Metastases to gastrointestinal or gynaecological tracts are more likely in invasive lobular carcinoma than invasive ductal cancer. The pathologist should determine whether or not they check estrogen and progesterone receptor status not simply by signet ring cell morphology but also by consideration of clinic-pathological correlation of the patient, such as the presence of a past history of breast cancer, or the colorectal localization of poorly differentiated carcinoma, which may occur less frequently than in the stomach.
The primary cilium is a solitary, sensory, non-motile microtubule-based structure that arises from the centrosome and is projected from the surface of most human cells. The objective of the current pilot study was to conduct an investigation of presence and frequency of cilia in gastrointestinal stromal tumors (GIST).The presence of primary cilia in GIST was evaluated in 9 patients, including 8 primary tumors and 1 liver metastasis. In 2 patients the presence of primary cilia was evaluated not only in the primary tumor, but also in recurrence: in 1 patient in recurrence without previous treatment with imatinib and in 1 patient in recurrence after treatment with imatinib. The primary cilia of GIST cells were immunofluorescently stained with primary monoclonal anti-acetylated tubulin alpha antibody and cell nuclei with DAPI.We observed 9985 nuclei of cells of GISTs and 425 primary cilia in total. The median of frequency of primary cilia in cells of GISTs in all examined samples was 4.26%, in primary tumors was 4.32% and in metastases was 3.64%, respectively.This pilot study provides the evidence of the presence of primary cilia in GISTs in different organs. Primary cilia were identified in all examined cases of GIST, including primary tumors, metastases and recurrent lesions without and with previous treatment with imatinib.
There is a growing corpus of evidence indicating that anti-VEGF therapy may normalize the abnormal tumor vasculature with the potential to re-program the tumor immune microenvironment to a more immunosupportive profile. Tumor vessel normalization increases tumor perfusion, and, consequently, oxygen and nutrient supply, and thus can be assumed to improve the general response to anticancer immunotherapy. The increased antitumor immunity responses seen following anti-VEGF therapy may also be associated with the inhibition of the immunosuppressive action deployed by VEGF on effector T cells. Bearing in mind the recent advances of combination immunotherapy, combinations of anti-VEGF therapy with immune checkpoint inhibitors now appear to represent an attractive strategy. Key to the successful implementation of a combination strategy for treating cancer is understanding the interaction of these two therapeutic interventions, particularly in regards to appropriate reprogramming of the tumor immune microenvironment to improve antitumor immunity.
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