Evidence map›Paper›PMID 36619305›Full record

ArticleBioMed research international2022

The Oxidative Drug Combination for Suppressing KRAS G12D Inducible Tumour Growth.

Dinara Begimbetova, Assiya Kukanova, Fatima Fazyl, Kenzhekyz Manekenova, Talgat Omarov, Agata N Burska, Medina Khamijan, Alexandr Gulyayev, Bakytgul Yermekbayeva, Abay Makishev and 5 more

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

Article in BioMed research international, 2022. 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
0.3field-weighted citation impact, top 44% 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. 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

15 authors at 4 institutions in 1 country.

Dinara BegimbetovaNational Laboratory Astana, Nazarbayev University, Astana, Kazakhstan.
Assiya KukanovaNational Laboratory Astana, Nazarbayev University, Astana, Kazakhstan.
Fatima FazylNational Laboratory Astana, Nazarbayev University, Astana, Kazakhstan.
Kenzhekyz ManekenovaDepartment of Pathological Anatomy, Astana Medical University, Astana, Kazakhstan.
Talgat OmarovDepartment of Pathological Anatomy, Astana Medical University, Astana, Kazakhstan.
Agata N BurskaNational Laboratory Astana, Nazarbayev University, Astana, Kazakhstan.
Medina KhamijanDepartment of Biology, School of Sciences and Humanities, Nazarbayev University, Astana, Kazakhstan.
Alexandr GulyayevNational Laboratory Astana, Nazarbayev University, Astana, Kazakhstan.
Bakytgul YermekbayevaNational Laboratory Astana, Nazarbayev University, Astana, Kazakhstan.
Abay MakishevDepartment of Oncology, Astana Medical University, Astana, Kazakhstan.
Timur SalievS.D. Asfendiyarov Kazakh National Medical University, Almaty, Kazakhstan.
Kanat BatyrbekovNational Research Oncological Centre, Astana, Kazakhstan.
Chokan AitbayevNational Research Oncological Centre, Astana, Kazakhstan.
Zhanat SpatayevNational Research Oncological Centre, Astana, Kazakhstan.
Dos SarbassovNational Laboratory Astana, Nazarbayev University, Astana, Kazakhstan.ORCID https://orcid.org/0000-0002-6848-1133
Nazarbayev University · KZAstana Medical University · KZNational Research Center for Maternal and Child Health · KZKazakh National Medical University · KZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Kirsten rat sarcoma (KRAS) protein is an essential contributor to the development of pancreatic ductal adenocarcinoma (PDAC). KRAS G12D and G12V mutant tumours are significant challenges in cancer therapy due to high resistance to the treatment. Objective: To determine how effective is the ATO/D-VC combination in suppression of PDAC the mouse transgenic model. This study investigated the antitumour effect of a novel combination of arsenic trioxide (ATO) and D-ascorbic acid isomer (D-VC). Such a combination can be used to treat KRAS mutant cancer by inducing catastrophic oxidative stress. Methods: In this study, we examined the effectiveness of ATO and D-VC on xenograft models-AK192 cells transplanted into mice. Previously, it has been shown that a high concentration of Vitamin C (VC) selectively can kill the cells expressing KRAS. Results: The results of this study demonstrated that the combination of VC with a low dose of the oxidizing drug ATO led to the enhancement of the therapeutic effect. These findings suggest that the combined treatment using ATO and D-VC is a promising approach to overcome the limitation of drug selectivity and efficacy.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAnimalsArsenic TrioxideAscorbic AcidCell Line, TumorDisease Models, AnimalDrug CombinationsHumansMiceOxidation-ReductionOxidative StressProto-Oncogene Proteins p21(ras)Arsenic TrioxideAscorbic AcidDrug CombinationsKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID36619305
PMCPMC9822755
OpenAlexW4313364835

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.