PuSH - Publication Server of Helmholtz Zentrum München: Interleukin-1β provided by KIT-competent mast cells is required for KRAS-mutant lung adenocarcinoma.

Navigation

Home

Deutsch

Research

Advanced Search

Browse by ...

... Journal

... Publication Type

... Research Data

... Publication Year

Publication overview

Support & Contact

Contact persons

Help

Data protection

Lilis, I.* ; Ntaliarda, G.* ; Papaleonidopoulos, V.* ; Giotopoulou, G.A.* ; Oplopoiou, M.* ; Marazioti, A.* ; Spella, M.* ; Marwitz, S.* ; Goldmann, T.* ; Bravou, V.* ; Giopanou, I.* ; Stathopoulos, G.T.

Interleukin-1β provided by KIT-competent mast cells is required for KRAS-mutant lung adenocarcinoma.

OncoImmunology 8:1593802 (2019)

Publ. Version/Full Text

DOI

PMC

	Open Access Gold (Paid Option)

Abstract
Metrics
Extra information

Mast cells (MC) have been identified in human lung adenocarcinoma (LADC) tissues, but their functional role has not been investigated in vivo. For this, we applied three mouse models of KRAS-mutant LADC to two different MC-deficient mouse strains (cKit^Wsh and Cpa3.Cre). Moreover, we derived MC gene signatures from murine bone marrow-derived MC and used them to interrogate five human cohorts of LADC patients. Tumor-free cKit^Wsh and Cpa3.Cre mice were deficient in alveolar and skin KIT-dependent (KIT+) MC, but cKit^Wsh mice retained normal KIT-independent (KIT-) MC in the airways. Both KIT+ and KIT- MC infiltrated murine LADC to varying degrees, but KIT+ MC were more abundant and promoted LADC initiation and progression through interleukin-1β secretion. KIT+ MC and their transcriptional signature were significantly enriched in human LADC compared to adjacent normal tissue, especially in the subset of patients with KRAS mutations. Importantly, MC density increased with tumor stage and high overall expression of the KIT+ MC signature portended poor survival. Collectively, our results indicate that KIT+ MC foster LADC development and represent marked therapeutic targets.

Altmetric

Additional Metrics?

[➜Log in]

Edit extra informations Login

Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords 1β/lung Cancer/urethane ; Carboxypeptidase 3/mutation/il; Cancer; Gene; Deficient; Mice; Classification; Angiogenesis; Macrophages; Recruitment; Expression; Hallmarks

ISSN (print) / ISBN 2162-4011

e-ISSN 2162-402X

Journal OncoImmunology

Quellenangaben Volume: 8, Issue: 7, Article Number: 1593802

Publisher Taylor & Francis

Publishing Place Philadelphia

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Lung Health and Immunity (LHI)