Routine CNLD as an adjunct to total thyroidectomy identifies positive nodes in over 30% of patients with PTC. The discovery of positive nodes is associated with higher doses of RAI for postoperative ablation, and there is a trend toward decreased recurrence in patients undergoing CNLD.

Tumors were more easily established and grew more aggressively after laparotomy than after insufflation. These results, coupled with those that demonstrate an immune advantage to laparoscopy over laparotomy, suggest that the difference in observed tumor growth may be related to immune function. While much work remains to be done, we believe these data provide evidence of a previously undemonstrated benefit of laparoscopic intervention.

CAPTEM is highly active, well tolerated and may prolong survival in patients with well-differentiated, metastatic NET who have progressed on previous therapies.

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Purpose: Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic-a (PIK3CA) gene in various human solid tumors. More than 75% of those somatic mutations are clustered in the helical (exon 9) and kinase domains (exon 20). The three hot-spot mutations, E542K, E545K, and H1047R, have been proven to elevate the lipid kinase activity of PIK3CA and activate the Akt signaling pathway. The mutational status of PIK3CA in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMC) has not been evaluated previously. Experimental Design: To evaluate a possible role for PIK3CA in the tumorigenesis of IPMN and IPMC, exons 1, 4, 5, 6, 7, 9, 12, 18, and 20 were analyzed in 36 IPMN/IPMC and two mucinous cystadenoma specimens by direct genomic DNA sequencing. Results: We identified four missense mutations in the nine screened exons of PIK3CA from 36 IPMN/IPMC specimens (11%). One of the four mutations, H1047R, has been previously reported as a hot-spot mutation. The remaining three mutations, T324I, W551G, and S1015F, were novel and somatic. Conclusion: This is the first report of PIK3CA mutation in pancreatic cancer. Our data provide evidence that the oncogenic properties of PIK3CA contribute to the tumorigenesis of IPMN/ IPMC.

Background Laparoscopic distal pancreatectomy (LDP) is increasingly performed for lesions of the body and tail of the pancreas. The aim of this study was to investigate short-term outcomes after LDP compared to open distal pancreatectomy (ODP) at a single, high-volume institution. Methods We reviewed records of patients who underwent distal pancreatectomy (DP) and compared perioperative data between LDP and ODP. Continuous variables were compared using Student’s t- or Wilcoxon rank-sum tests. Categorical variables were compared using chi-square or Fisher’s exact test. Results A total of 360 patients underwent DP. Beginning in 2001, 95 were attempted and 71 completed laparoscopically with a 25.3% conversion rate. Compared to ODP, LDP had similar rates of splenic preservation, pancreatic fistula, and mortality. LDP had lower blood loss (150 vs. 900 mL, p<0.01), smaller tumor size (2.5 vs. 3.6 cm, p<0.01), and shorter length of resected pancreas (7.7 vs. 10.0 cm, p<0.01). LDP had fewer complications (28.2% vs. 43.8%, p=0.02) as well as shorter hospital stays (5 vs. 6 days, p<0.01). Conclusions LDP can be performed safely and effectively in patients with benign or low-grade malignant neoplasms of the distal pancreas. When feasible in selected patients, LDP offers fewer complications and shorter hospital stays.

Attempts to enhance patients’ immune responses to malignancies have been largely unsuccessful. We now describe an immune-escape mechanism mediated by the inhibitory receptor Ig-like transcript 3 (ILT3) that may be responsible for such failures. Using a humanized SCID mouse model, we demonstrate that soluble and membrane ILT3 induce CD8+ T suppressor cells and prevent rejection of allogeneic tumor transplants. Furthermore, we found that patients with melanoma, and carcinomas of the colon, rectum, and pancreas produce the soluble ILT3 protein, which induces the differentiation of CD8+ T suppressor cells and impairs T cell responses in MLC. These responses are restored by anti-ILT3 mAb or by depletion of soluble ILT3 from the serum. Immunohistochemical staining of biopsies from the tumors and metastatic lymph nodes suggests that CD68+ tumor-associated macrophages represent the major source of soluble ILT3. Alternative splicing, resulting in the loss of the ILT3 transmembrane domain, may contribute to the release of ILT3 in the circulation. These data suggest that ILT3 depletion or blockade is crucial to the success of immunotherapy in cancer. In contrast, the inhibitory activity of soluble ILT3 on T cell alloreactivity in vitro and in vivo suggests the potential usefulness of rILT3 for immunosuppressive treatment of allograft recipients or patients with autoimmune diseases.

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