The RAD51 135G&gt;C polymorphism is related to the effect of adjuvant therapy in early breast cancer

Leifler, Karin Söderlund; Asklid, Anna; Fornander, Tommy; Askmalm, Marie Stenmark

doi:10.1007/s00432-014-1859-0

Cited by 7 publications

(5 citation statements)

References 22 publications

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“…CMF chemotherapy reduced the risk of distant recurrence only for carriers of at least one C‐allele (RR = 0.29, 95% C.I. 0.10–0.88, p = 0.03) . There was no significant survival difference in Chinese patients with early‐stage NSCLC undergoing potentially curative tumor resection followed by adjuvant platinum‐based chemotherapy depending on the RAD51 135 G/C genotype …”

Section: Rad51 As a Surrogate For Resistance To Dna Damaging Cancer Treatmentmentioning

confidence: 98%

“…Soderlund et al . studied the effect of RAD51 135 G/C on radiotherapy and cyclophosphamide, methotrexate and 5‐fluorouracil (CMF) chemotherapy in 306 breast cancer patients . Homozygous carriers of the RAD51 G allele had a decreased risk of local recurrence following radiotherapy compared to carriers of the C allele (RR = 0.32, 95% C.I.…”

Section: Rad51 As a Surrogate For Resistance To Dna Damaging Cancer Treatmentmentioning

confidence: 99%

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RAD51 as a potential surrogate marker for DNA repair capacity in solid malignancies

Gachechiladze

Škarda

Soltermann

et al. 2017

Intl Journal of Cancer

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Targeting deficient mechanisms of cellular DNA repair still represents the basis for the treatment of the majority of solid tumors, and increased DNA repair capacity is a hallmark mechanism of resistance not only to DNA-damaging treatments such as cytotoxic drugs and radiotherapy, but also to small molecule targeted drugs such as inhibitors of poly-ADP ribose polymerase (PARP). Hence, there is substantial medical need for potent and convenient biomarkers of individual response to DNA-targeted treatment in personalized cancer care. RAD51 is a highly conserved protein that catalyzes DNA repair via homologous recombination, a major DNA repair pathway which directly modulates cellular sensitivity to DNA-damaging treatments. The clinical and biological significance of RAD51 protein expression is still under investigation. Pre-clinical studies consistently show the important role of nuclear RAD51 immunoreactivity in chemo- and radioresistance. Validating data from clinical trials however is limited at present, and some clinical studies show controversial results. This review gives a comprehensive overview on the current knowledge about the prognostic and predictive value of RAD51 protein expression and genetic variability in patients with solid malignancies.

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Section: Rad51 As a Surrogate For Resistance To Dna Damaging Cancer Treatmentmentioning

confidence: 98%

Section: Rad51 As a Surrogate For Resistance To Dna Damaging Cancer Treatmentmentioning

confidence: 99%

RAD51 as a potential surrogate marker for DNA repair capacity in solid malignancies

Gachechiladze

Škarda

Soltermann

et al. 2017

Intl Journal of Cancer

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“…We observed down-regulation of hsa-mir-574-5p (logFC −0.29) and hsa-mir-320c (logFC −0.36), which targets RAB18 gene, a member of RAS oncogene family [25], ABHD13 [26], DKDG [27] and FOX12 [28]. hsa-mir-320c also indirectly regulates TNBC by targeting known biomarker genes such as MCL1 [29] and RAD51 [30]. Another established breast cancer prognostic miRNA, hsa-mir-1290, was down-regulated (logFC −0.58) TNCB samples and target critical genes such as SGOL1, a member of Shougoshin family member [31], FAM53C [32] and transcription factor II-I GTF21 [33].…”

Section: Mirnas Differentially Expressed Among the Tumour Subtypesmentioning

confidence: 80%

Model-Based Integration Analysis Revealed Presence of Novel Prognostic miRNA Targets and Important Cancer Driver Genes in Triple-Negative Breast Cancers

Zaka

Sutton

Peng

et al. 2020

Cancers

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Background: miRNAs (microRNAs) play a key role in triple-negative breast cancer (TNBC) progression, and its heterogeneity at the expression, pathological and clinical levels. Stratification of breast cancer subtypes on the basis of genomics and transcriptomics profiling, along with the known biomarkers’ receptor status, has revealed the existence of subgroups known to have diverse clinical outcomes. Recently, several studies have analysed expression profiles of matched mRNA and miRNA to investigate the underlying heterogeneity of TNBC and the potential role of miRNA as a biomarker within cancers. However, the miRNA-mRNA regulatory network within TNBC has yet to be understood. Results and Findings: We performed model-based integrated analysis of miRNA and mRNA expression profiles on breast cancer, primarily focusing on triple-negative, to identify subtype-specific signatures involved in oncogenic pathways and their potential role in patient survival outcome. Using univariate and multivariate Cox analysis, we identified 25 unique miRNAs associated with the prognosis of overall survival (OS) and distant metastases-free survival (DMFS) with “risky” and “protective” outcomes. The association of these prognostic miRNAs with subtype-specific mRNA genes was established to investigate their potential regulatory role in the canonical pathways using anti-correlation analysis. The analysis showed that miRNAs contribute to the positive regulation of known breast cancer driver genes as well as the activation of respective oncogenic pathway during disease formation. Further analysis on the “risk associated” miRNAs group revealed significant regulation of critical pathways such as cell growth, voltage-gated ion channel function, ion transport and cell-to-cell signalling. Conclusion: The study findings provide new insights into the potential role of miRNAs in TNBC disease progression through the activation of key oncogenic pathways. The results showed previously unreported subtype-specific prognostic miRNAs associated with clinical outcome that may be used for further clinical evaluation.

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“…Michalska et al [22] found that the polymorphism of RAD51 may be positively associated with the incidence of triple-negative breast carcinoma while Sekhar et al [23] indicated that RAD51 135G > C substitution in the homozygous form (CC) increases the risk of breast cancer in an ethnic-specific manner. Söderlund et al [24] suggest that RAD51 135G>C polymorphism predicts cyclophosphamide/methotrexate/5-fluorouracil chemotherapy effect in early breast cancer.…”

Section: Discussionmentioning

confidence: 99%

RAD51 and XRCC3 Polymorphisms Are Associated with Increased Risk of Prostate Cancer

Nowacka-Zawisza

Raszkiewicz

Kwasiborski

et al. 2019

Journal of Oncology

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Genetic polymorphisms in DNA repair genes may affect DNA repair efficiency and may contribute to the risk of developing cancer. The aim of our study was to investigate single nucleotide polymorphisms (SNPs) in RAD51 (rs2619679, rs2928140, and rs5030789) and XRCC3 (rs1799796) involved in DNA double-strand break repair and their relationship to prostate cancer. The study group included 99 men diagnosed with prostate cancer and 205 cancer-free controls. SNP genotyping was performed using the PCR-RFLP method. A significant association was detected between RAD51 rs5030789 polymorphism and XRCC3 rs1799796 polymorphism and an increased risk of prostate cancer. Our results indicate that RAD51 and XRCC3 polymorphism may contribute to prostate cancer.

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The RAD51 135G>C polymorphism is related to the effect of adjuvant therapy in early breast cancer

Abstract: The results suggest that the RAD51 135G>C polymorphism predicts CMF chemotherapy effect in early breast cancer.

Cited by 7 publications

References 22 publications

RAD51 as a potential surrogate marker for DNA repair capacity in solid malignancies

RAD51 as a potential surrogate marker for DNA repair capacity in solid malignancies

Model-Based Integration Analysis Revealed Presence of Novel Prognostic miRNA Targets and Important Cancer Driver Genes in Triple-Negative Breast Cancers

RAD51 and XRCC3 Polymorphisms Are Associated with Increased Risk of Prostate Cancer

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