ArticleOncogene2003
Hypermethylation of the Ink4b locus in murine myeloid leukemia and increased susceptibility to leukemia in p15(Ink4b)-deficient mice.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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
19 citing papers in PubMed, 42 citations in OpenAlex.
- A Comprehensive Guide on Epigenetics' Precision Role in Uncommon "Rare" Cancers' Biology and Treatment Frontiers.Sub-cellular biochemistry · 2026Review
- Role of microRNAs, circRNAs and long noncoding RNAs in acute myeloid leukemia.Journal of hematology & oncology · 2019Review
- CD93 Marks a Non-Quiescent Human Leukemia Stem Cell Population and Is Required for Development of MLL-Rearranged Acute Myeloid Leukemia.Cell stem cell · 2015Article
- Brief report: Loss of p15Ink4b accelerates development of myeloid neoplasms in Nup98-HoxD13 transgenic mice.Stem cells (Dayton, Ohio) · 2014Article
- Cyclin-dependent kinase inhibitor 2B regulates efferocytosis and atherosclerosis.The Journal of clinical investigation · 2014Article
- p15Ink4b Functions in determining hematopoietic cell fates: implications for its role as a tumor suppressor.Blood cells, molecules & diseases · 2013Review
- The role of tumor suppressor p15Ink4b in the regulation of hematopoietic progenitor cell fate.Blood cancer journal · 2013Article
- Article
- p15(INK4b) plays a crucial role in murine lymphoid development and tumorigenesis.Carcinogenesis · 2012Article
- Mechanisms of transforming growth factor β induced cell cycle arrest in palate development.Journal of cellular physiology · 2011Article
- Article
- Article
- Myeloid-specific inactivation of p15Ink4b results in monocytosis and predisposition to myeloid leukemia.Blood · 2010Article
- Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop acute B-lineage leukemia.Oncogene · 2010Article
- Article
- Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia.Leukemia research · 2008Article
- Article
- Zeb1 links epithelial-mesenchymal transition and cellular senescence.Development (Cambridge, England) · 2008Article
- JunB is a gatekeeper for B-lymphoid leukemia.Oncogene · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ink4b gene (Cdkn2b) encodes p15(Ink4b), a cyclin-dependent kinase inhibitor. It has been implicated in playing a role in the development of acute myeloid leukemia (AML) in man, since it is hypermethylated with high frequency. We provide evidence that the gene is a tumor suppressor for myeloid leukemia in mice. The evidence is twofold: (1) retrovirus-induced myeloid leukemias of the myelomonocytic phenotype were found to have hypermethylation of the 5' CpG island of the Ink4b gene, and this could be correlated with reduced mRNA expression, as demonstrated by TaqMan real-time PCR. p15(Ink4b) mRNA expression in a leukemia cell line, with hypermethylation at the locus, was induced following treatment with 5-aza-2'-deoxycytidine. (2) Targeted deletion of one allele in mice by removal of exon 2 increases their susceptibility to retrovirus-induced myeloid leukemia. Mice deficient in both alleles were not more susceptible to myeloid disease than those deficient in one allele, raising the possibility that there are opposing forces related to the development of myeloid leukemia in Ink4b null mice.
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.