Blood malignancies arise from the dysregulation of haematopoiesis. The type of blood cell and the specific order of oncogenic events initiating abnormal growth ultimately determine the cancer subtype and subsequent clinical outcome. HOXA9 plays an important role in acute myeloid leukaemia (AML) prognosis by promoting blood cell expansion and altering differentiation; however, the function of HOXA9 in other blood malignancies is still unclear. Here, we highlight the biological switch and prognosis marker properties of HOXA9 in AML and chronic myeloproliferative neoplasms (MPN). First, we establish the ability of HOXA9 to stratify AML patients with distinct cellular and clinical outcomes. Then, through the use of a computational network model of MPN, we show that the self-activation of HOXA9 and its relationship to JAK2 and TET2 can explain the branching progression of JAK2/TET2 mutant MPN patients towards divergent clinical characteristics. Finally, we predict a connection between the RUNX1 and MYB genes and a suppressive role for the NOTCH pathway in MPN diseases.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9530117 | PMC |
| http://dx.doi.org/10.1038/s41467-022-33189-w | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The 2024 APLAR Consensus on the Management of Lupus Nephritis.
Int J Rheum Dis
January 2025
The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
The APLAR has published a set of recommendations on the management of systemic lupus erythematosus (SLE) in 2021. The current consensus paper supplements and updates specifically the treatment of lupus nephritis (LN) according to two rounds of Delphi exercise from members of the APLAR SLE special interest group, invited nephrologists, histopathologists, and lupus nephritis patients. For initial treatment of LN, we recommend a combination of glucocorticoids (GCs) with cyclophosphamide (CYC), mycophenolate mofetil (MMF), or the calcineurin inhibitors (CNIs) as first-line options.
View Article and Find Full Text PDFA H2S-activated NIR-II imaging probe for precise diagnosis and pathological evaluation of colorectal tumor.
Theranostics
January 2025
Lab of Molecular Imaging and Translational Medicine (MITM), Engineering Research Center of Molecular and Neuro Imaging, Ministry of Education, School of Life Science and Technology, Xidian University & International Joint Research Center for Advanced Medical Imaging and Intelligent Diagnosis and Treatment, Xi'an, Shaanxi, 710126, P. R. China.
The quick and accurate detection of colorectal cancer (CRC) is essential for improving the treatment efficacy and patient survival, which nevertheless remains challenging due to low specificity and sensitivity of current CRC diagnostic approaches. Therefore, providing a robust solution for real-time and accurate tumor delineation is highly desirable. We report a novel polyacrylic acid-mediated strategy to develop the endogenous hydrogen sulfide (HS)-activated NIR-II probe DCNP@PB for specific visualization of CRC and image-guided tumor surgery.
View Article and Find Full Text PDFLKB1 inactivation promotes epigenetic remodeling-induced lineage plasticity and antiandrogen resistance in prostate cancer.
Cell Res
January 2025
Key Laboratory of Multi-Cell Systems, Shanghai Key Laboratory of Molecular Andrology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China.
Epigenetic regulation profoundly influences the fate of cancer cells and their capacity to switch between lineages by modulating essential gene expression, thereby shaping tumor heterogeneity and therapy response. In castration-resistant prostate cancer (CRPC), the intricacies behind androgen receptor (AR)-independent lineage plasticity remain unclear, leading to a scarcity of effective clinical treatments. Utilizing single-cell RNA sequencing on both human and mouse prostate cancer samples, combined with whole-genome bisulfite sequencing and multiple genetically engineered mouse models, we investigated the molecular mechanism of AR-independent lineage plasticity and uncovered a potential therapeutic strategy.
View Article and Find Full Text PDFFBP1 controls liver cancer evolution from senescent MASH hepatocytes.
Nature
January 2025
Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, School of Medicine, University of California San Diego (UCSD), La Jolla, CA, USA.
Hepatocellular carcinoma (HCC) originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses or metabolic-dysfunction-associated steatohepatitis (MASH). While increasing HCC risk, MASH triggers p53-dependent hepatocyte senescence, which we found to parallel hypernutrition-induced DNA breaks. How this tumour-suppressive response is bypassed to license oncogenic mutagenesis and enable HCC evolution was previously unclear.
View Article and Find Full Text PDFTreatment Persistence Among Anti-Tumor Necrosis Factor-experienced Patients With Ulcerative Colitis Switching to a Biologic With a Different Mode of Action or Cycling to Another Anti-Tumor Necrosis Factor Agent.
Clin Ther
December 2024
Analysis Group, Inc, Montreal, Quebec, Canada.
Purpose: In ulcerative colitis (UC), anti-tumor necrosis factor (TNF) agents often are first-line biologic therapy. Switching to a biologic with a different mode of action (ustekinumab and vedolizumab) or cycling to another anti-TNF agent (adalimumab, infliximab, and golimumab) is necessary if an initial anti-TNF fails. This study compared real-world persistence in patients with UC who switched to a biologic with a different mode of action or cycled with another anti-TNF after nonresponse to an anti-TNF.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!