Evidence map›Paper›PMID 42282109›Full record

ReviewBioImpacts : BI2026

Integrin-linked kinase (ILK) in hematologic malignancies: Bridging molecular mechanisms to therapeutic innovation.

Omer Qutaiba B Allela, Abdulkareem Shareef, Ashishkumar Kyada, H Malathi, Laxmidhar Maharana, Dinesh Puri, Harshit Gupta, Djamila Polatova, Hayder Naji Sameer, Ahmed Yaseen and 2 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in BioImpacts : BI, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

12 authors.

Omer Qutaiba B AllelaCollege of Pharmacy, Alnoor University, Mosul, Iraq.ORCID https://orcid.org/0000-0001-6803-9794
Abdulkareem ShareefAhl al bayt University, Kerbala, Iraq.
Ashishkumar KyadaMarwadi University Research Center, Department of Pharmaceutical Sciences, Faculty of Health Sciences, Marwadi University, Rajkot, Gujarat, India.
H MalathiDepartment of Biotechnology and Genetics, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India.
Laxmidhar MaharanaDepartment of Pharmaceutical Sciences, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha-751030, India.
Dinesh PuriDepartment of Pharmacy, Graphic Era Hill University, Dehradun, India.
Harshit GuptaCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India.
Djamila PolatovaScientific-Practical Medical Center for Pediatric Oncology, Hematology and Immunology, Tashkent, Uzbekistan.
Hayder Naji SameerCollage of Pharmacy, National University of Science and Technology, Dhi Qar, 64001, Iraq.
Ahmed YaseenGilgamesh Ahliya University, Baghdad, Iraq.
Zainab H AthabDepartment of Pharmacy, Al-Zahrawi University College, Karbala, Iraq.
Mohaned AdilPharmacy College, Al-Farahidi University, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapy resistance remains a formidable challenge in hematologic malignancies despite significant advances in targeted therapies. This comprehensive review examines integrin-linked kinase (ILK) as a critical molecular hub at the nexus of cell adhesion, signal transduction, and therapy resistance across leukemias, lymphomas, and multiple myeloma. Unlike in solid tumors, where ILK primarily drives invasion and metastasis, in hematologic malignancies it uniquely mediates microenvironmental protection and therapy resistance through distinct signaling networks. ILK functions as a central mediator connecting microenvironmental signals to intracellular survival pathways, with expression levels 5-20-fold higher in malignant cells compared to normal counterparts. Through systematic analysis of structural properties, expression patterns, downstream signaling, and microenvironmental interactions, we present compelling evidence for ILK as a promising therapeutic target capable of overcoming resistance mechanisms. Current data demonstrate that ILK inhibition simultaneously disrupts multiple survival pathways, sensitizes resistant cells to established therapies, and selectively targets therapy-resistant leukemic stem cells while sparing normal progenitors. This review provides a comprehensive framework for translating ILK-targeted approaches into innovative therapeutic strategies with significant potential to improve outcomes in treatment-refractory hematologic malignancies.

Indexed as

Hematologic malignanciesIntegrin-linked kinaseLeukemic stem cellsTherapy resistanceTumor microenvironment

Identifiers

PMID42282109
PMCPMC13250408

What Socratic 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 Socratic graph.