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Poster session 12

1731P - Lung cancer predisposition in Li-Fraumeni syndrome: Cohort from Gustave Roussy Institute

Date

10 Sep 2022

Session

Poster session 12

Topics

Cancer Biology;  Laboratory Diagnostics;  Pathology/Molecular Biology;  Molecular Oncology;  Genetic and Genomic Testing

Tumour Site

Non-Small Cell Lung Cancer

Presenters

Hela Sassi

Citation

Annals of Oncology (2022) 33 (suppl_7): S772-S784. 10.1016/annonc/annonc1079

Authors

H. Sassi1, D. Vasseur1, L. Mezquita2, D. Planchard3, B. Besse3, B. Bressac1, A. Fievet1, O. Cabaret1, M.A. Robert De Rancher1, S. COTTERET1, V. Goldbarg4, O. Caron4, J. Scoazec1, L. lacroix1, E. Rouleau1

Author affiliations

  • 1 Medical Biology And Pathology Department, Institut Gustave Roussy, 94805 - Villejuif/FR
  • 2 Medical Oncology, Hospital Clinic y Provincial de Barcelona, 08036 - Barcelona/ES
  • 3 Thoracic Oncology Group, Cancer Medicine Department, Institut Gustave Roussy, 94805 - Villejuif/FR
  • 4 Oncogenetic Department, Institut Gustave Roussy, 94805 - Villejuif/FR

Resources

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Abstract 1731P

Background

Li–Fraumeni syndrome (LFS) is a rare autosomal hereditary predisposition to multiples cancers, mainly affecting young individuals. It is characterized by a broad tumor spectrum, comprising early breast cancers (BC), sarcomas, adrenocortical tumors and brain tumors.

Methods

Retrospective study of clinical and genetic results of LFS patients with non-small-cell lung carcinoma (NSCLC).

Results

We reviewed medical reports of 194 LFS patients (105 index cases + 89 relatives) harboring 82 distinct TP53 germline variants with a follow-up at Gustave Roussy (1976-2021). We found 10 LFS patients with NSCLC, from 10 different families, 6M/4F, median age of 48y. These patients carried 10 distinct TP53 germline variants: p.(Val73fs), p.(Thr125=), p.(Arg196*), p.(His214fs), c.783-1G>A, p.(Arg267Gly), p.(Cys275Ser), p.(Arg282Gly), p.(Arg282Pro) and p.(Arg337His). For available personal and family cancers, Chompret criteria were fulfilled in 6/10, patients were non-smoker (5/6) with late onset advanced-stage disease (4/6) and adenocarcinoma subtype (6/6). BC was common among female patients. All six profiled tumors showed oncogenic somatic mutations in EGFR: p.(Leu858Arg) (1/6), exon 20 insertion(1/6), exon 19 deletion(4/6) with EGFR p.(Thr790Met) mutation in (3/6) cases and two of which had a concurrently PIK3CA mutation p.(Glu545Asp) and p.(His1047Arg).

Conclusions

NSCLC is known to occur in a rare proportion of LFS patients with frequently the variant p.(Arg337His) and with an enrichment of EGFR somatic alterations lung adenocarcinoma. Our study showed the diversity of germline TP53 variants associated with NSCLC and confirm the presence of the oncogenic dependency on EGFR somatic mutations. Face to a lung cancer, alterations in ATM, BRCA2 and EGFR gene p.(Thr790Met) in TKI-naïve patients with NSCLC should open the possibility of germline mutations with lung cancer predisposition. The TP53 gene is also a candidate for this risk.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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