Prognosis of Patients with Melanoma and Microsatellitosis Undergoing Sentinel Lymph Node Biopsy

INTRODUCTION: Melanoma microsatellitosis is classified as stage IIIB/C disease and is associated with a poor prognosis. Prognostic factors within this group, however, have not been well characterized. METHODS: We performed a retrospective analysis of 1621 patients undergoing sentinel lymph node (SLN) biopsy at our institution (1996–2011) to compare patients with (n=98) and patients without (n=1523) microsatellites. Univariate and multivariate logistic and Cox regression analyses were used to identify factors associated with SLN positivity and melanoma-specific survival (MSS) in patients with microsatellites. RESULTS: Patients with microsatellites were older and had lesions with higher Clark level and greater thickness that more frequently had mitoses, ulceration, and lymphovascular invasion (LVI) (all p<0.0001). In microsatellite patients, the SLN positivity rate was 43%. Lesional ulceration (OR=2.9, 95% CI: 1.5–8.6), absent tumor infiltrating lymphocytes (OR=2.8, 95% CI: 1.1–7.1), and LVI (OR=3.3, 95% CI: 1.7–10.0) were significantly associated with SLN positivity by multivariate analysis. With a median follow up of 4.5 years in survivors, ulceration (HR=3.4, 95% CI: 1.5–7.8) and >1 metastatic LN (HR=2.7, 95% CI: 1.1–6.6) were significantly associated with decreased MSS by multivariate analysis. In patients without these prognostic factors, the 5-year MSS was 90% (n=49), compared to 50% (n=23) among patients with ulceration only, 51% (n=12) in those with >1 metastatic LN only, or 25% in those with both (n=14, p<0.01). DISCUSSION: Microsatellitosis was frequently associated with multiple adverse pathologic features. In the absence of ulceration and >1 metastatic LN, however, the outcome for patients with microsatellites compared favorably to stage IIIB patients overall

Tumor microenvironment participates in metastasis of pancreatic cancer

Abstract Pancreatic cancer is a deadly disease with high mortality due to difficulties in its early diagnosis and metastasis. The tumor microenvironment induced by interactions between pancreatic epithelial/cancer cells and stromal cells is critical for pancreatic cancer progression and has been implicated in the failure of chemotherapy, radiation therapy and immunotherapy. Microenvironment formation requires interactions between pancreatic cancer cells and stromal cells. Components of the pancreatic cancer microenvironment that contribute to desmoplasia and immunosuppression are associated with poor patient prognosis. These components can facilitate desmoplasia and immunosuppression in primary and metastatic sites or can promote metastasis by stimulating angiogenesis/lymphangiogenesis, epithelial-mesenchymal transition, invasion/migration, and pre-metastatic niche formation. Some molecules participate in both microenvironment formation and metastasis. In this review, we focus on the mechanisms of pancreatic cancer microenvironment formation and discuss how the pancreatic cancer microenvironment participates in metastasis, representing a potential target for combination therapy to enhance overall survival