Somatic mTOR mutation in clonally expanded T lymphocytes associated with chronic graft versus host disease.

doi:10.1038/s41467-020-16115-w

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Somatic mTOR mutation in clonally expanded T lymphocytes associated with chronic graft versus host disease.

Nature communications - 7 May 2020

Kim Daehong, Park Giljun, Huuhtanen Jani, Lundgren Sofie, Khajuria Rajiv K, Hurtado Ana M, Muñoz-Calleja Cecilia, Cardeñoso Laura, Gómez-García de Soria Valle, Chen-Liang Tzu Hua, Eldfors Samuli, Ellonen Pekka, Hannula Sari, Kankainen Matti, Bruck Oscar, Kreutzman Anna, Salmenniemi Urpu, Lönnberg Tapio, Jerez Andrés, Itälä-Remes Maija, Myllymäki Mikko, Keränen Mikko A I, Mustjoki Satu

Abstract excerpt

Graft versus host disease (GvHD) is the main complication of allogeneic hematopoietic stem cell transplantation (HSCT). Here we report studies of a patient with chronic GvHD (cGvHD) carrying persistent CD4+ T cell clonal expansion harboring somatic mTOR, NFKB2, and TLR2 mutations. In the screening cohort (n = 134), we detect the mTOR P2229R kinase domain mutation in two additional cGvHD patients, but not in...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Blotting, Western

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Proliferation

Share to Graft vs Host Disease

Share to HEK293 Cells

Share to Immunity, Cellular

Share to Immunoprecipitation

Share to T-Lymphocytes

Share to TOR Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 32382059
DOI: 10.1038/s41467-020-16115-w
PMCID: PMC7206083

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Somatic mTOR mutation in clonally expanded T lymphocytes associated with chronic graft versus host disease.PMID 32382059Read ↗

Somatic Mutations in Clonally Expanded T-lymphocytes in Patients with Chronic Graft-Versus-Host DiseaseSemantic proximity Read ↗

A diverse array of cancer-associated MTOR mutations are hyperactivating and can predict rapamycin sensitivity.Semantic proximity Read ↗

TSC2 S1365A mutation potently regulates CD8+ T cell function and differentiation and improves adoptive cellular cancer therapy.Semantic proximity Read ↗

mTOR activation is a biomarker and a central pathway to autoimmune disorders, cancer, obesity, and agingSemantic proximity Read ↗

New Mechanisms of mTOR Pathway Activation in KIT-mutant Malignant GISTs.Semantic proximity Read ↗

mTORC1 upregulates B7-H3/CD276 to inhibit antitumor T cells and drive tumor immune evasionSemantic proximity Read ↗

The Multifunctional Role of mTOR in Innate Immunity: Implications for Transplant ImmunitySemantic proximity Read ↗

Targeting the mTOR Pathway in LeukemiaSemantic proximity Read ↗

Genetic polymorphisms of mTOR and cancer risk: a systematic review and updated meta-analysis.Semantic proximity Read ↗

Hyperactive mTOR pathway promotes lymphoproliferation and abnormal differentiation in autoimmune lymphoproliferative syndromeSemantic proximity Read ↗

Midkine expression by stem-like tumor cells drives persistence to mTOR inhibition and rewires the microenvironment toward an immune-suppressive stateSemantic proximity Read ↗

Signaling Node at TSC2 S1365 Potently Regulates T-Cell Differentiation and Improves Adoptive Cellular Cancer TherapySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.