Robotic versus open total mesorectal excision for rectal cancer: comparative study of short and long-term outcomes.

BACKGROUND: Despite the several series in which the short-term outcomes of robotic-assisted surgery were investigated, data concerning the long-term outcomes are still scarce. METHODS: The prospectively collected records of 65 consecutive patients with extraperitoneal rectal cancer who underwent robotic total mesorectal excision (RTME) were compared with those of 109 consecutive patients treated with open surgery (OTME). Patient characteristics, pathological findings, local and systemic recurrence rates and 5-year survival rates were compared. RESULTS: There were no statistically significant differences in postoperative complications, reoperation and 30-day mortality. There were significant differences comparing groups: number of lymph nodes harvested (RTME: 20.1 vs. OTME: 14.1, P < 0.001), estimated blood loss (RTME: 0 vs. OTME: 150 ml, P = 0.003), operation time (RTME: 299.0 vs. OTME: 207.5 min, P < 0.001) and length of postoperative stay (RTME: 6 vs. OTME: 9 days, P < 0.001). The rate of circumferential resection margin involvement and distal resection margin were not statistically different between groups. There were no statistically significant differences at the 5-year follow-up: overall survival, disease-free survival and cancer-specific survival. The cumulative local recurrence rate was statistically lower in the robotic group (RTME: 3.4% vs. OTME: 16.1%, P = 0.024). CONCLUSION: RTME showed a significant reduction in local recurrence rate and a higher, although not statistically significant, long-term cancer-specific survival with respect to OTME. Prospective randomized studies are needed to confirm or deny significantly better local control rates with robotic surgery.

Is there any association between TACSTD2, KIAA1253, Ku70 and mutant KRAS gene expression and clinical-pathological features of colorectal cancer?

AIM: To determine the quantitative gene expression of KRAS codon 12 mutant, TACSTD2, Ku70 and SERIN1 in samples of tumor tissue and to relate them with clinical-pathological characteristics of colorectal cancer. METHODS: Samples of tumor and normal tissue of patients surgically treated for colorectal cancer between July 2005 and July 2009 were stored in a tissue bank. These samples were studied with the technique of real-time polymerase chain reaction in respect to expression of the following genes: KRAS codon 12 mutation, TACSTD2, Ku70, and SERIN1. RESULTS: Tumor samples of 37 patients were studied. The mean age was 65.5 years. Twenty one patients (56.8%) were male. Nine patients (24.3%) were classified as TNM stage I, 11 patients (29.8%) as TNM stage II, eight patients (21.6%) as TNM stage III and nine patients (24.3%) as TNM stage IV. The Ku70 expression in poorly-differentiated tumors is significantly higher than in well and moderately-differentiated tumors (2.76 vs. 1.13; p < 0.05). SERIN1, TACSTD2 and KRAS codon 12 mutation are not associated with clinical-pathological characteristics of colorectal cancer. CONCLUSION: Ku70 expression in poorly-differentiated tumors is significantly higher than in well and moderately-differentiated colorectal tumors.

Insulin receptor tyrosine kinase activity in colon carcinoma.

Colon carcinoma is the most common tumor of the gastrointestinal tract. According to some investigators, insulin, epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I) man be involved in the neoplastic proliferation. Insulin-binding and receptor tyrosine kinase activity were investigated in colon carcinomas and in normal colons. The insulin receptor concentration, as shown by binding assays, was 17.4 +/- 4.3 fmol/micrograms in normal colon and 29.69 +/- 9.4 fmol/micrograms in colon carcinoma. Nevertheless, the insulin affinity of the receptor was similar in both groups (Kd identical to 1 nM). Both normal and neoplastic colon showed phosphorylation of the insulin receptor. The electrophoretic migration of the beta-subunit of the insulin receptors purified from colon carcinomas was similar to that of normal colon and both tissues demonstrated an insulin-dependent autophosphorylation. The receptor tyrosine kinase activity was measured by the incorporation of [gamma 32P]ATP into the beta-subunit. The basal and the insulin-stimulated tyrosine kinase activities were significantly higher in colon carcinomas compared to normal colon tissues (2.2 and 1.6 times, respectively). Understanding the metabolism of neoplastic cells may contribute to the development of prevention strategies as well as new therapies. It is now necessary to study other steps of the insulin signal transduction pathway, such as insulin receptor substrate 1 phosphorylation.

Insulin receptors tyrosine kinase activity in colon carcinoma

Colon carcinoma is the most common tumor of the gastrointestinal tract. According to some investigators, insulin, epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I) may be involved in the neoplastic proliferation. Insulin-binding and receptor tyrosine kinase activity were investigated in colon carcinomas and in normal colons. The insulin receptor concentration, as shown by binding assays, was 17.4 ñ 4.3 fmol/mug in normal colon and 29.69 ñ 9.4 fmol/mug in colon carcinoma. Nevertheless, the insulin affinity of the receptor was similar in both groups (Kd ( 1 nM). Both normal and neoplastic colon showed phosphorylation of the insulin receptor. The electrophoretic migration of the Beta-subunit of the insulin receptors purified from colon carcinomas was similar to that of normal colon and both tissues demonstrated an insulin-dependent autophosphorylation. The receptor tyrosine kinase activity was measured by the incorporation of [gamma32P]ATP into the Beta-subunit. The basal and the insulin-stimulated tyrosine kinase activities were significantly higher in colon carcinomas compared to normal colon tissues (2.2 and 1.6 times, respectively). Understanding the metabolism of neoplastic cells may contribute to the development of prevention strategies as well as new therapies. It is now necessary to study other steps of the insulin signal transduction pathway, such as insulin receptor substrate 1 phosphorylation.