Evidence map›Paper›PMID 27018785›Full record

ArticleCancer2016

Intratumoral heterogeneity: Role of differentiation in a potentially lethal phenotype of testicular cancer.

Shi-Ming Tu, Mehmet Asim Bilen, Kenneth R Hess, Russell R Broaddus, Scott Kopetz, Chongjuan Wei, Lance C Pagliaro, Jose A Karam, John F Ward, Christopher G Wood and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 44 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

19 authors at 1 institution in 1 country.

Shi-Ming TuDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Mehmet Asim BilenDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Kenneth R HessDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Russell R BroaddusDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Scott KopetzDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Chongjuan WeiDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Lance C PagliaroDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jose A KaramDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
John F WardDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Christopher G WoodDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Priya RaoDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Zachary H TuDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Rosale GeneralDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Adrienne H ChenDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Yago L NietoDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Sai-Ching J YeungDepartment of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Sue-Hwa LinDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Christopher J LogothetisDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Louis L PistersDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

backgroundIntratumoral heterogeneity presents a major obstacle to the widespread implementation of precision medicine. The authors assessed the origin of intratumoral heterogeneity in nonseminomatous germ cell tumor of the testis (NSGCT) and identified distinct tumor subtypes and a potentially lethal phenotype.

methodsIn this retrospective study, all consecutive patients who had been diagnosed with an NSGCT between January 2000 and December 2010 were evaluated. The histologic makeup of primary tumors and the clinical course of disease were determined for each patient. A Fine and Gray proportional hazards regression analysis was used to determine the prognostic risk factors, and the Gray test was used to detect differences in the cumulative incidence of cancer death. In a separate prospective study, next-generation sequencing was performed on tumor samples from 9 patients to identify any actionable mutations.

resultsSix hundred fifteen patients were included in this study. Multivariate analysis revealed that the presence of yolk sac tumor in the primary tumor (P = .0003) was associated with an unfavorable prognosis. NSGCT could be divided into 5 subgroups. Patients in the yolk sac-seminoma subgroup had the poorest clinical outcome (P = .0015). These tumors tended to undergo somatic transformation (P < .0001). Among the 9 NSGCTs that had a yolk sac tumor phenotype, no consistent gene mutation was detected.

conclusionsThe current data suggest that intratumoral heterogeneity is caused in part by differentiation of pluripotent progenitor cells. Integrated or multimodal therapy may be effective at addressing intratumoral heterogeneity and treating distinct subtypes as well as a potentially lethal phenotype of NSGCT. Cancer 2016;122:1836-43. © 2016 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Indexed as

AdolescentAdultAgedCell DifferentiationChildGenetic HeterogeneityHumansMaleMiddle AgedMultivariate AnalysisNeoplasms, Germ Cell and EmbryonalNeoplastic Stem CellsPhenotypeProportional Hazards ModelsRetrospective StudiesTesticular Neoplasmsintegrated therapyintratumoral heterogeneitylethal phenotypeprecision medicinetesticular canceryolk sac tumor

Identifiers

PMID27018785
PMCPMC5071733
OpenAlexW2323631311

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.