Evidence map›Paper›PMID 37621144›Full record

ArticleCancer biology & therapy2023

Mutant PIK3CA as a negative predictive biomarker for treatment with a highly selective PIM1 inhibitor in human colon cancer.

Yoon Sun Park, Joseph Kim, Yea Seong Ryu, Jai-Hee Moon, Yu Jin Shin, Jeong Hee Kim, Seung-Woo Hong, Soo-A Jung, Seul Lee, Seung-Mi Kim and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cancer biology & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
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

18 authors at 2 institutions in 1 country.

Yoon Sun ParkAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Joseph KimAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Yea Seong RyuAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Jai-Hee MoonAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Yu Jin ShinAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Jeong Hee KimAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Seung-Woo HongAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Soo-A JungAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Seul LeeAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Seung-Mi KimAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Dae Hee LeeAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Do Yeon KimAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Hyeseon YunAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Ji-Eun YouAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Dong Il YoonAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Chul Hee KimAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Dong-In KohAsan Institute for Life Science, Asan Medical Center, Seoul, Republic of Korea.
Dong-Hoon JinDepartment of Pharmacology, University of Ulsan College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-1124-1518
Asan Medical Center · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Significant improvement in targeted therapy for colorectal cancer (CRC) has occurred over the past few decades since the approval of the EGFR inhibitor cetuximab. However, cetuximab is used only for patients possessing the wild-type oncogene KRAS, NRAS, and BRAF, and even most of these eventually acquire therapeutic resistance, via activation of parallel oncogenic pathways such as RAS-MAPK or PI3K/Akt/mTOR. The two aforementioned pathways also contribute to the development of therapeutic resistance in CRC patients, due to compensatory and feedback mechanisms. Therefore, combination drug therapies (versus monotherapy) targeting these multiple pathways may be necessary for further efficacy against CRC. In this study, we identified

Indexed as

Colonic NeoplasmsPhosphatidylinositol 3-KinasesBiomarkersCetuximabClass I Phosphatidylinositol 3-KinasesHumansProto-Oncogene Proteins c-pim-1BiomarkersCetuximabClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPIK3CA protein, humanPIM1 protein, humanProto-Oncogene Proteins c-pim-1colorectal cancermutant KRASPIK3CAPIM1predictive marker

Identifiers

PMID37621144
PMCPMC10461515
OpenAlexW4386151771

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.