Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster viewing 06

422P - Molecular mechanism in prostate cancer with TP53 mutation

Date

03 Dec 2022

Session

Poster viewing 06

Topics

Tumour Site

Prostate Cancer

Presenters

Bin Hu

Citation

Annals of Oncology (2022) 33 (suppl_9): S1598-S1618. 10.1016/annonc/annonc1135

Authors

B. Hu1, H. Liu2, Y. Zhang3, H. Wang3

Author affiliations

  • 1 Urinary Surgery, Liaoning Cancer Hospital and Institute, 110801 - Shenyang/CN
  • 2 Department Of Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College - National Cancer Center, Cancer Hospital, 100021 - Beijing/CN
  • 3 Medicine Dept., Beijing Acornmed Biotechnology Co., Ltd., 100176 - Beijing/CN

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 422P

Background

The key roles of the TP53 mutation in cancer have been well established. However, the molecular mechanism differences of prostate cancer (PC) stratified by the TP53 mutation status has not yet been described.

Methods

Patients diagnosed with prostate cancer were enrolled in the study. Tumor tissue and matching blood were sequenced by next-generation sequencing (NGS) techniques with AcornMed panel with 808 cancer-related genes. Comprehensive molecular characterization was analyzed.

Results

A total of 599 patients with PC were enrolled including 90 patients with TP53 mutation (mut) and 509 patients with TP53 wild-type (wt). In TP53 mutation cohorts, the five most frequently mutated genes were TP53 (100%), BRD4 (19%), KMT2D (18%), ATRX (17%), and BRCA2 (15%). For TP53 wt cohorts, the five most frequently mutated genes were BRD4 (18%), AR (14%), FOXA1 (13%), CDK12 (12%), and BBC3 (11%). 88 frequently mutated genes were significant difference between TP53-mut and TP53-wt cohorts, such as KMT2D, ATRX, KMT2C, BRCA2 and PTEN, excluding the TP53 gene. There was no distinct signature between TP53-mut and TP53-wt cohorts. Signature 13 for APOBEC Cytidine Deaminase signatures, signature 5 for aging and signature 6 for defective DNA mismatch repair were only existed in TP53-mut cohorts, whereas signature 1 for spontaneous deamination of 5−methylcytosine and signature 3 for defects in DNA−DSB repair by HR were only discovered in TP53 wildtype cohorts. In the TP53 mutation cohorts, mutated genes were mainly enriched in the cancer pathway, PI3K-Akt signaling pathway, and Ras signaling pathway. However, in the TP53 wildtype cohorts, the primary pathways included the cancer pathway, PI3K-Akt signaling pathway, and Focal adhesion pathway.

Conclusions

There were characterized the genomic differences and similarities, stratified by the TP53 status, which may reflect the PC patients with TP53 mutation harbored specific molecular mechanism.Patients with TP53 wt are more likely to benefit from immunotherapy, PARPI.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

H. Wang: Financial interests, Personal, Full or part-time Employment: Beijing AcornMed Biotechnology Co., Ltd. All other authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.

  • Analytics cookies help us improve our website by collecting and reporting information on its usage.

  • We use marketing cookies to build a profile of you as a user through your actions on our site in order to better understand your interests and provide you with pertinent suggestions.