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Poster Display session

498P - Predictive modeling of oncogenic RNA expression using DNA alterations: Insights from Asian rare cancer patients

Date

07 Dec 2024

Session

Poster Display session

Presenters

Kathleen de Almeida

Citation

Annals of Oncology (2024) 35 (suppl_4): S1580-S1594. 10.1016/annonc/annonc1694

Authors

K.Y. de Almeida1, H.S. Okuma2, M.S. Imasa3, P. Voon4, S.H. Hwoei Fen5, T.W. Chen6, S. Yusak7, R. Ramachandran8, N. Abu Bakar9, M. Chen10, K. Nakamura1, K. Yonemori1

Author affiliations

  • 1 Department Of International Clinical Development, NCCH - National Cancer Center Hospital-Tsukiji Campus, 104-0045 - Chuo-ku/JP
  • 2 Department Of International Clinical Development, National Cancer Center - Tsukiji Campus, 104-0045 - Chuo-ku/JP
  • 3 Cancer Institute, St. Luke's Medical Center - Quezon City, 1112 - Quezon City/PH
  • 4 Department Radiotherapy, Oncology And Palliative Care, Sarawak General Hospital, 93586 - Kuching/MY
  • 5 Department Of Oncology, Radiotherapy And Palliative Care, Penang General Hospital, 10990 - Pulau Pinang/MY
  • 6 Oncology Department, NTU - National Taiwan University - College of Medicine, 10051 - Taipei City/TW
  • 7 Radiotherapy And Oncology Dept, National Cancer Institute, 62250 - Putrajaya/MY
  • 8 Oncology And Radiotherapy Dept., UMMC - University Malaya Medical Centre, 59100 - Kuala Lumpur/MY
  • 9 Department Of Radiotherapy And Oncology, General Hospital Kuala Lumpur, 50586 - Kuala Lumpur/MY
  • 10 Oncology Department, Taipei Veterans General Hospital, 11217 - Taipei City/TW

Resources

This content is available to ESMO members and event participants.

Abstract 498P

Background

Rare cancers, defined as malignant tumors with an incidence of less than 6 per 100,000 individuals per year, are complex for diagnosis and treatment due to limited clinical data. However, pan-cancer analysis suggests consistent mutational processes across diverse cancer types, offering insights into universal cancer mechanisms, regardless of their origin. To understand molecular mechanisms and inform personalized treatment strategies, this study aimed to analyze predictive models of oncogenic RNA expression based on DNA mutations, using multi-omics data from Asian rare cancer patients.

Methods

This research was a observational prospective study from the MASTER KEY Asia project, involving hospitals from Malaysia, the Philippines, and Taiwan. DNA and RNA were extracted from formalin-fixed paraffin-embedded (FFPE) specimens for next-generation sequencing (NGS) analysis using the TOP2 panel, alongside the evaluation of clinicopathological data for 128 rare cancer patients (50 ± 15 years old). RNA oncogene expression was analyzed using TPM Z-scores and Stepwise Linear Regression assessed the use of DNA alterations as predictive factors.

Results

DNA alterations predicted the RNA expression of 15 oncogenes/tumor suppressor genes. Higher BRCA1 expression correlated (p=0.001, R2 0.103) with alterations in PIK3CA (OR: 2.025, p=0.001) and KMT2D (OR: 1.696, p=0.008). ERBB2 expression was associated (p<0.001; R2 0.198) with alterations in ERBB2 (OR: 4.844, p=0.001) and ARID1A (OR: 3.110, p<0.001). TP53 alterations predicted lower expression of MDM2 (p<0.001, R2 0.143, OR: -3.159 of z-score). Patients with BRCA1 overexpression and DNA alterations in either PIK3CA or KMT2D had a higher frequency of disease progression after drug treatment (p=0.008). Additionally, patients with TP53 gain of function had a higher rate of disease progression (p=0.007), with a trend of higher MDM2 expression compared to TP53 loss of function (p=0.08).

Conclusions

In this study, DNA alterations effectively predicted the RNA expression of some oncogenes. This genomic analysis uncovers significant associations that can inform targeted therapies and personalized treatment strategies, improving outcomes for patients with rare cancers.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Daiichi Sankyo, Eisai, Otsuka Pharmaceutical.

Disclosure

All authors have declared no conflicts of interest.

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