# The impact of genetic variants of the IGF-1 axis on surgical outcomes and prognosis in ovarian cancer

**Authors:** Inês de Almeida Lopes, Mariana Moreira Pires, Deolinda Pereira, Valéria Tavares, Inês Guerra de Melo, Rui Medeiros

PMC · DOI: 10.1007/s11033-026-11508-4 · 2026-02-04

## TL;DR

This study explores how genetic variations in the IGF-1 axis affect ovarian cancer outcomes, finding that certain SNPs are linked to survival differences in specific patient groups.

## Contribution

The study identifies context-dependent associations between IGF-1 axis SNPs and ovarian cancer prognosis, suggesting potential molecular markers.

## Key findings

- G allele carriers of IGF1 rs6220 had improved survival in patients with suboptimal cytoreduction.
- The TT genotype of IGF1R rs2016347 was linked to shorter disease-free survival in well-differentiated tumors.

## Abstract

Ovarian cancer (OC) remains the most lethal gynaecological malignancy, largely due to late-stage diagnosis, tumour heterogeneity, and high recurrence rates. The insulin-like growth factor-1 (IGF-1) axis has been implicated in tumour proliferation, survival, and treatment resistance. Yet, the prognostic relevance of its genetic variants in OC is not well established. The present study aims to evaluate the impact of two IGF-1-related single-nucleotide polymorphisms (SNPs), IGF1 rs6220 and IGF1R rs2016347, on the clinical outcome of 330 OC patients.

SNP genotyping was performed using the TaqMan® Allelic Discrimination methodology. Regarding IGF1 rs6220, G allele carriers presented significantly improved overall survival compared with AA homozygotes within the subgroup of women undergoing suboptimal cytoreductive surgery (residual disease ≥ 1 cm) (p = 0.039). As for IGF1R rs2016347, the TT genotype was associated with shorter disease-free survival than A allele carriers within the well-differentiated tumour group (p = 0.028).

These results indicate a context-dependent impact of IGF-1 axis polymorphisms on OC prognosis, suggesting their potential utility as molecular markers. Further validation in larger, independent cohorts, together with functional studies, is warranted to confirm these results and clarify the biological mechanisms underlying the influence of IGF-1-related genetic variants on OC behaviour.

## Linked entities

- **Genes:** IGF1 (insulin like growth factor 1) [NCBI Gene 3479], IGF1R (insulin like growth factor 1 receptor) [NCBI Gene 3480]
- **Diseases:** ovarian cancer (MONDO:0005140)

## Full-text entities

- **Genes:** GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, IGF1R (insulin like growth factor 1 receptor) [NCBI Gene 3480] {aka CD221, IGFIR, IGFR, JTK13}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, GGH (gamma-glutamyl hydrolase) [NCBI Gene 8836] {aka GATD10, GH}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, ZHX2 (zinc fingers and homeoboxes 2) [NCBI Gene 22882] {aka AFR1, RAF}, MUC16 (mucin 16, cell surface associated) [NCBI Gene 94025] {aka CA125}
- **Diseases:** Well-differentiated tumours (MESH:D015451), ovarian carcinogenesis (MESH:D010049), serous tumours (MESH:D018297), inflammation (MESH:D007249), FIGO (MESH:D048949), endometrioid (MESH:D018269), death (MESH:D003643), OC (MESH:D010051), Solid Tumours (MESH:D009369), mucinous (MESH:D002288)
- **Chemicals:** carboplatin (MESH:D016190), EDTA (MESH:D004492), cisplatin (MESH:D002945), NO (MESH:D009569), paclitaxel (MESH:D017239), platinum (MESH:D010984)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** rs6220, 3129G > T, rs2016347

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12872681/full.md

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Source: https://tomesphere.com/paper/PMC12872681