Nature Search

Author Correction: ATF4 couples MYC-dependent translational activity to bioenergetic demands during tumour progression

Feven Tameire
Ioannis I. Verginadis
Constantinos Koumenis
Amendments and Corrections17 Jul 2019
Nature Cell Biology

Volume: 21, P: 1052
A stromal Integrated Stress Response activates perivascular cancer-associated fibroblasts to drive angiogenesis and tumour progression

Verginadis et al. show that ATF4 regulates Col1a1 expression and collagen biosynthesis in perivascular cancer-associated fibroblasts, thereby supporting angiogenesis and progression in melanoma and pancreatic cancer.

Ioannis I. Verginadis
Harris Avgousti
Constantinos Koumenis
ResearchOpen Access02 Jun 2022
Nature Cell Biology

Volume: 24, P: 940-953
ATF4 couples MYC-dependent translational activity to bioenergetic demands during tumour progression

Activating transcription factor 4 (ATF4) promotes MYC-driven tumour progression. Tameire et al. identify ATF4 and its target eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) as regulators of MYC-mediated amino acid biosynthesis and protein synthesis, thereby modulating tumour progression and survival in mice.

Feven Tameire
Ioannis I. Verginadis
Constantinos Koumenis
Research01 Jul 2019
Nature Cell Biology

Volume: 21, P: 889-899
FLASH radiation reprograms lipid metabolism and macrophage immunity and sensitizes medulloblastoma to CAR-T cell therapy

Fan and colleagues show that FLASH radiation promotes proinflammatory polarization of tumor-associated macrophages, which in turn increases T cell influx in medulloblastoma and synergizes with CAR-T cell therapy.

Haiwei Ni
Zachary J. Reitman
Yi Fan
Research05 Feb 2025
Nature Cancer

Volume: 6, P: 460-473
Targeting PARP11 to avert immunosuppression and improve CAR T therapy in solid tumors

Fuchs and colleagues delineate a mechanism by which PARP11-mediated IFNAR1 loss sustains an immunosuppressive tumor microenvironment and show that PARP11 inactivation can enhance chimeric antigen receptor T efficacy in preclinical solid tumor models.

Hongru Zhang
Pengfei Yu
Serge Y. Fuchs
Research30 May 2022
Nature Cancer

Volume: 3, P: 808-820
Activation of p38α stress-activated protein kinase drives the formation of the pre-metastatic niche in the lungs

Gui et al. report that tumor-cell-derived factors induce p38a activation in lung fibroblasts, leading to inactivation of type I interferon signaling, matrix remodeling and neutrophil infiltration, thereby generating a metastasis-permissive niche.

Jun Gui
Farima Zahedi
Serge Y. Fuchs
Research25 May 2020
Nature Cancer

Volume: 1, P: 603-619
Pro-tumorigenic AMPK in glioblastoma

AMPK is a key metabolic sensor promoting cellular energy homeostasis under low-nutrient conditions and other stresses. However, its role in cancer is context-dependent and not fully understood. A study now shows that glioma stem cells co-opt an AMPK-dependent pathway to rewire metabolism, promoting tumour growth.

Nektaria Maria Leli
Constantinos Koumenis
News & Views18 Jun 2018
Nature Cell Biology

Volume: 20, P: 736-737
p53 promotes revival stem cells in the regenerating intestine after severe radiation injury

The tumor suppressor p53 is the guardian of the genome. Here, the authors use comprehensive approaches to demonstrate that transient p53 activity induces revival stem cells to promote the regeneration of severely irradiated intestinal epithelium in mice.

Clara Morral
Arshad Ayyaz
David G. Kirsch
ResearchOpen Access08 Apr 2024
Nature Communications

Volume: 15, P: 1-14
The radiogenomic and spatiogenomic landscapes of glioblastoma and their relationship to oncogenic drivers

Kazerooni et al. explore the associations between tumor imaging and spatial characteristics with cancer gene mutations and the inferred sequence of mutational events. Radiogenomics reflects glioblastoma's molecular heterogeneity and imaging biomarkers and spatial patterns can reveal key oncogenic drivers.

Anahita Fathi Kazerooni
Hamed Akbari
Christos Davatzikos
ResearchOpen Access01 Mar 2025
Communications Medicine

Volume: 5, P: 1-15
A PERK–miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival

PERK regulates tumour cell survival. Bu et al. show that the unfolded protein response protein PERK induces miR-211 repression of the circadian factor Bmal1 to regulate protein synthesis and stress responses, contributing to tumour progression.

Yiwen Bu
Akihiro Yoshida
J. Alan Diehl
Research11 Dec 2017
Nature Cell Biology

Volume: 20, P: 104-115
Signaling through alternative Integrated Stress Response pathways compensates for GCN2 loss in a mouse model of soft tissue sarcoma

Stacey L. Lehman
Sandra Ryeom
Constantinos Koumenis
ResearchOpen Access30 Jun 2015
Scientific Reports

Volume: 5, P: 1-13
Integrating imaging and genomic data for the discovery of distinct glioblastoma subtypes: a joint learning approach

Jun Guo
Anahita Fathi Kazerooni
Christos Davatzikos
ResearchOpen Access28 Feb 2024
Scientific Reports

Volume: 14, P: 1-11
Loss of AID exacerbates the malignant progression of CLL

Avery C. Lee
Sai Ravi Pingali
Chih-Hang Anthony Tang
ResearchOpen Access30 Aug 2022
Leukemia

Volume: 36, P: 2430-2442
Combination of CHEK1/2 inhibition and ionizing radiation results in abscopal tumor response through increased micronuclei formation

Hann-Hsiang Chao
Ilias V. Karagounis
Amit Maity
Research25 Apr 2020
Oncogene

Volume: 39, P: 4344-4357
YAP1 enhances NF-κB-dependent and independent effects on clock-mediated unfolded protein responses and autophagy in sarcoma

Adrian Rivera-Reyes
Shuai Ye
T. S. Karin Eisinger-Mathason
ResearchOpen Access31 Oct 2018
Cell Death & Disease

Volume: 9, P: 1-17

Search

Filter By:

Search

Quick links