Evidence map›Paper›PMID 24752337›Full record

ArticlePloS one2014

The expression patterns of p53 and p16 and an analysis of a possible role of HPV in primary adenocarcinoma of the urinary bladder.

Riley E Alexander, Sean R Williamson, Justin Richey, Antonio Lopez-Beltran, Rodolfo Montironi, Darrell D Davidson, Muhammad T Idrees, Carol L Jones, Shaobo Zhang, Lisha Wang and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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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

16 authors at 7 institutions in 4 countries.

Riley E AlexanderDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Sean R WilliamsonDepartment of Pathology, Henry Ford Hospital, Detroit, Michigan, United States of America.
Justin RicheyDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Antonio Lopez-BeltranDepartment of Pathology, Cordoba University, Cordoba, Spain.
Rodolfo MontironiInstitute of Pathological Anatomy and Histopathology, School of Medicine, Polytechnic University of the Marche Region (Ancona), United Hospitals, Ancona, Italy.
Darrell D DavidsonDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Muhammad T IdreesDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Carol L JonesDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Shaobo ZhangDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Lisha WangDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Qiu RaoDepartment of Pathology, Nanjing Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
Jose A PedrosaDepartment of Urology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Hristos Z KaimakliotisDepartment of Urology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
M Francesca MonnDepartment of Urology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Michael O KochDepartment of Urology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Liang ChengDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America; Department of Urology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USFudan University Shanghai Cancer Center · CNHenry Ford Hospital · USMarche Polytechnic University · ITNanjing General Hospital of Nanjing Military Command · CNUniversity of Córdoba · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrimary adenocarcinoma of the urinary bladder is rare. The molecular and cellular events leading to its pathogenesis are not well delineated. The goal of this study was to investigate p53 and p16 expression, as well as HPV status, in a relatively large series of primary bladder adenocarcinomas. MATERIALS AND

methodsThirty six cases of urinary bladder adenocarcinoma were chosen from participating institutions. The diagnosis and available clinical history were reviewed in each case. Immunostains for p53, p16 and HPV and high-risk and low-risk HPV-ISH were performed on all tumors.

resultsPatients had an average age of 61 years with a male predominance (1.5 ∶ 1 male ∶ female ratio). The average tumor size in cystectomy specimens was 4.3 cm. Of the cases managed by transurethral resection, 40% were pT2 at the time of diagnosis. In cystectomy specimens, 77% were either pT3 or pT4. Strong nuclear p16 expression was seen in 67% of all cases and p53 expression was present in 58% of the cases. Expression of both markers was seen in 33% of cases. Expression of p16 or p53 alone was present in 12 (33%) and 9 (25%) cases, respectively. Neither marker was expressed in only 3 (8%) of the tumors. No significant correlation between clinical variables and any of the markers we studied was identified. No HPV infection was detected in any case.

conclusionsExpression of p53 and/or p16 is very common in urinary bladder adenocarcinoma. These findings implicate a high likelihood that alterations in these cell cycle proteins contribute to the pathogenesis of these tumors. Despite frequent immunohistochemical labeling for p16, no evidence of HPV infection was found.

Indexed as

AdenocarcinomaBiomarkers, TumorCyclin-Dependent Kinase Inhibitor p16FemaleHumansImmunohistochemistryIn Situ HybridizationMaleMiddle AgedNeoplasm ProteinsPapillomavirus InfectionsTumor Suppressor Protein p53Urinary Bladder NeoplasmsBiomarkers, TumorCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Neoplasm ProteinsTumor Suppressor Protein p53

Identifiers

PMID24752337
PMCPMC3994140
OpenAlexW1984314503

What OpenQuestion holds

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Registered trials

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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.