Abstract
The proto-oncogene c-MYC, located on chromosome 8q, can be upregulated through gain of 8q, causing alteration in biology of renal cell carcinoma (RCC). The aim of this study was to evaluate the prevalence of c-MYC through chromosome 8q gain and to correlate findings with cancer-specific mortality (CSM), and overall survival (OS). Cytogenetic analysis by conventional or Chromosomal Genomic Microarray Analysis (CMA) was performed on 414 renal tumors. Nonclear and nonpapillary RCC were excluded. Impact of gain in chromosome 8q status on CSM, OS, and its correlation with clinicopathological variables were evaluated. CSM and OS were assessed using log-rank test and the Cox proportional hazards model. A total of 297 RCC tumors with cytogenetic analysis were included. Gain of 8q was detected in 18 (6.1%) tumors (9 clear cell and 9 papillary RCC), using conventional method (n = 11) or CMA (n = 7). Gain of 8q was associated with higher T stage (p < 0.001), grade (p < 0.001), nodal involvement (p = 0.005), and distant metastasis (p < 0.001). No association between gain of 8q and age (p = 0.23), sex (p = 0.46), and Charlson comorbidity index (CCI, p = 0.59) were seen. Gain of 8q was associated with an 8.38-fold [95% confidence interval (CI), 3.83-18.34, p < 0.001] and 3.31-fold (95% CI, 1.56-7.04, p = 0.001) increase in CSM and decrease in OS, respectively, at a median follow up of 56 months. Chromosome 8q harbors the proto-oncogene c-MYC, which can be upregulated by gain of 8q. Our findings suggest that gain of 8q, can predict aggressive tumor phenotype and inferior survival in RCC.
Highlights
Kidney cancer, predominantly renal cell carcinoma (RCC), with an approximately 22% rate of cancer-specific mortality (CSM), is among the most lethal of urologic malignancies.[1]
The aim of our study is to report on the prevalence of chromosome 8q gain in our renal cancer tumor registry and to evaluate its prognostic significance on CSM and overall survival (OS) in clear cell, papillary, and sarcomatoid variant RCCs
As shown by cytogenetic analysis and histoimmunostaining (Figure 1), our findings suggest that proto-oncogene c-MYC is upregulated through gain of 8q in a subset of RCC tumors
Summary
Predominantly renal cell carcinoma (RCC), with an approximately 22% rate of cancer-specific mortality (CSM), is among the most lethal of urologic malignancies.[1]. Over the last several years, cytogenetic analysis by conventional or Chromosomal Microarray Analysis (CMA) has improved classifying RCCs and in predicting outcomes. The. The proto-oncogene c-MYC, located on chromosome 8q, can be upregulated through gain of 8q, causing alteration in biology of renal cell carcinoma (RCC). The aim of this study was to evaluate the prevalence of c-MYC through chromosome 8q gain and to correlate findings with cancer-specific mortality (CSM), and overall survival (OS). Methods: Cytogenetic analysis by conventional or Chromosomal Genomic Microarray Analysis (CMA) was performed on 414 renal tumors. Gain of 8q was detected in 18 (6.1%) tumors (9 clear cell and 9 papillary RCC), using conventional method (n = 11) or CMA (n = 7). Our findings suggest that gain of 8q, can predict aggressive tumor phenotype and inferior survival in RCC
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