to obtain blood samples from patients on a trial of MEK inhibition in prostate cancer to identify molecular predictors of sensitivity/resistance. These studies will also help us better understand the molecular basis of sensitivity or resistance to MEK inhibitors, which will help to provide new scientific insights into the pathogenesis of advanced prostate cancer and provide ideas of novel approaches that can be used to treat such tumors.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2018
Accession Number
AD1071921

Entities

People

  • Rajan P Kulkarni

Organizations

  • University of California, Los Angeles

Tags

DTIC Thesaurus Topics

  • Androgen Receptors
  • Androgens
  • Biological Markers
  • Biomedical Research
  • Castration
  • Data Analysis
  • Diseases And Disorders
  • Heterogeneity
  • Inhibition
  • Inhibitors
  • Neoplasms
  • Professional Development
  • Prostate
  • Prostate Cancer
  • Resistance
  • Sensitivity
  • Tissues

Fields of Study

  • Medicine

Readers

  • Oncology
  • Prostate Cancer Biology.