Abstract
Papillary thyroid carcinoma (PTC) variants exhibit different prognosis, but critical characteristics of PTC variants that contribute to differences in pathogenesis are not well-known. This study aims to characterize dysregulated immune-associated and cancer-associated genes in three PTC subtypes to explore how the interplay between cancer and immune processes causes differential prognosis. RNA-sequencing data from The Cancer Genome Atlas (TCGA) were used to identify dysregulated genes in each variant. The dysregulation profiles of the subtypes were compared using functional pathways clustering and correlations to relevant clinical variables, genomic alterations, and microRNA regulation. We discovered that the dysregulation profiles of classical PTC (CPTC) and the tall cell variant (TCPTC) are similar and are distinct from that of the follicular variant (FVPTC). However, unique cancer or immune-associated genes are associated with clinical variables for each subtype. Cancer-related genes MUC1, FN1, and S100-family members were the most clinically relevant in CPTC, while APLN and IL16, both immune-related, were clinically relevant in FVPTC. RAET-family members, also immune-related, were clinically relevant in TCPTC. Collectively, our data suggest that dysregulation of both cancer and immune associated genes defines the gene expression landscapes of PTC variants, but different cancer or immune related genes may drive the phenotype of each variant.
Highlights
Thyroid carcinoma is currently the fastest growing cancer in the world and is the most common endocrine carcinoma in the Western world [1]
The yearly occurrence of thyroid cancer has more than doubled in the past two decades, with most of this growth being attributed to papillary thyroid carcinoma (PTC), which constitutes over 80% of all thyroid cancer cases [1]
The three most common subtypes consist of classical (CPTC), follicular-variant (FVPTC), and tall cell (TCPTC) PTC, Cancers 2019, 11, 1179; doi:10.3390/cancers11081179
Summary
Thyroid carcinoma is currently the fastest growing cancer in the world and is the most common endocrine carcinoma in the Western world [1]. The yearly occurrence of thyroid cancer has more than doubled in the past two decades, with most of this growth being attributed to papillary thyroid carcinoma (PTC), which constitutes over 80% of all thyroid cancer cases [1]. Papillary thyroid carcinoma cases are divided into subtypes differentiated by physiology and clinical outcomes. The three most common subtypes consist of classical (CPTC), follicular-variant (FVPTC), and tall cell (TCPTC) PTC, Cancers 2019, 11, 1179; doi:10.3390/cancers11081179 www.mdpi.com/journal/cancers. Cancers 2019, 11, 1179 with CPTC being the most common subtype and TCPTC being the least common subtype. TCPTC is characterized by higher rates of mortality, tumor recurrence, distant metastasis, and lymph node metastasis than the other subtypes [2]
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