Showing posts with label Androgen receptor. Show all posts
Showing posts with label Androgen receptor. Show all posts

Sunday, 30 March 2025

Addressing Racial Disparities in Quadruple-Negative Breast Cancer: Insights Into Aggressive Biology, Therapeutic Targets, and Prevention Strategies |Chapter 3 | Disease and Health: Research Developments Vol. 7

Black/African-American (AA) women, relative to their White/European-American (EA) counterparts, experience disproportionately high breast cancer mortality. Central to this survival disparity, Black/AA women have an unequal burden of aggressive breast cancer subtypes, such as triple-negative breast cancer (ER/PR-, HER2-wild type; TNBC). TNBC is inherently more clinically aggressive than the other breast cancer subtypes as evidenced by the higher frequency of metastasis and recurrence within 5 years of diagnosis. While TNBC has been well characterized, recent studies have identified a highly aggressive androgen receptor (AR)-negative subtype of TNBC, quadruple-negative breast cancer (ER/PR-, HER2-wildtype, AR-; QNBC). QNBCs are significantly more aggressive than AR-positive TNBCs. QNBC is increasingly recognized as an aggressive, hard-to-treat breast cancer subtype. Similar to TNBC, QNBC disproportionately impacts Black/AA women and likely plays an important role in the breast cancer survival disparities experienced by Black/AA women. Here, a discussion has been developed on the racial disparities of QNBC and molecular signaling pathways that may contribute to the aggressive biology of QNBC in Black/AA women. This study intends to spotlight potential prevention and therapeutic targets for Black/AA QNBC; ultimately the goal of this study is to provide greater insight into reducing the breast cancer survival burden experienced by Black/AA women. Non-genetic risk factors include lifestyle, socioeconomic status, access to quality oncological care, reproductive factors, anthropometrics, and comorbidities have long been reported to contribute to the gap in survival rates between Black/AA and White/EA women with breast cancer. The Potential Role of Non-Genetic Risk Factors in the Racially Disparate Burden in QNBC is also discussed here. Addressing the racial disparity in the highly aggressive breast cancer subtype, QNBC could significantly contribute to reducing the racially disparate burden of breast cancer.

 

Author (s) Details

 

Nikita Jinna
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA.

 

Tijana Jovanovic- Talisman
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Mark LaBarge
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Rama Natarajan
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Rick Kittles
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Christopher Sistrunk
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA.

 

Padmashree Rida
Novazoi Theranostics, Salt Lake City, UT 84105, USA.

 

Victoria L. Seewaldt
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrd/v7/4732

Tuesday, 2 April 2024

Genetic Variants as a Prostate Cancer Risk | Chapter 11 | New Visions in Medicine and Medical Science Vol. 2

 Prostate cancer is one of the most frequent and potentially fatal cancers in males globally. Prostate cancer is a multifactorial disease caused by the interaction of one or more factors. In prostate cancer, several genetic alterations are involved. Due to their high complexity, these genetic modifications must be taken into consideration. These alterations not only account for a large portion of cancer deaths but also have a major impact on the effectiveness of medication. A significant challenge with advanced disease is that many hypothesized underlying pathways remain unknown or inadequately understood due to insufficient evidence. This chapter presents the available data on related pathways (DNA damage repair, androgen receptor and tumor suppression), examining each genetic anomaly (somatic copy number alterations, structural rearrangements, point mutations, SNPs, miRNA) and other related factors (P13K pathway, epigenetics, apoptosis inhibition, oxidative damage) that could be connected to the carcinogenesis of prostate cancer.


Author(s) Details:

Pradhumn,
Department of Genetics, Maharshi Dayanand University, Rohtak, Haryana-124001, India.

Preeti Chauhan,
Department of Biotechnology, CCT, Chandigarh Group of Colleges, Landran, Mohali, Chandigarh-140307, India.

Shalu Ranga,
Department of Genetics, Maharshi Dayanand University, Rohtak, Haryana-124001, India.

Ritu Yadav,
Department of Genetics, Maharshi Dayanand University, Rohtak, Haryana-124001, India.

Please see the link here: https://stm.bookpi.org/NVMMS-V2/article/view/13806