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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...
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In circuit analysis, situations often arise where resistors are neither in series nor parallel configurations. To tackle such scenarios, three-terminal equivalent networks like the wye (Y) (Figure 1 (a)) or tee (T) and delta (Δ) (Figure 1 (b)) or pi (π) networks come into play. These networks offer versatile solutions and are frequently encountered in various applications, including three-phase electrical systems, electrical filters, and matching networks.
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A conductor's DC resistance at a given temperature is influenced by its resistivity, length, and cross-sectional area. Resistivity is an inherent property of the conductor material, with annealed copper serving as the international standard for measurement. For instance, the resistivity of hard-drawn aluminum at 20 degrees Celsius is 61% of the standard conductivity of annealed copper.
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Profiling Prostate Cancer Therapeutic Resistance.

Cameron A Wade1, Natasha Kyprianou2,3,4

  • 1Departments of Urology, University of Kentucky College of Medicine, Lexington, Kentucky, KY 40536, USA. cameron.wade@uky.edu.

International Journal of Molecular Sciences
|March 23, 2018
PubMed
Summary

Therapeutic resistance in advanced prostate cancer is driven by the tumor microenvironment and epithelial-mesenchymal transition (EMT). Targeting EMT-MET dynamics offers a new strategy to overcome treatment resistance in metastatic castration-resistant prostate cancer (mCRPC).

Keywords:
androgen receptorepithelial plasticitymetabolic changestumor landscape

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Area of Science:

  • Oncology
  • Cancer Biology
  • Molecular Therapeutics

Background:

  • Advanced lethal prostate cancer often develops resistance to androgen-deprivation therapy (ADT) and chemotherapy.
  • Therapeutic resistance is influenced by the tumor microenvironment, not solely androgen receptor (AR) signaling.
  • Epithelial-mesenchymal transition (EMT), driven by transforming growth factor-β (TGF-β), promotes cancer cell survival, invasion, and stem cell properties via anoikis resistance.

Purpose of the Study:

  • To review recent evidence on targeting the dynamic interconversions between EMT and mesenchymal-epithelial transition (MET) to overcome therapeutic resistance in prostate cancer.
  • To explore the role of the tumor microenvironment and phenotypic plasticity in conferring treatment resistance.
  • To identify potential new drug targets and therapeutic strategies for advanced, treatment-resistant prostate cancer.

Main Methods:

  • Review of current scientific literature focusing on EMT, MET, anoikis, and the tumor microenvironment in prostate cancer.
  • Analysis of signaling pathways involved in therapeutic resistance, including AR and TGF-β.
  • Discussion of potential therapeutic interventions targeting EMT-MET dynamics and associated biomarkers.

Main Results:

  • EMT facilitates resistance to anoikis, promoting metastasis and chemoresistance through mechanisms like E-cadherin loss.
  • The plasticity of prostate tumor epithelium allows for EMT and MET, contributing to tumor progression and treatment resistance.
  • The lead agent DZ-50 shows potential efficacy in metastatic castration-resistant prostate cancer (mCRPC) by inducing an anoikis-driven therapeutic response.

Conclusions:

  • Targeting the EMT-MET dynamic is a promising strategy to overcome therapeutic resistance in advanced prostate cancer.
  • Understanding the tumor microenvironment's role is crucial for developing effective treatments for resistant prostate cancer.
  • Further research into targeting androgen/AR and TGF-β signaling interactions may optimize therapeutic regimens for mCRPC.