Discover Community Create You

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

Article

A metabolic synthetic lethality of phosphoinositide 3-kinase-driven cancer

4 Mar 2025

Abstract excerpt

The deregulated activation of the phosphoinositide 3-kinase (PI3K) pathway is a hallmark of aggressive tumors with metabolic plasticity, eliciting their adaptation to the microenvironment and resistance to chemotherapy. A significant gap lies between the biological features of PI3K-driven tumors and the specific targeting of their vulnerabilities. Here, we explore the metabolic liabilities of PI3K-altered T-cell...

Read the complete abstract on PubMed

Topics

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

Share to Acute Myeloid Leukemia Research
Share to Cancer, Hypoxia, and Metabolism
Share to Hematopoietic Stem Cell Transplantation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 40038309
DOI: 10.1038/s41467-025-57225-7

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A metabolic synthetic lethality of phosphoinositide 3-kinase-driven cancerPMID 40038309Read ↗

Metabolic reprogramming in the tumour microenvironment: a hallmark shared by cancer cells and T lymphocytes.Semantic proximity Read ↗

WEE1 inhibition induces glutamine addiction in T-cell acute lymphoblastic leukemiaSemantic proximity Read ↗

Mechanisms of T‑cell metabolic reprogramming in the microenvironment of acute myeloid leukemia and its therapeutic potential (Review)Semantic proximity Read ↗

Glutaminolysis is a metabolic dependency in FLT3ITD acute myeloid leukemia unmasked by FLT3 tyrosine kinase inhibition.Semantic proximity Read ↗

Metabolic Reprogramming in Hematologic Malignancies: Advances and Clinical PerspectivesSemantic proximity Read ↗

Exploiting metabolic vulnerabilities for personalized therapy in acute myeloid leukemiaSemantic proximity Read ↗

The Glycolytic Gatekeeper PDK1 defines different metabolic states between genetically distinct subtypes of human acute myeloid leukemia.Semantic proximity Read ↗

The metabolic alterations of cancer cells.Semantic proximity Read ↗

Cancer Metabolism: Phenotype, Signaling and Therapeutic Targets.Semantic proximity Read ↗

Metabolic reprogramming in cancer: unraveling the role of glutamine in tumorigenesis.Semantic proximity Read ↗

Metabolic reprogramming in KRAS-mutant cancers: Proven targetable vulnerabilities and potential therapeutic strategies.Semantic proximity Read ↗

Adapt and conquer: Metabolic flexibility in cancer growth, invasion and evasion.Semantic proximity Read ↗

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