Nature Search

Kupffer cell programming by maternal obesity triggers fatty liver disease

In a mouse model, maternal obesity during pregnancy can lead to fatty liver disease in the offspring, driven by aberrant developmental programming of Kuppfer cells.

Hao Huang
Nora R. Balzer
Elvira Mass
ResearchOpen Access18 Jun 2025
Nature

P: 1-9
Anaplastic large cell lymphoma: the current state of play from a European prospective as presented at the second annual meeting of the European Research Initiative on ALCL, 27–28 June 2011

O Merkel
L Kenner
S D Turner
Editorial14 Dec 2011
Leukemia

Volume: 25, P: 1795-1796
Super-enhancer-based identification of a BATF3/IL-2R−module reveals vulnerabilities in anaplastic large cell lymphoma

Anaplastic large cell lymphoma (ALCL) is an aggressive T-cell lymphoma often with poor prognosis. To identify genes defining ALCL cell state and dependencies, the authors here characterize ALCL-specific super-enhancers and describe the BATF3/IL-2R−module as a therapeutic opportunity for ALCL.

Huan-Chang Liang
Mariantonia Costanza
Olaf Merkel
ResearchOpen Access22 Sept 2021
Nature Communications

Volume: 12, P: 1-12
Correction: Corrigendum: Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins

Rainer Zenz
Robert Eferl
Erwin F. Wagner
Amendments and Corrections30 Mar 2006
Nature

Volume: 440, P: 708
The targetable kinase PIM1 drives ALK inhibitor resistance in high-risk neuroblastoma independent of MYCN status

Anaplastic lymphoma kinase (ALK) inhibitors are currently being considered in neuroblastoma (NB), but its acquired resistance is reported in non-small cell lung cancers. Here, the authors have found PIM1 overexpression decreases sensitivity to ALK inhibitors in NB and combined ALK and PIM1 inhibition enhances anti-tumour efficacy in vitro and in PDX models.

Ricky M. Trigg
Liam C. Lee
Suzanne D. Turner
ResearchOpen Access28 Nov 2019
Nature Communications

Volume: 10, P: 1-13
Erratum: STAT3 regulated ARF expression suppresses prostate cancer metastasis

Jan Pencik
Michaela Schlederer
Lukas Kenner
Amendments and CorrectionsOpen Access26 Oct 2015
Nature Communications

Volume: 6, P: 1
STAT3 regulated ARF expression suppresses prostate cancer metastasis

IL6-STAT3 signaling is activated in prostate cancer, however inhibiting this pathway has not lead to a survival advantage in patients. Here, Pencik et al.show that loss of the IL6-STAT3 axis in mice and humans leads to metastasis due to loss of ARF, unravelling STAT3 and ARF as potential prognostic markers in prostate cancer.

Jan Pencik
Michaela Schlederer
Lukas Kenner
ResearchOpen Access22 Jul 2015
Nature Communications

Volume: 6, P: 1-15
A dual role for autophagy in a murine model of lung cancer

Autophagy prolongs the survival of cells in stressful conditions but its role in cancer is unclear. Here, Rao et al. show that loss of the autophagic protein Atg5 enhanced cancer incidence but impaired tumour progression in a mouse model of lung cancer.

Shuan Rao
Luigi Tortola
Josef M. Penninger
Research20 Jan 2014
Nature Communications

Volume: 5, P: 1-15
Screening for oncogenic AF1q expression predicts disease recurrence in gastric cancer patients

Elisabeth S. Gruber
Georg Oberhuber
Lukas Kenner
ResearchOpen Access10 Jul 2024
Scientific Reports

Volume: 14, P: 1-8
Targeting NRAS via miR-1304-5p or farnesyltransferase inhibition confers sensitivity to ALK inhibitors in ALK-mutant neuroblastoma

Targeting oncogenic ALK activity in neuroblastoma is an attractive therapeutic strategy but success has been limited by resistance to ALK inhibitors. Here, the authors identify loss of miR-1304-5p as a driver of ALK inhibitor resistance via regulation of NRAS, and therapeutically target this axis with the addition of a farnesyltransferase inhibitor in preclinical models of neuroblastoma.

Perla Pucci
Liam C. Lee
Suzanne D. Turner
ResearchOpen Access23 Apr 2024
Nature Communications

Volume: 15, P: 1-19
A mouse model to identify cooperating signaling pathways in cancer

The mouse cancer model 'Multi-Hit' allows for the evaluation of oncogene cooperativities in tumor development based on stochastic Cre-recombination events. Cells with cooperating oncogenes are positively selected and give rise to tumors. The approach is used to study Ras downstream effector pathways in tumorigenesis.

Monica Musteanu
Leander Blaas
Robert Eferl
Research05 Aug 2012
Nature Methods

Volume: 9, P: 897-900
A modular self-adjuvanting cancer vaccine combined with an oncolytic vaccine induces potent antitumor immunity

Successful cancer immune therapy correlates with a T cell-inflamed tumour microenvironment. Authors show here that co-administration of a self-adjuvanting protein vaccine and an antigen-expressing oncolytic virus in an optimised regimen strongly enhances T cell immunogenicity and may turn non-inflamed tumours proinflammatory and less resistant to checkpoint blockade therapy.

Krishna Das
Elodie Belnoue
Guido Wollmann
ResearchOpen Access31 Aug 2021
Nature Communications

Volume: 12, P: 1-14
The adsorption of drugs on nanoplastics has severe biological impact

Leonard Dick
Patrick R. Batista
Oldamur Hollóczki
ResearchOpen Access28 Oct 2024
Scientific Reports

Volume: 14, P: 1-17
Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis

STAT3 is an intracellular transducer of cytokine signals that cooperates with Ras in tumour formation and is often activated in lung cancer. Here the authors show that STAT3 acts as a tumour suppressor in a mouse model of Kras-driven lung adenocarcinoma.

Beatrice Grabner
Daniel Schramek
Emilio Casanova
ResearchOpen Access03 Mar 2015
Nature Communications

Volume: 6, P: 1-14
Cold aortic flush after ventricular fibrillation cardiac arrest reduces inflammatory reaction but not neuronal loss in the pig cerebral cortex

Lisa Barones
Wolfgang Weihs
Sandra Högler
ResearchOpen Access04 Apr 2025
Scientific Reports

Volume: 15, P: 1-14
RANK links thymic regulatory T cells to fetal loss and gestational diabetes in pregnancy

RANK promotes the hormone-mediated development of thymic regulatory T cells during pregnancy; loss of RANK is associated with impaired maturation of maternal regulatory T cells, leading to fetal loss and the development of gestational diabetes.

Magdalena Paolino
Rubina Koglgruber
Josef M. Penninger
Research23 Dec 2020
Nature

Volume: 589, P: 442-447
Structural and functional consequences of the STAT5B^N642H driver mutation

Hyper-activated STAT5B and its disease-causing variants are of interest as cancer drug targets. Here the authors combine cell based studies, X-ray crystallography, biophysical experiments and MD simulations to structurally and functionally characterize the STAT5B^N642H mutant found in aggressive T-cell leukemia and lymphomas and find that it has an increased affinity for self-dimerization.

Elvin D. de Araujo
Fettah Erdogan
Patrick T. Gunning
ResearchOpen Access07 Jun 2019
Nature Communications

Volume: 10, P: 1-15
Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins

Rainer Zenz
Robert Eferl
Erwin F. Wagner
Research15 Sept 2005
Nature

Volume: 437, P: 369-375
Anaplastic large cell lymphoma arises in thymocytes and requires transient TCR expression for thymic egress

Anaplastic large cell lymphoma is characterized by an NPM–ALK fusion but the cell of origin for this cancer is unclear. Here, the authors show that, in an NPM–ALK mouse model, the tumours likely arise from early thmyocytes and require an initial burst of TCR signalling for initiation.

Tim I. M. Malcolm
Patrick Villarese
Suzanne D. Turner
ResearchOpen Access12 Jan 2016
Nature Communications

Volume: 7, P: 1-12
p38α suppresses normal and cancer cell proliferation by antagonizing the JNK–c-Jun pathway

Lijian Hui
Latifa Bakiri
Erwin F Wagner
Research29 Apr 2007
Nature Genetics

Volume: 39, P: 741-749
Overexpression of LAPTM4B-35 is a negative prognostic factor in head and neck squamous cell carcinoma

Ulana Kotowski
Lorenz Kadletz
Gregor Heiduschka
ResearchOpen Access11 Dec 2019
Scientific Reports

Volume: 9, P: 1-8
PDGFR blockade is a rational and effective therapy for NPM-ALK–driven lymphomas

Anaplastic large cell lymphomas (ALCL) often express the oncoprotein NPM-ALK. This study shows that the activator protein 1 family members JUN and JUNB promote lymphoma development through platelet-derived growth factor receptor-β (PDGFRB). Inhibition of PDGFRB prolonged survival of NPM-ALK transgenic mice and increased the efficacy of an ALK-specific inhibitor against transplanted NPM-ALK tumors. Inhibition of PDGFR in a patient with ALCL also resulted in rapid, complete and sustained remission.

Daniela Laimer
Helmut Dolznig
Lukas Kenner
Research14 Oct 2012
Nature Medicine

Volume: 18, P: 1699-1704
Dependency on the TYK2/STAT1/MCL1 axis in anaplastic large cell lymphoma

Nicole Prutsch
Elisabeth Gurnhofer
Olaf Merkel
ResearchOpen Access21 Aug 2018
Leukemia

Volume: 33, P: 696-709
Retraction Note: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation

Tahereh Javaheri
Zahra Kazemi
Richard Moriggl
Amendments and CorrectionsOpen Access13 Aug 2019
Cell Death & Disease

Volume: 10, P: 1
Correction: Dependency on the TYK2/STAT1/MCL1 axis in anaplastic large cell lymphoma

Nicole Prutsch
Elisabeth Gurnhofer
Olaf Merkel
Amendments and CorrectionsOpen Access14 Jul 2020
Leukemia

Volume: 34, P: 3105
Epidermal JunB represses G-CSF transcription and affects haematopoiesis and bone formation

Arabella Meixner
Rainer Zenz
Erwin F. Wagner
Research20 Jul 2008
Nature Cell Biology

Volume: 10, P: 1003-1011
Osteoclast differentiation factor RANKL controls development of progestin-driven mammary cancer

Progestins, used in contraceptives and hormone replacement therapy, have been linked to breast cancer. These authors provide a mechanistic basis for this association. They show in a mouse model that synthetic progestins can promote mammary tumour formation by inducing RANKL (receptor activator of NF-KB ligand), which acts on mammary epithelial cells through the RANKL receptor RANK.

Daniel Schramek
Andreas Leibbrandt
Josef M. Penninger
Research29 Sept 2010
Nature

Volume: 468, P: 98-102
The AP-1-BATF and -BATF3 module is essential for growth, survival and TH17/ILC3 skewing of anaplastic large cell lymphoma

Nikolai Schleussner
Olaf Merkel
Stephan Mathas
ResearchOpen Access28 Mar 2018
Leukemia

Volume: 32, P: 1994-2007
Immunosuppressive plasma cells impede T-cell-dependent immunogenic chemotherapy

IgA plasmocytes are shown to promote resistance to the immunogenic chemotherapeutic oxaliplatin in prostate cancer mouse models by inhibiting activation of cytotoxic T cells; immunosuppressive plasma cells, which are also found in human-therapy-resistant prostate cancer, are generated in response to TGFβ, and their functionality depends on PD-L1 expression and IL-10 secretion.

Shabnam Shalapour
Joan Font-Burgada
Michael Karin
Research29 Apr 2015
Nature

Volume: 521, P: 94-98
Parathyroid hormone induces a browning program in human white adipocytes

Oana C. Hedesan
Anna Fenzl
Florian W. Kiefer
Research05 Dec 2018
International Journal of Obesity

Volume: 43, P: 1319-1324
TYK2 licenses non-canonical inflammasome activation during endotoxemia

Andrea Poelzl
Caroline Lassnig
Birgit Strobl
Research14 Sept 2020
Cell Death & Differentiation

Volume: 28, P: 748-763
IDO1⁺ Paneth cells promote immune escape of colorectal cancer

Pflügler, Svinka et al. identify a subset of Paneth cells in mouse intestinal crypts and tumors, which express the immune checkpoint molecule Ido1 in a Stat1-dependent manner and promote tumor growth. Gene expression data from human colorectal cancer (CRC) suggest that a similar population is present in human cancer and opens the door for further studies of immune escape mechanisms in CRC.

Sandra Pflügler
Jasmin Svinka
Robert Eferl
ResearchOpen Access22 May 2020
Communications Biology

Volume: 3, P: 1-14
STAT3 promotes melanoma metastasis by CEBP-induced repression of the MITF pathway

Alexander Swoboda
Robert Soukup
Richard Moriggl
Research15 Dec 2020
Oncogene

Volume: 40, P: 1091-1105
YAP/TAZ inhibition reduces metastatic potential of Ewing sarcoma cells

Lisa Bierbaumer
Anna M. Katschnig
Heinrich Kovar
ResearchOpen Access08 Jan 2021
Oncogenesis

Volume: 10, P: 1-13
AIF-regulated oxidative phosphorylation supports lung cancer development

Shuan Rao
Laura Mondragón
Josef M. Penninger
ResearchOpen Access27 May 2019
Cell Research

Volume: 29, P: 579-591
Absence of PD-L1 on tumor cells is associated with reduced MHC I expression and PD-L1 expression increases in recurrent serous ovarian cancer

Stefanie Aust
Sophie Felix
Dietmar Pils
ResearchOpen Access07 Mar 2017
Scientific Reports

Volume: 7, P: 1-12
Hepatic Deletion of Janus Kinase 2 Counteracts Oxidative Stress in Mice

Madeleine Themanns
Kristina M. Mueller
Richard Moriggl
ResearchOpen Access07 Oct 2016
Scientific Reports

Volume: 6, P: 1-13
RETRACTED ARTICLE: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation

Tahereh Javaheri
Zahra Kazemi
Richard Moriggl
ResearchOpen Access13 Oct 2016
Cell Death & Disease

Volume: 7, P: e2419
Correction: Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation

Tahereh Javaheri
Zahra Kazemi
Richard Moriggl
Amendments and CorrectionsOpen Access23 Jul 2018
Cell Death & Disease

Volume: 9, P: 1-2
JunB and PTEN in prostate cancer: ‘loss is nothing else than change’

P Birner
G Egger
L Kenner
Editorial09 Mar 2015
Cell Death & Differentiation

Volume: 22, P: 522-523
Longitudinal study of murine microbiota activity and interactions with the host during acute inflammation and recovery

Clarissa Schwab
David Berry
Tim Urich
ResearchOpen Access09 Jan 2014
The ISME Journal

Volume: 8, P: 1101-1114
RANKL/RANK control Brca1 mutation-driven mammary tumors

Verena Sigl
Kwadwo Owusu-Boaitey
Josef M Penninger
ResearchOpen Access31 May 2016
Cell Research

Volume: 26, P: 761-774
Phylotype-level 16S rRNA analysis reveals new bacterial indicators of health state in acute murine colitis

David Berry
Clarissa Schwab
Alexander Loy
Research10 May 2012
The ISME Journal

Volume: 6, P: 2091-2106

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