Lineage plasticity-mediated therapy resistance in prostate cancer

Alexandra Blee, Haojie Huang

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Therapy resistance is a significant challenge for prostate cancer treatment in clinic. Although targeted therapies such as androgen deprivation and androgen receptor (AR) inhibition are effective initially, tumor cells eventually evade these strategies through multiple mechanisms. Lineage reprogramming in response to hormone therapy represents a key mechanism that is increasingly observed. The studies in this area have revealed specific combinations of alterations present in adenocarcinomas that provide cells with the ability to transdifferentiate and perpetuate AR-independent tumor growth after androgen-based therapies. Interestingly, several master regulators have been identified that drive plasticity, some of which also play key roles during development and differentiation of the cell lineages in the normal prostate. Thus, further study of each AR-independent tumor type and understanding underlying mechanisms are warranted to develop combinational therapies that combat lineage plasticity in prostate cancer.

Original languageEnglish (US)
Pages (from-to)241-248
Number of pages8
JournalAsian Journal of Andrology
Volume21
Issue number3
DOIs
StatePublished - May 1 2019

Fingerprint

Prostatic Neoplasms
Androgen Receptors
Androgens
Therapeutics
Neoplasms
Cell Lineage
Prostate
Adenocarcinoma
Hormones
Growth

Keywords

  • Lineage plasticity
  • Neuroendocrine
  • Prostate cancer
  • Therapy resistance
  • Transdifferentiation

ASJC Scopus subject areas

  • Urology

Cite this

Lineage plasticity-mediated therapy resistance in prostate cancer. / Blee, Alexandra; Huang, Haojie.

In: Asian Journal of Andrology, Vol. 21, No. 3, 01.05.2019, p. 241-248.

Research output: Contribution to journalReview article

@article{a4d0bc3447f14cc3955908cd41cd0361,
title = "Lineage plasticity-mediated therapy resistance in prostate cancer",
abstract = "Therapy resistance is a significant challenge for prostate cancer treatment in clinic. Although targeted therapies such as androgen deprivation and androgen receptor (AR) inhibition are effective initially, tumor cells eventually evade these strategies through multiple mechanisms. Lineage reprogramming in response to hormone therapy represents a key mechanism that is increasingly observed. The studies in this area have revealed specific combinations of alterations present in adenocarcinomas that provide cells with the ability to transdifferentiate and perpetuate AR-independent tumor growth after androgen-based therapies. Interestingly, several master regulators have been identified that drive plasticity, some of which also play key roles during development and differentiation of the cell lineages in the normal prostate. Thus, further study of each AR-independent tumor type and understanding underlying mechanisms are warranted to develop combinational therapies that combat lineage plasticity in prostate cancer.",
keywords = "Lineage plasticity, Neuroendocrine, Prostate cancer, Therapy resistance, Transdifferentiation",
author = "Alexandra Blee and Haojie Huang",
year = "2019",
month = "5",
day = "1",
doi = "10.4103/aja.aja_41_18",
language = "English (US)",
volume = "21",
pages = "241--248",
journal = "Asian Journal of Andrology",
issn = "1008-682X",
publisher = "Nature Publishing Group",
number = "3",

}

TY - JOUR

T1 - Lineage plasticity-mediated therapy resistance in prostate cancer

AU - Blee, Alexandra

AU - Huang, Haojie

PY - 2019/5/1

Y1 - 2019/5/1

N2 - Therapy resistance is a significant challenge for prostate cancer treatment in clinic. Although targeted therapies such as androgen deprivation and androgen receptor (AR) inhibition are effective initially, tumor cells eventually evade these strategies through multiple mechanisms. Lineage reprogramming in response to hormone therapy represents a key mechanism that is increasingly observed. The studies in this area have revealed specific combinations of alterations present in adenocarcinomas that provide cells with the ability to transdifferentiate and perpetuate AR-independent tumor growth after androgen-based therapies. Interestingly, several master regulators have been identified that drive plasticity, some of which also play key roles during development and differentiation of the cell lineages in the normal prostate. Thus, further study of each AR-independent tumor type and understanding underlying mechanisms are warranted to develop combinational therapies that combat lineage plasticity in prostate cancer.

AB - Therapy resistance is a significant challenge for prostate cancer treatment in clinic. Although targeted therapies such as androgen deprivation and androgen receptor (AR) inhibition are effective initially, tumor cells eventually evade these strategies through multiple mechanisms. Lineage reprogramming in response to hormone therapy represents a key mechanism that is increasingly observed. The studies in this area have revealed specific combinations of alterations present in adenocarcinomas that provide cells with the ability to transdifferentiate and perpetuate AR-independent tumor growth after androgen-based therapies. Interestingly, several master regulators have been identified that drive plasticity, some of which also play key roles during development and differentiation of the cell lineages in the normal prostate. Thus, further study of each AR-independent tumor type and understanding underlying mechanisms are warranted to develop combinational therapies that combat lineage plasticity in prostate cancer.

KW - Lineage plasticity

KW - Neuroendocrine

KW - Prostate cancer

KW - Therapy resistance

KW - Transdifferentiation

UR - http://www.scopus.com/inward/record.url?scp=85064839376&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85064839376&partnerID=8YFLogxK

U2 - 10.4103/aja.aja_41_18

DO - 10.4103/aja.aja_41_18

M3 - Review article

VL - 21

SP - 241

EP - 248

JO - Asian Journal of Andrology

JF - Asian Journal of Andrology

SN - 1008-682X

IS - 3

ER -