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Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV

On the basis of TP53 mutations and standardized uptake values (SUVs) from 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET), we sought to enhance our knowledge of the biology underlying low progesterone receptor (PR) expression in estrogen receptor (ER)-positive/human epidermal growt...

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Autores principales: Ahn, Sung Gwe, Yoon, Chang Ik, Lee, Jae Hoon, Lee, Hye Sun, Park, So Eun, Cha, Yoon Jin, Cha, Chihwan, Bae, Soong June, Lee, Kyung-A, Jeong, Joon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bioscientifica Ltd 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347277/
https://www.ncbi.nlm.nih.gov/pubmed/30407916
http://dx.doi.org/10.1530/ERC-18-0281
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author Ahn, Sung Gwe
Yoon, Chang Ik
Lee, Jae Hoon
Lee, Hye Sun
Park, So Eun
Cha, Yoon Jin
Cha, Chihwan
Bae, Soong June
Lee, Kyung-A
Jeong, Joon
author_facet Ahn, Sung Gwe
Yoon, Chang Ik
Lee, Jae Hoon
Lee, Hye Sun
Park, So Eun
Cha, Yoon Jin
Cha, Chihwan
Bae, Soong June
Lee, Kyung-A
Jeong, Joon
author_sort Ahn, Sung Gwe
collection PubMed
description On the basis of TP53 mutations and standardized uptake values (SUVs) from 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET), we sought to enhance our knowledge of the biology underlying low progesterone receptor (PR) expression in estrogen receptor (ER)-positive/human epidermal growth factor receptor-2 (HER2)-negative tumors. This study included 272 patients surgically treated for ER-positive, HER2-negative breast cancer and who had undergone TP53 gene sequencing. Of these, 229 patients also underwent 18F-FDG PET or PET/CT. Mutational analysis of exons 5–9 of the TP53 gene was conducted using PCR amplification and direct sequencing. The SUVs were measured using 18F-FDG-PET scan images. Twenty-eight (10.3%) tumors had a somatic TP53 mutation. The TP53 mutation rate was significantly higher in low-PR tumors than in high-PR tumors (17.1% vs 7.9%, P = 0.039). Low-PR tumors had significantly higher median SUVs than high-PR tumors (P = 0.046). The multivariable analysis revealed that SUV and age remained independent variables associated with low PR expression. An adverse impact of low PR expression on recurrence-free survival was observed in the multivariable Cox regression hazard model. We provide clinical evidence that genetic alteration of the TP53 gene and dysregulated glucose metabolism partly involve low PR expression in ER-positive and HER2-negative breast cancer.
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spelling pubmed-63472772019-01-29 Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV Ahn, Sung Gwe Yoon, Chang Ik Lee, Jae Hoon Lee, Hye Sun Park, So Eun Cha, Yoon Jin Cha, Chihwan Bae, Soong June Lee, Kyung-A Jeong, Joon Endocr Relat Cancer Research On the basis of TP53 mutations and standardized uptake values (SUVs) from 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET), we sought to enhance our knowledge of the biology underlying low progesterone receptor (PR) expression in estrogen receptor (ER)-positive/human epidermal growth factor receptor-2 (HER2)-negative tumors. This study included 272 patients surgically treated for ER-positive, HER2-negative breast cancer and who had undergone TP53 gene sequencing. Of these, 229 patients also underwent 18F-FDG PET or PET/CT. Mutational analysis of exons 5–9 of the TP53 gene was conducted using PCR amplification and direct sequencing. The SUVs were measured using 18F-FDG-PET scan images. Twenty-eight (10.3%) tumors had a somatic TP53 mutation. The TP53 mutation rate was significantly higher in low-PR tumors than in high-PR tumors (17.1% vs 7.9%, P = 0.039). Low-PR tumors had significantly higher median SUVs than high-PR tumors (P = 0.046). The multivariable analysis revealed that SUV and age remained independent variables associated with low PR expression. An adverse impact of low PR expression on recurrence-free survival was observed in the multivariable Cox regression hazard model. We provide clinical evidence that genetic alteration of the TP53 gene and dysregulated glucose metabolism partly involve low PR expression in ER-positive and HER2-negative breast cancer. Bioscientifica Ltd 2018-11-08 /pmc/articles/PMC6347277/ /pubmed/30407916 http://dx.doi.org/10.1530/ERC-18-0281 Text en © 2019 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 Research
Ahn, Sung Gwe
Yoon, Chang Ik
Lee, Jae Hoon
Lee, Hye Sun
Park, So Eun
Cha, Yoon Jin
Cha, Chihwan
Bae, Soong June
Lee, Kyung-A
Jeong, Joon
Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV
title Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV
title_full Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV
title_fullStr Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV
title_full_unstemmed Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV
title_short Low PR in ER(+)/HER2(−) breast cancer: high rates of TP53 mutation and high SUV
title_sort low pr in er(+)/her2(−) breast cancer: high rates of tp53 mutation and high suv
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347277/
https://www.ncbi.nlm.nih.gov/pubmed/30407916
http://dx.doi.org/10.1530/ERC-18-0281
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