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HighlightsRCC is the predominant primary tumor for isolated pancreatic metastases.Pancreatic metastases from RCC generally tends to slow growth and indolent behavior.Surgical resection may be curative and should be considered in selected patients.It is still controversial whether to perform typical or atypical surgical procedures.Pancreatic metastasis after a prolonged period may imply change in tumor biology.

Non-Hodgkin lymphomas commonly show extranodal involvement (25-30%) but primary diffuse large B-cell lymphomas (DLBCL) with extranodal localization represent clinically and molecularly distinct entities. The present study involved retrospective analysis of case records of 4 patients who were diagnosed with extranodal DLBCL between 2010 and 2016 at the Medical Oncology and Hematology Departments of the Ioannina University Hospital, Greece. Median age of presentation was 69 years (range 60-77 years). There were 2 males and 2 females. The sites of DLBCL involvement included adrenal gland, mandible, cervix uteri, and ileum. Two patients had B symptoms while none had bone marrow involvement. After staging workup, all the patients fell into IE stage. The treatment approach included chemotherapy combined with rituximab (R), whereas one patient received additionally irradiation therapy. Post-treatment positron emission tomography-computed tomography scan was performed in 3 patients. In terms of the outcome, 3 patients are alive in complete response, whereas one was lost in follow-up. Further prospective data analyses are required so as to better elucidate the biology and course of extranodal DLBCL.

11503 Background: Hormone refractory breast cancer (HRBC) is incurable due to malignant stem cells,which represent a potential nidus for the recurrent cancer that arises after treatment failure. Methods: From 126 metastatic HRBC patients,we obtained CSCs from recurrent tumor reservoirs missed from current chemotherapy,which had eradicated bulky tumor foliage.HRBC-CSCs were treated with DVC composed of vinorelbine linked onto anti-DNMT1/anti-SHH di-diabody. Results: Post treatment ,we observed antibody dependent cellular toxicity (ADCC),complement dependent cellular toxicity (CDC) ,and antibody mediated phagocytosis (AMP) mediated by the di-diabody.Next,we observed inhibition of SHH, which is overexpressed in CSCs,blocking HH binding to PTCH,and signaling from SMO and GLI. DNMT1 was downregulated blocking DNA methylation.This inhibited hTERT transcription blocking the telomerase activity of CSCs. DNA demethylation reactivated DEAF-1 upregulating PTEN,which antagonised PKB/mTOR,PI3K/AKT,src/VEGF , HIF-1a/survivin angiogenic and antiapoptotic pathways leading to synergistic inhibition of telomerase activity. RKIP was re-expressed inhibiting Raf-1/MEK1–2/ERK1–2,NFkB and STAT3 leading to downregulation of CD46 mediating CDC. PTEN by inhibiting AKT,it upregulated Drg-1.Also,PTEN re-expression inhibited synergistically with vinorelbine,the oncogenes bcl-2,bcl-xL and mcl-1 leading to upregulation of bid,bax and bak. DNA demethylation reactivated CDH1,RASSF1A,EDNRB,Kip1/p27,RhoE,NKX31,DLC-1,GSTP1, TIG1,TAP,Necl-1,RARb,NTRK2,MFPC7–8,p16/Rb,p53/p21,DOC- 2/DAB2,BTG2,maspin and DEFB1. Ki67,BrdU and MTT exhibited inhibition of CSC proliferation. DFF,PARP,TUNEL,SEM and TEM exhibited PCD type I,II and III in CSCs.We observed aponecrosis based on lysosomal damage independent of caspases.PCR exhibited inhibition of CSC markers CD44/a2b1/CD133,b-catenin,Sca1,Notch-1 and methylation marker SCNN1B. Conclusions: DVC eradicated efficiently HRBC-CSCs. No significant financial relationships to disclose.