Evidence map›Paper›PMID 18325103›Full record

ArticleBMC cancer2008

CDKN1C/p57kip2 is a candidate tumor suppressor gene in human breast cancer.

Pamela S Larson, Benjamin L Schlechter, Chia-Lin King, Qiong Yang, Chelsea N Glass, Charline Mack, Robert Pistey, Antonio de Las Morenas, Carol L Rosenberg

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Inhibition of MiR-199a-5p reduced cell proliferation in autosomal dominant polycystic kidney disease through targeting CDKN1C.Medical science monitor : international medical journal of experimental and clinical research · 2015
    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

9 authors at 3 institutions in 1 country.

Pamela S LarsonDepartment of Pathology and Laboratory Medicine, Boston University Medical Center, Boston, MA, USA. pamkent@bu.edu
Benjamin L Schlechter
Chia-Lin King
Qiong Yang
Chelsea N Glass
Charline Mack
Robert Pistey
Antonio de Las Morenas
Carol L Rosenberg
Boston Medical Center · USBoston University · USUniversity Medical Center · US

Funding

GENETIC ABNORMALITIES EARLY ON THE PATH OF BREAST CANCERR01CA081078 · NCI · BOSTON MEDICAL CENTER · PI ROSENBERG, CAROL L · 2001 to 2004
$851k
NCI NIH HHS CA081078NCI NIH HHS R01 CA081078
6 · The paper itself

Abstract

backgroundCDKN1C (also known as p57KIP2) is a cyclin-dependent kinase inhibitor previously implicated in several types of human cancer. Its family members (CDKN1A/p21CIP1 and B/p27KIP1) have been implicated in breast cancer, but information about CDKN1C's role is limited. We hypothesized that decreased CDKN1C may be involved in human breast carcinogenesis in vivo.

methodsWe determined rates of allele imbalance or loss of heterozygosity (AI/LOH) in CDKN1C, using an intronic polymorphism, and in the surrounding 11p15.5 region in 82 breast cancers. We examined the CDKN1C mRNA level in 10 cancers using quantitative real-time PCR (qPCR), and the CDKN1C protein level in 20 cancers using immunohistochemistry (IHC). All samples were obtained using laser microdissection. Data were analyzed using standard statistical tests.

resultsAI/LOH at 11p15.5 occurred in 28/73 (38%) informative cancers, but CDKN1C itself underwent AI/LOH in only 3/16 (19%) cancers (p = ns). In contrast, CDKN1C mRNA levels were reduced in 9/10 (90%) cancers (p < 0.0001), ranging from 2-60% of paired normal epithelium. Similarly, CDKN1C protein staining was seen in 19/20 (95%) cases' normal epithelium but in only 7/14 (50%) cases' CIS (p < 0.004) and 5/18 (28%) cases' IC (p < 0.00003). The reduction appears primarily due to loss of CDKN1C expression from myoepithelial layer cells, which stained intensely in 17/20 (85%) normal lobules, but in 0/14 (0%) CIS (p < 0.00001). In contrast, luminal cells displayed less intense, focal staining fairly consistently across histologies. Decreased CDKN1C was not clearly associated with tumor grade, histology, ER, PR or HER2 status.

conclusionCDKN1C is expressed in normal epithelium of most breast cancer cases, mainly in the myothepithelial layer. This expression decreases, at both the mRNA and protein level, in the large majority of breast cancers, and does not appear to be mediated by AI/LOH at the gene. Thus, CDKN1C may be a breast cancer tumor suppressor.

Indexed as

Genes, Tumor SuppressorAdultAgedAged, 80 and overBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, LobularCyclin-Dependent Kinase Inhibitor p57FemaleHumansLoss of HeterozygosityMiddle AgedPolymorphism, GeneticCDKN1C protein, humanCyclin-Dependent Kinase Inhibitor p57

Identifiers

PMID18325103
PMCPMC2323395
OpenAlexW2059212981

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.