Evidence map›Paper›PMID 32193285›Full record

ArticleCancer research2020

Inactivation of the Prolyl Isomerase Pin1 Sensitizes BRCA1-Proficient Breast Cancer to PARP Inhibition.

Man-Li Luo, Fang Zheng, Wenying Chen, Zhi-Mei Liang, Gurushankar Chandramouly, Jianan Tan, Nicholas A Willis, Chun-Hau Chen, Mateus de Oliveira Taveira, Xiao Zhen Zhou and 4 more

Open access · bronzeAbstract readComment
In one paragraph

Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  11. Abrogation of KLF5 sensitizesActa biochimica et biophysica Sinica · 2024
    Article
  12. Review
  13. Reciprocal antagonism of PIN1-APC/CNature communications · 2024
    Article
  14. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 2 countries.

Man-Li Luo *Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Fang Zheng *Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Wenying ChenDepartment of Oncology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Zhi-Mei LiangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.ORCID 0000-0002-0101-2818
Gurushankar ChandramoulyDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Jianan TanDepartment of Oncology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Nicholas A WillisDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Chun-Hau ChenDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Center for Life Science, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Mateus de Oliveira TaveiraDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.ORCID 0000-0001-8091-6593
Xiao Zhen ZhouDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Center for Life Science, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Kun Ping LuDivision of Translational Therapeutics, Department of Medicine and Cancer Research Institute, Center for Life Science, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Ralph ScullyDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Gerburg M WulfDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts. huhai@mail.sysu.edu.cn gwulf@bidmc.harvard.edu.
Hai HuDepartment of Oncology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China. huhai@mail.sysu.edu.cn gwulf@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USSun Yat-sen University · CN

Funding

ANALYSIS OF BRCA1 RECOMBINATION FUNCTIONSR01CA095175 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SCULLY, RALPH · 2002 to 2021
$4.9M
Optimization of PI3K-inhibitors to augment the efficacy of microtubule-disrupting chemotherapyR01CA226776 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WULF, GERBURG M · 2018 to 2022
$2.1M
NCI NIH HHS R01 CA095175NCI NIH HHS R01 CA226776
6 · The paper itself

Abstract

PARP inhibitor monotherapies are effective to treat patients with breast, ovary, prostate, and pancreatic cancer with BRCA1 mutations, but not to the much more frequent BRCA wild-type cancers. Searching for strategies that would extend the use of PARP inhibitors to BRCA1-proficient tumors, we found that the stability of BRCA1 protein following ionizing radiation (IR) is maintained by postphosphorylational prolyl-isomerization adjacent to Ser1191 of BRCA1, catalyzed by prolyl-isomerase Pin1. Extinction of Pin1 decreased homologous recombination (HR) to the level of BRCA1-deficient cells. Pin1 stabilizes BRCA1 by preventing ubiquitination of Lys1037 of BRCA1. Loss of Pin1, or introduction of a BRCA1-mutant refractory to Pin1 binding, decreased the ability of BRCA1 to localize to repair foci and augmented IR-induced DNA damage.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsTriple Negative Breast NeoplasmsBRCA1 ProteinCell Line, TumorFemaleHumansMaleNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePhthalazinesBRCA1 ProteinBRCA1 protein, humanNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePhthalazinesPIN1 protein, humanPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID32193285
PMCPMC7755124
OpenAlexW3011124659

What OpenQuestion holds

Textmetadata
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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.