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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
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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.
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  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Prostate Cancer Research: Tools, Cell Types, And Molecular Targets.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Prostate Cancer Research: Tools, Cell Types, And Molecular Targets.

Related Experiment Video

Pre-clinical Orthotopic Murine Model of Human Prostate Cancer
07:01

Pre-clinical Orthotopic Murine Model of Human Prostate Cancer

Published on: August 29, 2016

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Prostate cancer research: tools, cell types, and molecular targets.

Alvin Y Liu1

  • 1Department of Urology, Institute of Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA, United States.

Frontiers in Oncology
|April 10, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Prostate tumors contain diverse cancer cell types. Proenkephalin (PENK) can induce differentiation in stem-like prostate cancer cells by targeting stem cell transcription factors (scTF), offering a new therapeutic avenue.

Keywords:
AGR2 immunotherapycancer cell reprogrammingcancer differentiationdifferentiation therapy

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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Author Spotlight: Advancing Prostate Cancer Research Through Improved Tissue Sampling and Biobanking
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Author Spotlight: Advancing Prostate Cancer Research Through Improved Tissue Sampling and Biobanking

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Author Spotlight: Advancing Prostate Cancer Research Through Improved Tissue Sampling and Biobanking
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Author Spotlight: Advancing Prostate Cancer Research Through Improved Tissue Sampling and Biobanking

Published on: November 17, 2023

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Cell Biology

Background:

  • Prostate tumors exhibit heterogeneity, comprising luminal-like adenocarcinoma and less differentiated, stem-like non-adenocarcinoma and small cell carcinoma.
  • Dedifferentiation from luminal-like to stem-like phenotypes is driven by stem cell transcription factors (scTF) like LIN28A, NANOG, POU5F1, and SOX2, leading to β2-microglobulin (B2M) downregulation.

Purpose of the Study:

  • To investigate the role of stromal signaling, specifically proenkephalin (PENK), in regulating prostate cancer cell differentiation.
  • To explore therapeutic strategies targeting distinct prostate cancer cell types, including stem-like and adenocarcinoma cells.

Main Methods:

  • Investigated the effect of PENK on scTF and B2M expression in stem-like small cell carcinoma LuCaP 145.1 cells.
lineage relationship
stem cell transcription factors
stromal PENK
  • Utilized scTF and PENK transfection to induce dedifferentiation and differentiation in prostate cancer cells.
  • Examined extracellular anterior gradient 2 (eAGR2) as a targetable adenocarcinoma antigen.

    • Main Results:

    • PENK treatment downregulated scTF and upregulated B2M in stem-like cells, indicating a shift towards differentiation.
    • Prostate cancer cells could be reprogrammed to a dedifferentiated state by scTF transfection and subsequently differentiated by PENK transfection.
    • Extracellular AGR2 (eAGR2) is identified as a cancer-specific antigen on differentiated adenocarcinoma cells, while stem-like cells are AGR2-negative.

    Conclusions:

    • PENK acts as a differentiation-inducing factor for stem-like prostate cancer cells by modulating scTF and B2M.
    • Targeting scTF with factors like PENK presents a potential differentiation therapy for AGR2-negative, stem-like prostate cancers.
    • Therapeutic strategies should consider the distinct cell types within prostate tumors, leveraging antigens like eAGR2 for adenocarcinoma and PENK for stem-like cells.