Risk of adenoma recurrence after polypectomy in patients younger than 50 years vs. 50 years old and over with diminutive or small adenomas.

Background and aims: Current studies have shown that polyp recurrence occurs after colonic adenomas polypectomy (AP), but the difference in recurrence risk between patients in patients older than 50 years and younger than 50 years has not been clearly studied. Methods: 490 patients after AP were enrolled in the study. The patients were classified according to age (<50 years old or ≥50 years old), and then further categorized according to the baseline adenoma characteristics: Group 1: 1-2 non-advanced adenomas (NAAs) 1-5 mm in size; Group 2: ≥3 NAAs, 1-5 mm; Group 3: 1-2 NAAs, 6-9 mm; Group 4: ≥3 NAAs, 6-9 mm; and Group 5: advanced adenomas. Results: During a mean follow-up interval of 2.52 years (2.51 years for ≥50 years old and 2.55 years for patients <50 years old), NAA recurrence was detected in 147 patients (30.0%). Overall, the hazard ratio (HR) for NAA recurrence after AP was higher in patients ≥50 years old than that in patients <50 years old (HR, 1.774, P = 0.003). For patients <50 years old, HRs (Group 2-5 vs. G1, respectively) for NAA recurrence were 0.744 (P = 0.773), 3.885 (P = 0.007), 5.337 (P = 0.003), and 3.334 (P = 0.015). For patients ≥50 years old, HRs (Group 2-5 vs. G1, respectively) for NAA recurrence were 1.033 (P = 0.965), 1.250 (P = 0.405), 2.252 (P = 0.015), and 1.887 (P = 0.009). For G1, the risk of NAA recurrence was significantly higher in patients ≥50 years old (HR, 2.932, P = 0.011) than that in patients <50 years old; for G2-G5, the risk was similar in the two age groups (P > 0.05). Conclusions: For patients <50 years old with less than 3 NAAs that are 1-5 mm in size, the recurrence rate of NAA is less than that of patients ≥50 years old with the same index colonoscopy findings. When the adenomas are ≥5 mm, or their number exceeds 3, they have similar recurrence risk as that for patients ≥50 years old.

Role of Tetraspanins in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is characterized by high prevalence, morbidity, and mortality. Liver cancer is the sixth most common cancer worldwide; and its subtype, HCC, accounts for nearly 80% of cases. HCC progresses rapidly, and to date, there is no efficacious treatment for advanced HCC. Tetraspanins belong to a protein family characterized by four transmembrane domains. Thirty-three known tetraspanins are widely expressed on the surface of most nucleated cells and play important roles in different biological processes. In our review, we summarize the functions of tetraspanins and their underlying mechanism in the life cycle of HCC, from its initiation, progression, and finally to treatment. CD9, TSPAN15, and TSPAN31 can promote HCC cell proliferation or suppress apoptosis. CD63, CD151, and TSPAN8 can also facilitate HCC metastasis, while CD82 serves as a suppressor of metastasis. TSPAN1, TSPAN8, and CD151 act as prognosis indicators and are inversely correlated to the overall survival rate of HCC patients. In addition, we discuss the potential of role of the tetraspanin family proteins as novel therapeutic targets and as an approach to overcome drug resistance, and also provide suggestions for further research.

Tetraspanins: Novel Molecular Regulators of Gastric Cancer.

Gastric cancer is the fourth and fifth most common cancer worldwide in men and women, respectively. However, patients with an advanced stage of gastric cancer still have a poor prognosis and low overall survival rate. The tetraspanins belong to a protein superfamily with four hydrophobic transmembrane domains and 33 mammalian tetraspanins are ubiquitously distributed in various cells and tissues. They interact with other membrane proteins to form tetraspanin-enriched microdomains and serve a variety of functions including cell adhesion, invasion, motility, cell fusion, virus infection, and signal transduction. In this review, we summarize multiple utilities of tetraspanins in the progression of gastric cancer and the underlying molecular mechanisms. In general, the expression of TSPAN8, CD151, TSPAN1, and TSPAN4 is increased in gastric cancer tissues and enhance the proliferation and invasion of gastric cancer cells, while CD81, CD82, TSPAN5, TSPAN9, and TSPAN21 are downregulated and suppress gastric cancer cell growth. In terms of cell motility regulation, CD9, CD63 and CD82 are metastasis suppressors and the expression level is inversely associated with lymph node metastasis. We also review the clinicopathological significance of tetraspanins in gastric cancer including therapeutic targets, the development of drug resistance and prognosis prediction. Finally, we discuss the potential clinical value and current limitations of tetraspanins in gastric cancer treatments, and provide some guidance for future research.