ArticleLeukemia2006
Silencing of the tumor suppressor gene FHIT is highly characteristic for MLL gene rearranged infant acute lymphoblastic leukemia.
Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 61 citations in OpenAlex.
- Germinal epimutation of Fragile Histidine Triad (FHIT) gene is associated with progression to acute and chronic adult T-cell leukemia diseases.Molecular cancer · 2021Article
- Venetoclax in Combination with Decitabine for Relapsed T-Cell Acute Lymphoblastic Leukemia after Allogeneic Hematopoietic Cell Transplant.Case reports in hematology · 2018Article
- FHIT promoter DNA methylation and expression analysis in childhood acute lymphoblastic leukemia.Oncology letters · 2017Article
- Significance of Inactivated Genes in Leukemia: Pathogenesis and Prognosis.Cell journal · 2017Review
- PTPRG inhibition by DNA methylation and cooperation with RAS gene activation in childhood acute lymphoblastic leukemia.International journal of cancer · 2014Article
- Gene therapy model of X-linked severe combined immunodeficiency using a modified foamy virus vector.PloS one · 2013Article
- Elevated S100A8/S100A9 expression causes glucocorticoid resistance in MLL-rearranged infant acute lymphoblastic leukemia.Leukemia · 2012Article
- Genome-wide analysis of transcriptional reprogramming in mouse models of acute myeloid leukaemia.PloS one · 2011Article
- Promoter hypermethylation in MLL-r infant acute lymphoblastic leukemia: biology and therapeutic targeting.Blood · 2010Article
- Infant leukemia and parental infertility or its treatment: a Children's Oncology Group report.Human reproduction (Oxford, England) · 2010Article
- Fragile histidine triad protein: structure, function, and its association with tumorogenesis.Journal of cancer research and clinical oncology · 2010Review
- Infant acute lymphoblastic leukemia: Lessons learned and future directions.Current hematologic malignancy reports · 2009Review
- Therapeutic targeting of MLL.Blood · 2009Review
- High-risk childhood acute lymphoblastic leukemia.Clinical lymphoma & myeloma · 2009Review
- Epigenetics of acute lymphocytic leukemia.Seminars in hematology · 2009Review
- New therapeutic strategies for the treatment of acute lymphoblastic leukaemia.Nature reviews. Drug discovery · 2007Review
- Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia.Paediatric drugs · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MLL rearranged acute lymphoblastic leukemia (MLL) is an aggressive type of acute lymphoblastic leukemia (ALL), diagnosed predominantly in infants (<1 years of age). Since current chemotherapy fails in >50% of patients with MLL, new therapeutic strategies are desperately needed. For this, understanding the biological features characterizing MLL is necessary. Analysis of gene expression profiles revealed that the expression of the tumor suppressor gene FHIT is reduced in children with MLL rearranged ALL as compared to ALL patients carrying germ line MLL. This finding was confirmed by quantitative real-time PCR. In 100% of the infant MLL cases tested, methylation of the FHIT 5'CpG region was observed, resulting in strongly reduced mRNA and protein expression. In contrast, FHIT methylation in infant and non-infant ALL patients carrying germ line MLL was found in only approximately 60% (P< or =0.004). FHIT expression was restored upon exposing leukemic cells to the demethylating agent decitabine, which induced apoptosis. Likewise and more specifically, leukemic cell death was induced by transfecting MLL rearranged leukemic cells with expression vectors encoding wild-type FHIT, confirming tumor suppressor activity of this gene. These observations imply that suppression of FHIT may be required for the development of MLL, and provide new insights into leukemogenesis and therapeutic possibilities for MLL.
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.