ArticleCancer research2018
Targeting STAT5 or STAT5-Regulated Pathways Suppresses Leukemogenesis of Ph+ Acute Lymphoblastic Leukemia.
Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Expression and prognostic role of STAT5a across cancer types.Bioscience reports · 2023Pooled it
- Pro-apoptotic and cell cycle-modulating effects of lobaric and rhizocarpic acids in human leukemic cell lines.Molecular biology reports · 2026Article
- Combination of p-STAT5, CRLF2 and copy number alterations as a potential indicator of a high-risk subgroup of acute lymphoblastic leukemia.Discover oncology · 2026Article
- Long-acting IL-7 induces distinct transcriptomic features in peripheral T cells of patients with solid tumors.JCI insight · 2026Article
- BCR::ABL1-Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B-ALL Cells to Enhancer-Targeting Drugs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting STAT5A via CRISPR/Cas9 restores TKI sensitivity in resistant chronic myeloid leukemia cells.Medical oncology (Northwood, London, England) · 2026Article
- Toward a chemotherapy and allo-HSCT free future: the evolution of treatment for Philadelphia chromosome-positive acute lymphoblastic leukemia.Frontiers in immunology · 2026Review
- Counter-Therapeutic Strategies for Resistance of FLT3 Inhibitors in Acute Myeloid Leukemia.Cells · 2025Review
- Targeting senescent stemlike subpopulations in Philadelphia chromosome-like acute lymphoblastic leukemia.Blood · 2025Article
- Differential activation of basal and IL-7-induced PI3K/Akt/ mTOR and JAK/STAT5 signaling distinguishes pediatric from adult acute lymphoblastic leukemia.Haematologica · 2024Article
- JAK/STAT in leukemia: a clinical update.Molecular cancer · 2024Review
- Targeting Pim kinases in hematological cancers: molecular and clinical review.Molecular cancer · 2023Review
- STAT5 confers lactogenic properties in breast tumorigenesis and restricts metastatic potential.Oncogene · 2022Article
- Recent research on the association between signal transducer and activator of transcription 5 and childhood acute lymphoblastic leukemia.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022Review
- Review
- STAT5 inhibitor attenuates atherosclerosis via inhibition of inflammation: the role of STAT5 in atherosclerosis.American journal of translational research · 2021Article
- Article
- Involvement of STAT5 in Oncogenesis.Biomedicines · 2020Review
- Article
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
Abstract
Combining standard cytotoxic chemotherapy with BCR-ABL1 tyrosine kinase inhibitors (TKI) has greatly improved the upfront treatment of patients with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL). However, due to the development of drug resistance through both BCR-ABL1-dependent and -independent mechanisms, prognosis remains poor. The STAT5 transcription factor is activated by BCR-ABL1 and by JAK2-dependent cytokine signaling; therefore, inhibiting its activity could address both mechanisms of resistance in Ph+ ALL. We show here that genetic and pharmacologic inhibition of STAT5 activity suppresses cell growth, induces apoptosis, and inhibits leukemogenesis of Ph+ cell lines and patient-derived newly diagnosed and relapsed/TKI-resistant Ph+ ALL cells
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.