Evidence map›Paper›PMID 23370770›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2013

Lynch syndrome-associated breast cancers do not overexpress chromosome 11-encoded mucins.

Michael D Walsh, Margaret C Cummings, Sally-Ann Pearson, Mark Clendenning, Rhiannon J Walters, Belinda Nagler, John L Hopper, Mark A Jenkins, Graeme K Suthers, Jack Goldblatt and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 89% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

18 authors at 10 institutions in 2 countries.

Michael D WalshCancer and Population Studies Group, Queensland Institute of Medical Research, Herston, QLD 4006, Australia. Michael.Walsh@qimr.edu.au
Margaret C Cummings
Sally-Ann Pearson
Mark Clendenning
Rhiannon J Walters
Belinda Nagler
John L Hopper
Mark A Jenkins
Graeme K Suthers
Jack Goldblatt
Kathy Tucker
Michael R Gattas
Julie L Arnold
Susan Parry
Finlay A Macrae
Michael A McGuckin
Joanne P Young
Daniel D Buchanan
QIMR Berghofer Medical Research Institute · AUAuckland City Hospital · NZThe University of Melbourne · AUThe University of Queensland · AUMater Research · AUPrince of Wales Hospital · AURoyal Brisbane and Women's Hospital · AUSouth Australia Pathology · AUThe Royal Melbourne Hospital · AUThe University of Western Australia · AU

Funding

AUSTRALASIAN COLORECTAL CANCER FAMILY REGISTRYU01CA097735 · NCI · UNIVERSITY OF MELBOURNE · PI HOPPER, JOHN L · 2002 to 2007
$6.9M
NCI NIH HHS U01 CA097735
6 · The paper itself

Abstract

Mismatch repair-deficient breast cancers may be identified in Lynch syndrome mutation carriers, and have clinicopathological features in common with mismatch repair-deficient colorectal and endometrial cancers such as tumour-infiltrating lymphocytes and poor differentiation. Mismatch repair-deficient colorectal cancers frequently show mucinous differentiation associated with upregulation of chromosome 11 mucins. The aim of this study was to compare the protein expression of these mucins in mismatch repair-deficient and -proficient breast cancers. Cases of breast cancer (n=100) were identified from families where (1) both breast and colon cancer co-occurred and (2) families met either modified Amsterdam criteria or had at least one early-onset (<50 years) colorectal cancer. Tumour sections were stained for the epithelial mucins, MUC2, MUC5AC, MUC5B and MUC6, and the homeobox protein CDX2, a regulator of MUC2 expression. In all, 16 mismatch repair-deficient Lynch syndrome breast cancers and 84 non-Lynch breast cancers were assessed for altered mucin expression. No significant difference in the expression of MUC2, MUC5AC or MUC6 was observed between the mismatch repair-deficient and mismatch repair-proficient breast cancers; however, there was a trend for mismatch repair-deficient tumours to express high levels of MUC5B less frequently (P=0.07, OR=0.2 (0.0-1.0)). Co-expression of two or more gel-forming mucins was common. Ectopic expression of CDX2 was associated with expression of MUC2 (P=0.035, OR=8.7 (1.3-58.4)). Mismatch repair-deficient breast cancers do not show differential expression of the mucins genes on chromosome 11 when compared with mismatch repair-proficient breast cancers, in contrast with mismatch repair-deficient colorectal and endometrial cancers, which frequently have increased mucin protein expression when compared with their mismatch repair-proficient counterparts. In addition, ectopic CDX2 expression is positively associated with de novo MUC2 expression.

Indexed as

AdultAgedAged, 80 and overBreast NeoplasmsChromosomes, Human, Pair 11Colorectal Neoplasms, Hereditary NonpolyposisFemaleHumansMaleMiddle AgedMucinsMucins

Identifiers

PMID23370770
PMCPMC4204018
OpenAlexW2062132861

What OpenQuestion holds

Textmetadata
LicenceTDM
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.