Evidence map›Paper›PMID 32719131›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

A CRAF/glutathione-S-transferase P1 complex sustains autocrine growth of cancers with

Yoshiro Niitsu, Yasushi Sato, Kunihiro Takanashi, Tsuyoshi Hayashi, Naoko Kubo-Birukawa, Fumiko Shimizu, Naoki Fujitani, Rai Shimoyama, Takehiro Kukitsu, Wataru Kurata and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Implications of glutathione-S transferase P1 in MAPK signaling as a CRAF chaperone: In memory of Dr. Irving Listowsky.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022
    Review
  5. Article
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

12 authors at 4 institutions in 2 countries.

Yoshiro NiitsuDepartment of Molecular Target Exploration, Sapporo Medical University School of Medicine, 060-8556 Sapporo, Japan; y_niitu@shonankamakura.or.jp.
Yasushi SatoDepartment of Community Medicine for Gastroenterology and Oncology, Tokushima University Graduate School of Biomedical Sciences, 770-8503 Tokushima, Japan.ORCID 0000-0002-6776-4609
Kunihiro Takanashi4th Department of Internal Medicine, Sapporo Medical University, School of Medicine, 060-8556 Sapporo, Japan.
Tsuyoshi Hayashi4th Department of Internal Medicine, Sapporo Medical University, School of Medicine, 060-8556 Sapporo, Japan.
Naoko Kubo-BirukawaDepartment of Molecular Target Exploration, Sapporo Medical University School of Medicine, 060-8556 Sapporo, Japan.
Fumiko ShimizuDepartment of Molecular Target Exploration, Sapporo Medical University School of Medicine, 060-8556 Sapporo, Japan.
Naoki FujitaniDepartment of Molecular Target Exploration, Sapporo Medical University School of Medicine, 060-8556 Sapporo, Japan.
Rai ShimoyamaDivision of Gastroenterology, Shonan Kamakura General Hospital, 247-8533 Kamakura, Japan.ORCID 0000-0001-8601-0442
Takehiro Kukitsu4th Department of Internal Medicine, Sapporo Medical University, School of Medicine, 060-8556 Sapporo, Japan.
Wataru KurataOncology Section, Center of Advanced Medicine, Shonan Kamakura Innovation Park, Shonan Kamakura General Hospital, 247-8533 Kamakura, Japan.
Yasuyuki TashiroOncology Section, Center of Advanced Medicine, Shonan Kamakura Innovation Park, Shonan Kamakura General Hospital, 247-8533 Kamakura, Japan.
Irving ListowskyDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461.
Sapporo Medical University · JPShonan Kamakura General Hospital · JPAlbert Einstein College of Medicine · USTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ras/RAF/MEK/ERK pathway is an essential signaling cascade for various refractory cancers, such as those with mutant

Indexed as

AnimalsCarcinogenesisCell Line, TumorCell ProliferationGlutathione S-Transferase piHumansMiceMice, KnockoutMutationNeoplasmsProtein BindingProtein Interaction Domains and MotifsProtein MultimerizationProtein StabilityProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafBRAF protein, humanGlutathione S-Transferase piGSTP1 protein, humanKRAS protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafProto-Oncogene Proteins p21(ras)Raf1 protein, humanautocrine growth cycleCRAF/GSTP1 complexmKRAS and mBRAF cancersrefractory cancers

Identifiers

PMID32719131
PMCPMC7430992
OpenAlexW3045141434

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.