# CD36 rs1761667 Polymorphism and Its Impact on Molecular Signatures in Bladder Cancer

**Authors:** Mihai Ioan Pavalean, Ioana Maria Lambrescu, Gisela Gaina, Victor Lucian Madan, Mihail Eugen Hinescu, Laura Cristina Ceafalan

PMC · DOI: 10.3390/diseases14020044 · Diseases · 2026-01-28

## TL;DR

This study explores how a genetic variant in CD36 affects gene expression in bladder cancer patients.

## Contribution

The study is the first to investigate the CD36 rs1761667 polymorphism in relation to bladder cancer.

## Key findings

- CD36 expression varied significantly across rs1761667 genotypes in bladder cancer patients.
- AA carriers showed reduced CD36 expression compared to GG carriers.
- No significant genotype-related differences were observed in controls.

## Abstract

Background: Bladder cancer remains a heterogeneous disease, and genetic factors are increasingly recognized as potential contributors to its pathogenesis. CD36, a multifunctional scavenger receptor implicated in lipid metabolism and tumor progression, has not been previously investigated in relation to bladder cancer-associated polymorphisms. Objectives: This study examined the relationship between the rs1761667 variant and CD36 mRNA expression. Methods: Our study included 30 patients with bladder cancer and 19 controls. PCR–RFLP genotyping for rs1761667 and RT–qPCR quantification of CD36 mRNA expression, with GAPDH as the reference gene, were performed. Expression levels were analyzed using the 2−ΔΔCt method, and statistical significance was defined as p < 0.05. Results: In patients, CD36 expression varied significantly across rs1761667 genotypes with reduced expression in AA carriers compared with GG carriers (post hoc, p = 0.009, with a Holm-adjusted p = 0.03). No significant genotype-related differences were observed among controls. Genotype distributions did not differ significantly between cases and controls (χ2, p = 0.053). Conclusions: These results indicate that rs1761667 may modulate CD36 transcription in a genotype-dependent manner, particularly in the disease context. Overall, our findings point to a potential biological connection between inherited CD36 variation and bladder cancer-related pathways, underscoring the need for further validation in tumor tissues

## Linked entities

- **Genes:** CD36 (CD36 molecule (CD36 blood group)) [NCBI Gene 948], GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597]
- **Diseases:** bladder cancer (MONDO:0004986)

## Full-text entities

- **Genes:** GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}
- **Diseases:** metabolic disease (MESH:D008659), metabolic and oncological disorders (MESH:D000072716), BC (MESH:D001749), T2DM (MESH:D003924), hepatic steatosis (MESH:D005234), lymph node (MESH:D000072717), obese (MESH:D009765), adiposity (MESH:D018205), bladder carcinogenesis (MESH:D063646), cardiovascular disease (MESH:D002318), Tumor (MESH:D009369), familial adenomatous polyposis (MESH:D011125), MIBC (MESH:D000093284), insulin resistance (MESH:D007333), injury to (MESH:D014947), inflammation (MESH:D007249), death (MESH:D003643), dyslipidemia (MESH:D050171), colorectal cancer (MESH:D015179), urothelial cancer (MESH:D014523)
- **Chemicals:** lipid (MESH:D008055), agarose (MESH:D012685), Ethidium bromide (MESH:D004996), EDTA (MESH:D004492), fatty acid (MESH:D005227), long-chain fatty acids (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** rs1527483, G > A

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12938890/full.md

## References

23 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938890/full.md

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Source: https://tomesphere.com/paper/PMC12938890