Evidence map›Paper›PMID 7942844›Full record

ArticleAmerican journal of human genetics1994

A common region of deletion on chromosome 17q in both sporadic and familial epithelial ovarian tumors distal to BRCA1.

A K Godwin, L Vanderveer, D C Schultz, H T Lynch, D A Altomare, K H Buetow, M Daly, L A Getts, A Masny, N Rosenblum

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of human genetics, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Article
  3. Integrating network pharmacology and Mendelian randomization to explore potential targets of matrine against ovarian cancer.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024
    Article
  4. Article
  5. In Vitro Reconstitution of BRCA1-BARD1/RAD51-Mediated Homologous DNA Pairing.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  6. Article
  7. BRCA1 and BRCA2 Tumor Suppressor Function in Meiosis.Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. Article
  10. TP53 Mutations in Breast and Ovarian Cancer.Cold Spring Harbor perspectives in medicine · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Expression of FK506 binding protein 65 (FKBP65) is decreased in epithelial ovarian cancer cells compared to benign tumor cells and to ovarian epithelium.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
    Article
  16. Genomic aberrations in borderline ovarian tumors.Journal of translational medicine · 2010
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

A K GodwinDepartment of Medical Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111.
L Vanderveer
D C Schultz
H T Lynch
D A Altomare
K H Buetow
M Daly
L A Getts
A Masny
N Rosenblum
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
GENETIC CHANGES INVOLVED IN OVARIAN CANCER INITIATIONR01CA060643 · NCI · FOX CHASE CANCER CENTER · PI GODWIN, ANDREW K · 1993 to 1995
–
NCI NIH HHS CA60643NCI NIH HHS P30 CA006927
6 · The paper itself

Abstract

Linkage analysis in familial breast and ovarian cancer and studies of allelic deletion in sporadic ovarian tumors have identified a region on chromosome 17q containing a candidate tumor-suppressor gene (referred to as BRCA1) of likely importance in ovarian carcinogenesis. We have examined normal and tumor DNA samples from 32 patients with sporadic and 8 patients with familial forms of the disease, for loss of heterozygosity (LOH) at 21 loci on chromosome 17 (7 on 17p and 14 on 17q). LOH on 17p was 55% (22/40) for informative 17p13.1 and 17p13.3 markers. When six polymorphic markers flanking the familial breast/ovarian cancer susceptibility locus on 17q12-q21 were used, LOH was 58% (23/40), with one tumor showing telomeric retention. Evaluation of a set of markers positioned telomeric to BRCA1 resulted in the highest degree of LOH, 73% (29/40), indicating that a candidate locus involved in ovarian cancer may reside distal to BRCA1. Five of the tumors demonstrating allelic loss for 17q markers were from individuals with a strong family history of breast and ovarian cancer. More important, two of these tumors (unique patient number [UPN] 57 and UPN 79) retained heterozygosity for all informative markers spanning the BRCA1 locus but showed LOH at loci distal to but not including the anonymous markers CMM86 (D17S74) and 42D6 (D17S588), respectively. Deletion mapping of seven cases (two familial and five sporadic) showing limited LOH on 17q revealed a common region of deletion, distal to GH and proximal to D17S4, that spans approximately 25 cM. These results suggest that a potential tumor-suppressor gene involved in both sporadic and familial ovarian cancer may reside on the distal portion of chromosome 17q and is distinct from the BRCA1 gene.

Indexed as

Chromosome DeletionChromosomes, Human, Pair 17Genes, Tumor SuppressorPolymorphism, Restriction Fragment LengthBase SequenceCarcinomaChromosome MappingDNA PrimersDNA ProbesFemaleHumansMolecular Sequence DataOvarian NeoplasmsPolymerase Chain ReactionDNA PrimersDNA Probes

Identifiers

PMID7942844
PMCPMC1918278
OpenAlexW1498750456

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.