Evidence map›Paper›PMID 31207547›Full record

ArticleTranslational oncology2019

Telomere Maintenance-Associated PML Is a Potential Specific Therapeutic Target of Human Colorectal Cancer.

Peng Gong, Hua Wang, Jingsong Zhang, Yudong Fu, Zhengmao Zhu, Jinmiao Wang, Yu Yin, Haiying Wang, Zhongcheng Zhou, Jiao Yang and 10 more

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 13 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

20 authors at 5 institutions in 2 countries.

Peng GongState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Hua WangState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jingsong ZhangDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yudong FuState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Zhengmao ZhuState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jinmiao WangDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yu YinState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Haiying WangState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Zhongcheng ZhouState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jiao YangState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Linlin LiuState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Mo GouState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Ming ZengState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jinghua YuanDepartment of Genetics, Tianjin Medical University, Tianjin, 300070, China.
Feng WangDepartment of Genetics, Tianjin Medical University, Tianjin, 300070, China.
Xinghua PanDepartment of Genetics, Yale School of Medicine, New Haven, CT, 06520, USA.
Rong XiangState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy.
Sherman M WeissmanDepartment of Genetics, Yale School of Medicine, New Haven, CT, 06520, USA.
Feng QiDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, China. Electronic address: qf@medmail.com.cn.
Lin LiuState Key Laboratory of Medicinal Chemical Biology, 2011 Collaborative Innovation Center for Biotherapy; Department of Cell Biology and Genetics, College of Life Sciences, Nankai University, Tianjin, 300071, China. Electronic address: liulin@nankai.edu.cn.
State Key Laboratory of Medicinal Chemical BiologyNankai University · CNTianjin Medical University General Hospital · CNTianjin Medical University · CNYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomere length maintenance is essential for cell proliferation, which is particularly prominent in cancer. We validate that the primary colorectal tumors exhibit heterogeneous telomere lengths but mostly (90%) short telomeres relative to normal tissues. Intriguingly, relatively short telomeres are associated with tumor malignancy as indicated by poorly differentiated state, and these tumors contain more cancer stem-like cells (CSLCs) identified by several commonly used markers CD44, EPHB2 or LGR5. Moreover, promyelocytic leukemia (PML) and ALT-associated PML nuclear bodies (APBs) are frequently found in tumors with short telomeres and high proliferation. In contrast, distant normal tissues rarely or only minimally express PML. Inhibition of PML and APBs by an ATR inhibitor decreases proliferation of CSLCs and organoids, suggesting a potential therapeutic target to progressive colorectal tumors. Together, telomere maintenance underling tumor progression is connected with CSLCs.

Identifiers

PMID31207547
PMCPMC6580093
OpenAlexW2952103177

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.