Evidence map›Paper›PMID 33157517›Full record

ArticleTranslational oncology2021

Increased chromosomal instability characterizes metastatic renal cell carcinoma.

Qin Ma, Jilu Wang, Jie Qi, Ding Peng, Bao Guan, Jianye Zhang, Zhongwu Li, Hongxian Zhang, Ting Li, Yue Shi and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Establishment of a Seven-Gene Signature Associated with CD8International journal of molecular sciences · 2023
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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

14 authors at 2 institutions in 1 country.

Qin MaDepartment of Urology, Peking University First Hospital, Beijing 100034, China; Key Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China.
Jilu WangKey Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China.
Jie QiKey Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China.
Ding PengDepartment of Urology, Peking University First Hospital, Beijing 100034, China; Key Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China.
Bao GuanDepartment of Urology, Peking University First Hospital, Beijing 100034, China; Key Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China; Institute of Urology, Peking University, Beijing 100034, China; National Urological Cancer Centre, Beijing 100034, China.
Jianye ZhangDepartment of Urology, Peking University First Hospital, Beijing 100034, China; Key Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China; Institute of Urology, Peking University, Beijing 100034, China; National Urological Cancer Centre, Beijing 100034, China.
Zhongwu LiDepartment of Pathology, Peking University School of Oncology, 100142 Beijing, China.
Hongxian ZhangDepartment of Urology, School of Life Sciences, Third Hospital, Peking University, Beijing 100083, China.
Ting LiDepartment of Urology, Peking University First Hospital, Beijing 100034, China; Institute of Urology, Peking University, Beijing 100034, China; National Urological Cancer Centre, Beijing 100034, China.
Yue ShiKey Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China.
Xuesong LiDepartment of Urology, Peking University First Hospital, Beijing 100034, China; Institute of Urology, Peking University, Beijing 100034, China; National Urological Cancer Centre, Beijing 100034, China. Electronic address: pineneedle@sina.com.
Liqun ZhouDepartment of Urology, Peking University First Hospital, Beijing 100034, China; Institute of Urology, Peking University, Beijing 100034, China; National Urological Cancer Centre, Beijing 100034, China. Electronic address: zhoulqmail@sina.com.
Ke ChenKey Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China. Electronic address: chenke@big.ac.cn.
Weimin CiKey Laboratory of Genomics and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China; Institute of Stem cell and Regeneration, Chinese Academy of Sciences, Beijing 100101, China. Electronic address: ciwm@big.ac.cn.
Chinese Academy of Sciences · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evolutionary trajectories of treatment-naïve metastatic tumour are largely unknown. Such knowledge is crucial for cancer prevention and therapeutic interventions. Herein, we performed whole genome or exome sequencing of 19 tumour specimens and 8 matched normal kidney tissues from 8 clear cell renal cell carcinoma (ccRCC) patients. The clonal origin and parallel evolution of the metastatic lesions and primary tumour is identified in all 8 patients. But the evolutionary branches of primary and metastatic clones diverge early in the development of the tumour. More importantly, larger scale genomic aberrations including somatic copy number alteration (SCNA) or loss of heterozygosity (LOH) differentiate the metastasis lesions from primary tumour. Based on it, we identify that LOH at 14q, loss of 14q32.31 and gain of 6p22.2 are highly selected events during metastatic evolution. Further functional validations of multiple genes within the SCNA regions indicated that these selected events interact to drive metastatic risk with potential therapeutic relevance. Collectively, we described increased genome instability in metastatic ccRCC and validated it via molecular biology, providing an evolution pattern which may facilitate the translation of basic finding.

Indexed as

Clear cell renal cell carcinomaEvolutionary trajectoryLoss of heterozygosityMetastasisSomatic copy number alteration

Identifiers

PMID33157517
PMCPMC7649528
OpenAlexW3095909167

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.