Evidence map›Paper›PMID 41569191›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2026

Innovative Strategies in Oral Carcinoma: Disrupting Cell Signaling for Therapeutic Advances.

Ibrahim Mahmood Mahdi, Maitha Sameer Kadhim, Maysaa Sameer Kadhim, Hawraa Kadhum Falhi, Douglas Law, Shazrul Fazry, Ahmed Abdulkareem Najm

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Article in Asian Pacific journal of cancer prevention : APJCP, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Ibrahim Mahmood MahdiDentistry Department, Al-Rafidain University College, Baghdad, Iraq.ORCID 0000-0003-2001-1842
Maitha Sameer KadhimMedical Laboratory Techniques Department, Al-Rafidain University College, Baghdad, Iraq.
Maysaa Sameer KadhimMedical Laboratory Techniques Department, Al-Rafidain University College, Baghdad, Iraq.
Hawraa Kadhum FalhiAl-Kindi Teaching Hospital, Baghdad, Iraq.
Douglas LawFaculty of Health and Life Sciences, INTI International University, Nilai, Negeri Sembilan, Malaysia.
Shazrul FazryDepartment of Food Sciences, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia.
Ahmed Abdulkareem NajmDepartment of Food Sciences, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aimed to evaluate the therapeutic efficacy of multi-pathway inhibition, targeting EGFR, MAPK, and PI3K/Akt in oral carcinoma.

methodsIn vitro experiments were conducted using human oral carcinoma cell lines (HSC-3 and SCC-4) treated with EGFR, MAPK, and PI3K/Akt inhibitors individually and in combination. Cell viability was assessed using the MTT assay, apoptosis with Annexin V-FITC/PI staining, and pathway inhibition through Western blot. In vivo, nude mice (n=30, equal gender distribution) with xenograft tumours were treated with the same inhibitors, and tumour volume was measured over a period of 3 weeks.

resultsCombination therapy reduced cell viability by 65% (vs. 40-45% for monotherapies) and increased apoptosis to 55% (vs. 25-30% for monotherapies). In vivo, tumour volume decreased by 64% with combination therapy (vs. 28-44% for monotherapies). Western blot analysis confirmed synergistic suppression of all three pathways in the combination group (p<0.05 for all comparisons).

conclusionMulti-pathway inhibition significantly enhances therapeutic efficacy in oral carcinoma by concurrently disrupting EGFR, MAPK, and PI3K/Akt signaling.

Indexed as

Antineoplastic AgentsCarcinoma, Squamous CellMouth NeoplasmsProtein Kinase InhibitorsSignal TransductionAnimalsApoptosisCell ProliferationCell SurvivalErbB ReceptorsFemaleHumansMiceMice, NudePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAntineoplastic AgentsEGFR protein, humanErbB ReceptorsPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktCell signaling disruption. Tumor suppressionmulti-pathway inhibitionoral carcinoma

Identifiers

PMID41569191
PMCPMC13384154

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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.