Evidence map›Paper›PMID 36567450›Full record

ArticleJournal of the National Cancer Institute2023

Association of longer telomere length in cancer cells and cancer-associated fibroblasts with worse prognosis.

Yoko Matsuda, Juanjuan Ye, Keiko Yamakawa, Yuri Mukai, Kazuki Azuma, Linxuan Wu, Kenkichi Masutomi, Taro Yamashita, Yataro Daigo, Yohei Miyagi and 17 more

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

Article in Journal of the National Cancer Institute, 2023. 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
2.5field-weighted citation impact, top 10% 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, 17 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

27 authors at 5 institutions in 1 country.

Yoko MatsudaOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.ORCID 0000-0002-3235-655X
Juanjuan YeOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Keiko YamakawaOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Yuri MukaiOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Kazuki AzumaOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Linxuan WuOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Kenkichi MasutomiDivision of Cancer Stem Cell, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Taro YamashitaDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan.
Yataro DaigoDepartment of Medical Oncology and Cancer Center.
Yohei MiyagiKanagawa Cancer Center Research Institute, Asahi-ku, Yokohama, Japan.
Tomoyuki YokoseDepartment of Pathology, Kanagawa Cancer Center, Asahi-ku, Yokohama, Japan.ORCID 0000-0002-9403-9592
Takashi OshimaDepartment of Gastrointestinal Surgery, Kanagawa Cancer Center, Asahi-ku, Yokohama, Japan.
Hiroyuki ItoDepartment of Thoracic Surgery, Kanagawa Cancer Center, Asahi-ku, Yokohama, Japan.ORCID 0000-0003-0983-6093
Soichiro MorinagaDepartment of Hepato-Biliary and Pancreatic Surgery, Kanagawa Cancer Center, Asahi-ku, Yokohama, Japan.
Takeshi KishidaDepartment of Urology, Kanagawa Cancer Center, Asahi-ku, Yokohama, Japan.
Toshinari MinamotoDivison of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Motohiro KojimaDivision of Pathology, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa-shi, Chiba, Japan.
Shuichi KanekoDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan.
Reiji HabaDiagnostic Pathology, Kagawa University, Kita-gun, Kagawa, Japan.
Keiichi KontaniDepartment of Thoracic, Breast and Endocrine Surgery, Kagawa University, Kita-gun, Kagawa, Japan.
Nobuhiro KanajiDepartment of Internal Medicine, Division of Hematology, Rheumatology and Respiratory Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Keiichi OkanoDepartment of Gastroenterological Surgery, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Mariko Muto-IshizukaOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Masanao YokohiraOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Kousuke SaooOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Katsumi ImaidaOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
Futoshi SuizuOncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.ORCID 0000-0003-0206-4289
Kagawa University · JPKanagawa Prefectural Hospital Organization · JPKanazawa University · JPChiba Cancer Center · JPShiga University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTelomere dysfunction has been reported to be directly involved in carcinogenesis owing to chromosomal instability and immortalization; however, the clinicopathological significance of telomeres remains controversial. We have shown that telomere shortening occurs in normal-appearing duct cells at initiation and then continues during the progression of pancreatic cancer. In this study, we determined the clinicopathological and prognostic value of telomere length (TL) in cancer progression.

methodsTL in both cancer cells and cancer-associated fibroblasts (CAFs) was analyzed by high-throughput quantitative fluorescence in situ hybridization using a previously reported cohort comprising 1434 cases of adenocarcinoma (ADC), squamous cell carcinoma (SCC), adenosquamous carcinoma, hepatocellular carcinoma, and renal cell carcinoma (RCC), which are known cancers with a statistically significantly low incidence of alternative lengthening of telomeres. Cases were divided into 2 groups as follows: longer and shorter telomeres, according to the median TL of cancer cells and CAFs. The statistical significance of TL in cancer cells and CAFs on clinicopathological characteristics and prognosis was analyzed.

resultsThere was a close association between TL in cancer cells and CAFs. Longer telomeres in cancer cells and CAFs were associated with aggressive features such as advanced stage, high mitosis score and nuclear score, poorly differentiated cancer, and desmoplastic stroma in ADC. Furthermore, a longer TL was an independent prognostic factor for ADC, SCC, and RCC.

conclusionsLonger telomeres are associated with worse prognosis in ADC, SCC, and RCC. Thus, TL is a novel biomarker for the diagnosis of aggressive cancers with poor prognoses.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Renal CellCarcinoma, Squamous CellKidney NeoplasmsLiver NeoplasmsHumansIn Situ Hybridization, FluorescencePrognosisTelomereTelomere HomeostasisTelomere Shortening

Identifiers

PMID36567450
PMCPMC9905972
OpenAlexW4312194827

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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.