Evidence map›Paper›PMID 36241658›Full record

ArticleScientific reports2022

KIR-HLA gene diversities and susceptibility to lung cancer.

Marjan Hematian Larki, Elham Ashouri, Shaghik Barani, Seiyed Mohammad Ali Ghayumi, Abbas Ghaderi, Raja Rajalingam

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Mapping malignant T-cell states and immune circuits in Sézary syndrome by single-cell analysis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Article
  2. Article
  3. Article
  4. Advances in the Basic Sciences in Thoracic Oncology in the Last 20 Years and Their Translational Impact.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2026
    Review
  5. Article
  6. The Role of Killer Ig-like Receptors in Diseases from A to Z.International journal of molecular sciences · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. 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

6 authors at 2 institutions in 2 countries.

Marjan Hematian LarkiShiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID 0000-0002-0246-5050
Elham AshouriShiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Shaghik BaraniShiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Seiyed Mohammad Ali GhayumiDepartment of Internal Medicine, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Abbas GhaderiShiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. ghaderia@sums.ac.ir.ORCID 0000-0003-0849-3375
Raja RajalingamImmunogenetics and Transplantation Laboratory, Department of Surgery, University of California San Francisco, San Francisco, CA, USA. Rajalingam.Raja@ucsf.edu.ORCID 0000-0001-8821-7877
Shiraz University of Medical Sciences · IRUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Killer-cell immunoglobulin-like receptors (KIR) are essential for acquiring natural killer (NK) cell effector function, which is modulated by a balance between the net input of signals derived from inhibitory and activating receptors through engagement by human leukocyte antigen (HLA) class I ligands. KIR and HLA loci are polygenic and polymorphic and exhibit substantial variation between individuals and populations. We attempted to investigate the contribution of KIR complex and HLA class I ligands to the genetic predisposition to lung cancer in the native population of southern Iran. We genotyped 16 KIR genes for a total of 232 patients with lung cancer and 448 healthy controls (HC), among which 85 patients and 178 HCs were taken into account for evaluating combined KIR-HLA associations. KIR2DL2 and 2DS2 were increased significantly in patients than in controls, individually (OR 1.63, and OR 1.42, respectively) and in combination with HLA-C1 ligands (OR 1.99, and OR 1.93, respectively). KIR3DS1 (OR 0.67) and 2DS1 (OR 0.69) were more likely presented in controls in the absence of their relative ligands. The incidence of CxTx subset was increased in lung cancer patients (OR 1.83), and disease risk strikingly increased by more than fivefold among genotype ID19 carriers (a CxTx genotype that carries 2DL2 in the absence of 2DS2, OR 5.92). We found that genotypes with iKIRs > aKIRs (OR 1.67) were more frequently presented in lung cancer patients. Additionally, patients with lung cancer were more likely to carry the combination of CxTx/2DS2 compared to controls (OR 2.04), and iKIRs > aKIRs genotypes in the presence of 2DL2 (OR 2.05) increased the likelihood of lung cancer development. Here we report new susceptibility factors and the contribution of KIR and HLA-I encoding genes to lung cancer risk, highlighting an array of genetic effects and disease setting which regulates NK cell responsiveness. Our results suggest that inherited KIR genes and HLA-I ligands specifying the educational state of NK cells can modify lung cancer risk.

Indexed as

Lung NeoplasmsReceptors, KIRGene FrequencyGenotypeHistocompatibility Antigens Class IHLA AntigensHumansImmunoglobulinsLigandsHistocompatibility Antigens Class IHLA AntigensImmunoglobulinsLigandsReceptors, KIR

Identifiers

PMID36241658
PMCPMC9568660
OpenAlexW4306168668

What OpenQuestion holds

Textmetadata
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.