ArticleThe American journal of pathology2001
Putative tumor suppressor loci at 6q22 and 6q23-q24 are involved in the malignant progression of sporadic endocrine pancreatic tumors.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Utilization of ancillary studies in the cytologic diagnosis of biliary and pancreatic lesions: the Papanicolaou Society of Cytopathology guidelines for pancreatobiliary cytology.Diagnostic cytopathology · 2014Guideline
- Cyclin C promotes pancreatic developmentand suppresses cancer initiation by maintenance of the autophagy-lysosome pathway.iScience · 2026Article
- Genetic Variation and Recurrent Haplotypes on Chromosome 6q23-25 Risk Locus in Familial Lung Cancer.Cancer research · 2021Article
- The Impact ofInternational journal of hypertension · 2021Article
- PTPRK suppresses progression and chemo-resistance of colon cancer cells via direct inhibition of pro-oncogenic CD133.FEBS open bio · 2019Article
- MicroRNA-205 promotes cell invasion by repressing TCF21 in human ovarian cancer.Journal of ovarian research · 2017Article
- Regulation of development and cancer by the R2B subfamily of RPTPs and the implications of proteolysis.Seminars in cell & developmental biology · 2015Review
- Knockdown of protein tyrosine phosphatase receptor U inhibits growth and motility of gastric cancer cells.International journal of clinical and experimental pathology · 2014Article
- Utilization of ancillary studies in the cytologic diagnosis of biliary and pancreatic lesions: The Papanicolaou Society of Cytopathology Guidelines.CytoJournal · 2014Article
- Article
- SASH1 regulates proliferation, apoptosis, and invasion of osteosarcoma cell.Molecular and cellular biochemistry · 2013Article
- MSH2 and CXCR4 involvement in malignant VIPoma.World journal of surgical oncology · 2012Article
- Overexpression of SASH1 related to the decreased invasion ability of human glioma U251 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- Thermodynamic stability, unfolding kinetics, and aggregation of the N-terminal actin-binding domains of utrophin and dystrophin.Proteins · 2012Article
- Epigenetic deregulation of TCF21 inhibits metastasis suppressor KISS1 in metastatic melanoma.Carcinogenesis · 2011Article
- Localization of sporadic neuroendocrine tumors by gene expression analysis of their metastases.Clinical & experimental metastasis · 2011Article
- Insulin secretion and insulin-producing tumors.Expert review of endocrinology & metabolism · 2010Article
- Pancreatic endocrine neoplasms: epidemiology and prognosis of pancreatic endocrine tumors.Endocrine-related cancer · 2008Review
- UTRN on chromosome 6q24 is mutated in multiple tumors.Oncogene · 2007Article
- Molecular profiles of gastroenteropancreatic endocrine tumors.Virchows Archiv : an international journal of pathology · 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
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous comparative genomic hybridization study on sporadic endocrine pancreatic tumors (EPTs) revealed frequent losses on chromosomes 11q, 3p, and 6q. The aim of this study was to evaluate the importance of 6q losses in the oncogenesis of sporadic EPTs and to narrow down the smallest regions of allelic deletion. A multimodal approach combining polymerase chain reaction-based allelotyping, double-target fluorescence in situ hybridization, and comparative genomic hybridization was used in a collection of 109 sporadic EPTs from 93 patients. Nine polymorphic microsatellite markers (6q13 to 6q25-q27) were investigated, demonstrating a loss of heterozygosity (LOH) in 62.2% of the patients. A LOH was significantly more common in tumors >2 cm in diameter than below this threshold as well as in malignant than in benign tumors. We were able to narrow down the smallest regions of allelic deletion at 6q22.1 (D6S262) and 6q23-q24 (D6S310-UTRN) with LOH-frequencies of 50.0% and 41.2 to 56.3%, respectively. Several promising tumor suppressor candidates are located in these regions. Additional fluorescence in situ hybridization analysis on 46 EPTs using three locus-specific probes (6q21, 6q22, and 6q27) as well as a centromere 6-specific probe revealed complete loss of chromosome 6 especially in metastatic disease. We conclude that the two hot spots found on 6q may harbor putative tumor suppressor genes involved not only in the oncogenesis but maybe also in the malignant and metastatic progression of sporadic EPTs.
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.