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Gastrointest Cancer (Jersey City). 2016;1(1). pii: 1005. Epub 2016 Aug 3.

Gene Expression Analysis of Sporadic Early-Onset Rectal Adenocarcinoma.

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UA Cancer Center, 1515 N Campbell Avenue, Tucson, AZ 85724, USA; UA Department of Surgery, Division of Surgical Oncology, 1501 N Campbell Avenue, Tucson, AZ 85724, USA.
NanoString Technologies, 530 Fairview Avenue North, Seattle, WA 98109, USA.
UA Department of Surgery, Division of Surgical Oncology, 1501 N Campbell Avenue, Tucson, AZ 85724, USA.



Overall declines in incidence of rectal cancer (RC) in patients older than 50 years have been mostly attributed to improvement in treatment modalities and introduction of age-based screening. Recent studies, however, have shown a rise in the incidence of RC in patients younger than 50 years. The etiology of early-onset (EO) RC is not well understood. The aim of this study is to elucidate the molecular features of (EO) RC and show its uniqueness compared to late-onset (LO) disease.


Two cohorts of patients with sporadic RC were identified. Tumors and matching non-involved tissues from six (EO) RC patients (< 50 years) and six (LO) RC patients (>65 years) were obtained from Pathology archives. Deparaffinized tissues were macro-dissected from FFPE sections, RNA isolated and used for expression profiling of 770 cancer related genes representing 13 canonical pathways. Statistical analysis was performed using the Gene Expression R-script module within the nCounter software v2.6. A gene was considered to be above background if the average count for the target gene was greater than the average counts for the eight negative control genes and if the P value of the t-test was less than 0.05.


When we compared rectal tumors to non-involved rectal tissues, changes in expression levels of 171 genes were statistically significant in early-onset group and 151 genes in late-onset group. Further comparative gene expression analysis between early- and late-onset rectal tumors normalized to their matching non-involved tissues revealed that changes in expression of 65 genes were unique to early-onset rectal tumors with 16 genes being up- and 49 genes down-regulated using the cutoff criteria of expression levels difference >2 fold and p-value <0.01. At the pathway level, MAPK signaling was the most deregulated pathway in early-onset rectal tumors compared to PI3K-AKT signaling pathway being the most deregulated in late-onset rectal tumors.


Results of this study suggest that sporadic early-onset rectal cancer is characterized by distinct molecular events compared to late-onset disease.


Gene expression profiling; Pathway analysis; Sporadic early- and late-onset rectal cancer


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