Integrated clinicomolecular characterization identifies RAS activation and CDKN2A deletion as independent adverse prognostic factors in cancer of unknown primary.


Journal

International journal of cancer
ISSN: 1097-0215
Titre abrégé: Int J Cancer
Pays: United States
ID NLM: 0042124

Informations de publication

Date de publication:
01 06 2020
Historique:
received: 31 10 2019
revised: 08 01 2020
accepted: 09 01 2020
pubmed: 24 1 2020
medline: 8 1 2021
entrez: 24 1 2020
Statut: ppublish

Résumé

Cancer of unknown primary (CUP) denotes a malignancy with histologically confirmed metastatic spread while the primary tumor remains elusive. Here, we address prognostic and therapeutic implications of mutations and copy number variations (CNVs) detected in tumor tissue in the context of a comprehensive clinical risk assessment. Targeted panel sequencing was performed in 252 CUP patients. 71.8% of patients had unfavorable CUP according to ESMO guidelines. 74.7% were adeno- and 13.7% squamous cell carcinomas. DNA was extracted from microdissected formalin-fixed, paraffin-embedded tissues. For library preparation, mostly multiplex PCR-based Ion Torrent AmpliSeq™ technology with Oncomine comprehensive assays was used. Most frequent genetic alterations were mutations/deletions of TP53 (49.6%), CDKN2A (19.0%) and NOTCH1 (14.1%) as well as oncogenic activation of KRAS (23.4%), FGFR4 (14.9%) and PIK3CA (10.7%). KRAS activation was predominantly found in adenocarcinomas (p = 0.01), PIK3CA activation in squamous cell carcinomas (p = 0.03). Male sex, high ECOG score, unfavorable CUP, higher number of involved organs and RAS activation predicted decreased event-free and overall survival in multivariate analysis. Deletions of CDKN2A were prognostically adverse regarding overall survival. TP53 mutations did not significantly influence prognosis in the overall cohort, but worsened prognosis in otherwise favorable CUP subtypes. Although not standard in CUP, for 17/198 (8.6%) patients molecularly targeted treatment was recommended and 10 patients (5.1%) were treated accordingly. In conclusion, besides the identification of drug targets, panel sequencing in CUP is prognostically relevant, with RAS activation and CDKN2A deletion emerging as novel independent risk factors in a comprehensive assessment with clinicopathological data.

Identifiants

pubmed: 31970771
doi: 10.1002/ijc.32882
doi:

Substances chimiques

CDKN2A protein, human 0
Cyclin-Dependent Kinase Inhibitor p16 0
KRAS protein, human 0
NOTCH1 protein, human 0
Receptor, Notch1 0
TP53 protein, human 0
Tumor Suppressor Protein p53 0
Class I Phosphatidylinositol 3-Kinases EC 2.7.1.137
PIK3CA protein, human EC 2.7.1.137
FGFR4 protein, human EC 2.7.10.1
Receptor, Fibroblast Growth Factor, Type 4 EC 2.7.10.1
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3053-3064

Informations de copyright

© 2020 UICC.

Références

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Auteurs

Tilmann Bochtler (T)

Clinical Cooperation Unit Molecular Hematology/Oncology, German Cancer Research Center (DKFZ) and Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Department of Thoracic Oncology, Thoraxklinik Heidelberg, Heidelberg, Germany.
Translational Lung Research Center Heidelberg (TLRC-H), Member of the German Center for Lung Research (DZL), Germany.
Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.

Anna Reiling (A)

Clinical Cooperation Unit Molecular Hematology/Oncology, German Cancer Research Center (DKFZ) and Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.

Volker Endris (V)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
German Cancer Consortium (DKTK), Germany.

Thomas Hielscher (T)

Division of Biostatistics, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Anna-Lena Volckmar (AL)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Olaf Neumann (O)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Martina Kirchner (M)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Jan Budczies (J)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Lukas C Heukamp (LC)

Institute for Haematopathology Hamburg, Hamburg, Germany.

Jonas Leichsenring (J)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Michael Allgäuer (M)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Daniel Kazdal (D)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Harald Löffler (H)

Clinical Cooperation Unit Molecular Hematology/Oncology, German Cancer Research Center (DKFZ) and Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Marienhospital Stuttgart, Stuttgart, Germany.

Wilko Weichert (W)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
German Cancer Consortium (DKTK), Germany.
Institute of Pathology, Technical University Munich, Munich, Germany.

Peter Schirmacher (P)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.

Albrecht Stenzinger (A)

Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
German Cancer Consortium (DKTK), Germany.

Alwin Krämer (A)

Clinical Cooperation Unit Molecular Hematology/Oncology, German Cancer Research Center (DKFZ) and Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.
Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany.

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