Cargando…

A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers

Prostate and breast cancer are the two cancers with the highest incidence in men and women, respectively. Here, we focus on the known biology of acquired resistance to antihormone therapy of prostate and breast cancer and compare laboratory and clinical similarities in the evolution of the disease....

Descripción completa

Detalles Bibliográficos
Autores principales: Maximov, Philipp Y, Abderrahman, Balkees, Curpan, Ramona F, Hawsawi, Yousef M, Fan, Ping, Jordan, V Craig
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bioscientifica Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5771961/
https://www.ncbi.nlm.nih.gov/pubmed/29162647
http://dx.doi.org/10.1530/ERC-17-0416
_version_ 1783293329053581312
author Maximov, Philipp Y
Abderrahman, Balkees
Curpan, Ramona F
Hawsawi, Yousef M
Fan, Ping
Jordan, V Craig
author_facet Maximov, Philipp Y
Abderrahman, Balkees
Curpan, Ramona F
Hawsawi, Yousef M
Fan, Ping
Jordan, V Craig
author_sort Maximov, Philipp Y
collection PubMed
description Prostate and breast cancer are the two cancers with the highest incidence in men and women, respectively. Here, we focus on the known biology of acquired resistance to antihormone therapy of prostate and breast cancer and compare laboratory and clinical similarities in the evolution of the disease. Laboratory studies and clinical observations in prostate and breast cancer demonstrate that cell selection pathways occur during acquired resistance to antihormonal therapy. Following sex steroid deprivation, both prostate and breast cancer models show an initial increased acquired sensitivity to the growth potential of sex steroids. Subsequently, prostate and breast cancer cells either become dependent upon the antihormone treatment or grow spontaneously in the absence of hormones. Paradoxically, the physiologic sex steroids now kill a proportion of selected, but vulnerable, resistant tumor cells. The sex steroid receptor complex triggers apoptosis. We draw parallels between acquired resistance in prostate and breast cancer to sex steroid deprivation. Clinical observations and patient trials confirm the veracity of the laboratory studies. We consider therapeutic strategies to increase response rates in clinical trials of metastatic disease that can subsequently be applied as a preemptive salvage adjuvant therapy. The goal of future advances is to enhance response rates and deploy a safe strategy earlier in the treatment plan to save lives. The introduction of a simple evidence-based enhanced adjuvant therapy as a global healthcare strategy has the potential to control recurrence, reduce hospitalization, reduce healthcare costs and maintain a healthier population that contributes to society.
format Online
Article
Text
id pubmed-5771961
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher Bioscientifica Ltd
record_format MEDLINE/PubMed
spelling pubmed-57719612018-01-24 A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers Maximov, Philipp Y Abderrahman, Balkees Curpan, Ramona F Hawsawi, Yousef M Fan, Ping Jordan, V Craig Endocr Relat Cancer Review Prostate and breast cancer are the two cancers with the highest incidence in men and women, respectively. Here, we focus on the known biology of acquired resistance to antihormone therapy of prostate and breast cancer and compare laboratory and clinical similarities in the evolution of the disease. Laboratory studies and clinical observations in prostate and breast cancer demonstrate that cell selection pathways occur during acquired resistance to antihormonal therapy. Following sex steroid deprivation, both prostate and breast cancer models show an initial increased acquired sensitivity to the growth potential of sex steroids. Subsequently, prostate and breast cancer cells either become dependent upon the antihormone treatment or grow spontaneously in the absence of hormones. Paradoxically, the physiologic sex steroids now kill a proportion of selected, but vulnerable, resistant tumor cells. The sex steroid receptor complex triggers apoptosis. We draw parallels between acquired resistance in prostate and breast cancer to sex steroid deprivation. Clinical observations and patient trials confirm the veracity of the laboratory studies. We consider therapeutic strategies to increase response rates in clinical trials of metastatic disease that can subsequently be applied as a preemptive salvage adjuvant therapy. The goal of future advances is to enhance response rates and deploy a safe strategy earlier in the treatment plan to save lives. The introduction of a simple evidence-based enhanced adjuvant therapy as a global healthcare strategy has the potential to control recurrence, reduce hospitalization, reduce healthcare costs and maintain a healthier population that contributes to society. Bioscientifica Ltd 2017-11-21 /pmc/articles/PMC5771961/ /pubmed/29162647 http://dx.doi.org/10.1530/ERC-17-0416 Text en © 2018 The authors http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review
Maximov, Philipp Y
Abderrahman, Balkees
Curpan, Ramona F
Hawsawi, Yousef M
Fan, Ping
Jordan, V Craig
A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers
title A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers
title_full A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers
title_fullStr A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers
title_full_unstemmed A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers
title_short A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers
title_sort unifying biology of sex steroid-induced apoptosis in prostate and breast cancers
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5771961/
https://www.ncbi.nlm.nih.gov/pubmed/29162647
http://dx.doi.org/10.1530/ERC-17-0416
work_keys_str_mv AT maximovphilippy aunifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT abderrahmanbalkees aunifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT curpanramonaf aunifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT hawsawiyousefm aunifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT fanping aunifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT jordanvcraig aunifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT maximovphilippy unifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT abderrahmanbalkees unifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT curpanramonaf unifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT hawsawiyousefm unifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT fanping unifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers
AT jordanvcraig unifyingbiologyofsexsteroidinducedapoptosisinprostateandbreastcancers