Clinical and Translational Research
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Feb 24, 2022; 13(2): 135-146
Published online Feb 24, 2022. doi: 10.5306/wjco.v13.i2.135
Neurotrophic receptor tyrosine kinase family members in secretory and non-secretory breast carcinomas
Athina Stravodimou, Ioannis A Voutsadakis
Athina Stravodimou, Department of Medical Oncology, CHUV, Lausanne 1011, Switzerland
Ioannis A Voutsadakis, Department of Medical Oncology, Sault Area Hospital, Sault Ste Marie P6B0A8, Ontario, Canada
Author contributions: Both authors contributed to the conception of the study, literature review, data analysis, writing of the article and revising the article.
Institutional review board statement: No institutional review board approval was required or obtained as the study was not a clinical trial.
Clinical trial registration statement: This study was not registered as a clinical trial as it includes only data from publicly available previously published studies and no new patient information.
Informed consent statement: No informed consents have been obtained for this study as no new patients were included. The study analyzed publicly available data from previously published studies.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ioannis A Voutsadakis, MD, PhD, Associate Professor, Doctor, Department of Medical Oncology, Sault Area Hospital, 750 Great Northern Road, Sault Ste Marie P6B0A8, Ontario, Canada. ivoutsadakis@yahoo.com
Received: April 5, 2021
Peer-review started: April 5, 2021
First decision: July 6, 2021
Revised: July 11, 2021
Accepted: January 13, 2022
Article in press: January 13, 2022
Published online: February 24, 2022
ARTICLE HIGHLIGHTS
Research background

Breast cancer is a common female cancer. It constitutes a major cause of morbidity and mortality. Progress in breast cancer therapeutics has been attained with the introduction of targeted therapies for specific sub-sets. However, other breast cancer subsets lack targeted therapeutics.

Research motivation

Personalized therapies for breast cancer have the potential to improve outcomes. These therapies take consideration of specific molecular abnormalities that could be targeted for optimal results.

Research objectives

This article aims to analyze the landscape of neurotrophic receptor tyrosine kinase (NTRK) abnormalities in breast cancer. These are molecular lesions in a family of receptor tyrosine kinases. Specific drug inhibitors have been developed and have obtained regulatory approval, paving the way for effective patient treatment.

Research methods

An analysis of publicly available genomic breast cancer datasets was performed for identification and characterization of cases with fusions and other molecular abnormalities involving NTRK1, NTRK2 and NTRK3 genes.

Research results

NTRK fusions are rare in breast cancers as a whole. They are present in a small number of breast cancers at the extensive GENIE project data set which contains more than 10000 breast cancers. These cases are not identified as secretory in the database.

Research conclusions

NTRK lesions other than fusions are more common than fusions in breast cancers. However, confirmation of efficacy for the currently available inhibitors exist only for NTRK fusions.

Research perspectives

Amplifications of NTRK receptor genes are more common than fusions in breast cancers. Inhibitors effective for interfering with the activity of amplified NTRK receptors could advance therapeutics in this subset of breast cancers.