ArticleProceedings of the National Academy of Sciences of the United States of America1999
MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25).
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 174 citations in OpenAlex.
- SEPT9_i1 and Septin Dynamics in Oncogenesis and Cancer Treatment.Biomolecules · 2024Review
- SEPT9: From pan-cancer to lung squamous cell carcinoma.BMC cancer · 2024Article
- Circulating tumor cells: from new biological insights to clinical practice.Signal transduction and targeted therapy · 2024Review
- Membrane tension sensing molecule-FNBP1 is a prognostic biomarker related to immune infiltration in BRCA, LUAD and STAD.BMC immunology · 2022Article
- Proteomic profiling of the oncogenic septin 9 reveals isoform-specific interactions in breast cancer cells.Proteomics · 2021Article
- Article
- SEPT9_v2, frequently silenced by promoter hypermethylation, exerts anti-tumor functions through inactivation of Wnt/β-catenin signaling pathway via miR92b-3p/FZD10 in nasopharyngeal carcinoma cells.Clinical epigenetics · 2020Article
- Article
- A case ofCold Spring Harbor molecular case studies · 2018Article
- Septin remodeling is essential for the formation of cell membrane protrusions (microtentacles) in detached tumor cells.Oncotarget · 2017Article
- Septin 9_i2 is downregulated in tumors, impairs cancer cell migration and alters subnuclear actin filaments.Scientific reports · 2017Article
- The Relationship between the Methylated Septin-9 DNA Blood Test and Stool Occult Blood Test for Diagnosing Colorectal Cancer in Taiwanese People.Journal of clinical laboratory analysis · 2017Article
- Parallel Regulation of von Hippel-Lindau Disease by pVHL-Mediated Degradation of B-Myb and Hypoxia-Inducible Factor α.Molecular and cellular biology · 2016Article
- Septin Mutations in Human Cancers.Frontiers in cell and developmental biology · 2016Review
- Cancer-Related Functions and Subcellular Localizations of Septins.Frontiers in cell and developmental biology · 2016Review
- MiR-223-3p targeting SEPT6 promotes the biological behavior of prostate cancer.Scientific reports · 2014Article
- Plasma Septin9 versus fecal immunochemical testing for colorectal cancer screening: a prospective multicenter study.PloS one · 2014Article
- The expression patterns of Septin-9 after traumatic brain injury in rat brain.Journal of molecular neuroscience : MN · 2013Article
- Aberrant septin 9 DNA methylation in colorectal cancer is restricted to a single CpG island.BMC cancer · 2013Article
- Steps solidifying a role for SEPT9 in breast cancer suggest that greater strides are needed.Breast cancer research : BCR · 2012Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
MLL (ALL1, Htrx, HRX), which is located on chromosome band 11q23, frequently is rearranged in patients with therapy-related acute myeloid leukemia who previously were treated with DNA topoisomerase II inhibitors. In this study, we have identified a fusion partner of MLL in a 10-year-old female who developed therapy-related acute myeloid leukemia 17 months after treatment for Hodgkin's disease. Leukemia cells of this patient had a t(11;17)(q23;q25), which involved MLL as demonstrated by Southern blot analysis. The partner gene was cloned from cDNA of the leukemia cells by use of a combination of adapter reverse transcriptase-PCR, rapid amplification of 5' cDNA ends, and BLAST database analysis to identify expressed sequence tags. The full-length cDNA of 2.8 kb was found to be an additional member of the septin family, therefore it was named MSF (MLL septin-like fusion). Members of the septin family conserve the GTP binding domain, localize in the cytoplasm, and interact with cytoskeletal filaments. A major 4-kb transcript of MSF was expressed ubiquitously; a 1.7-kb transcript was found in most tissues. An additional 3-kb transcript was found only in hematopoietic tissues. By amplification with MLL exon 5 forward primer and reverse primers in MSF, the appropriately sized products were obtained. MSF is highly homologous to hCDCrel-1, which is a partner gene of MLL in leukemias with a t(11;22)(q23;q11.2). Further analysis of MSF may help to delineate the function of MLL partner genes in leukemia, particularly in therapy-related leukemia.
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.