Evidence map›Paper›PMID 27626065›Full record

ArticleCold Spring Harbor molecular case studies2016

A novel TP53-KPNA3 translocation defines a de novo treatment-resistant clone in osteosarcoma.

Kenneth S Chen, Woo Sun Kwon, Jiwoong Kim, Su Jin Heo, Hyo Song Kim, Hyo Ki Kim, Soo Hee Kim, Won Suk Lee, Hyun Cheol Chung, Sun Young Rha and 1 more

Abstract read
In one paragraph

Article in Cold Spring Harbor molecular case studies, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. JCO precision oncology · 2022
    Article
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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

11 authors.

Kenneth S ChenDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;; Gill Center for Cancer and Blood Disorders, Children's Medical Center, Dallas, Texas 75235, USA;
Woo Sun KwonSong-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, Republic of Korea;
Jiwoong KimQuantitative Biomedical Research Center, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;; Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;
Su Jin HeoDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea;
Hyo Song KimDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea;
Hyo Ki KimCelemics Inc., Seoul, Republic of Korea;
Soo Hee KimDepartment of Pathology, Yonsei University College of Medicine, Anatomic Pathology Reference Lab, Seegene Medical Foundation, Seoul, Republic of Korea;
Won Suk LeeSong-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, Republic of Korea;
Hyun Cheol ChungSong-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, Republic of Korea;; Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea;; Brain Korea 21 Project for Medical Sciences, Seoul, Republic of Korea.
Sun Young RhaSong-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, Republic of Korea;; Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea;; Brain Korea 21 Project for Medical Sciences, Seoul, Republic of Korea.
Tae Hyun HwangQuantitative Biomedical Research Center, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;; Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Sandi Leigh Pruitt · 2010 to 2026
$53.7M
NCI NIH HHS P30 CA142543
6 · The paper itself

Abstract

Osteosarcoma is the most common primary bone cancer. It can be cured by aggressive surgery and chemotherapy, but outcomes for metastatic or chemoresistant disease remain dismal. Cancer sequencing studies have shown that the p53 pathway is dysregulated in nearly every case, often by translocation; however, no studies of osteosarcoma evolution or intratumor heterogeneity have been done to date. We studied a patient with chemoresistant, metastatic disease over the course of 3 years. We performed exome sequencing on germline DNA and DNA collected from tumor at three separate time points. We compared variant calls and variant allele frequencies between different samples. We identified subclonal mutations in several different genes in the primary tumor sample and found that one particular subclone dominated subsequent tumor samples at relapse. This clone was marked by a novel TP53-KPNA3 translocation and loss of the opposite-strand wild-type TP53 allele. Future research must focus on the functional significance of such clones and strategies to eliminate them.

Indexed as

neoplasm of the skeletal systemosteosarcoma

Identifiers

PMID27626065
PMCPMC5002927

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.