A tumor is an abnormal mass of tissue that has formed a lump. It’s called a benign tumor if it grows slowly and is self-limiting; that is, if it doesn’t have the capacity to invade nearby tissues and spread beyond its original site. A malignant, or cancerous, tumor, on the other hand, is innately dangerous because its cells can divide uncontrollably and produce virtually immortal daughter cells. Malignant tumor cells can penetrate and destroy adjacent tissue, and can metastasize, or travel through the circulation to distant parts of the body and form new tumors.

Patients with pancreatic cancer often present with non-specific symptoms and are often diagnosed at an advanced stage. The relationship between diabetes and the development of pancreatic cancer has been an area of intense research. In the present study we specifically aim to look at the hypothesis that the incidence of insulin dependent diabetes increases after the onset of pancreatic cancer. Materials and Methods: We retrospectively reviewed the chart of all pancreatic cancer patients in tumor registry admitted to University of Florida Tumor Registry in Jacksonville, Florida. Data was collective from January 2000 and December 2006. Each patient’s record was reviewed for histologic biopsy, demographic information, presence of risk factors, co-morbidities, presence and duration of diabetes. Assessment of diabetes was based on the guidelines provided by American Diabetes Association. Results: 82 patients were identified from the University of Florida Cancer Registry from the year 2000-2006. Complete data was available on 76 patients. Mean age at diagnosis was 66.4 years. 53 (69.7%) were African American, 23 (30.26%) were white. There was an equal male/female distribution of 1:1.07 (43 males; 40 females). 35 (46.0%) patients were smokers. Most common presentation was with obstructive jaundice (33/76 or 43.4%) followed by typical symptoms of weight loss, fatigue, abdominal and back pain (31/76 or 40.78%). In 11 (14.47%) patients, pancreatic cancer was noted as an incidental finding. Staging at the time of diagnosis was available in 76 patients. 48 (63.1%) patients were in Stage 4, 13 (17.1%) patients were in Stage 3, 10 (13.15%) patients were at stage 2 and 5 (6.5%) patients were in Stage 1. 15(19.7%) patients had diabetes at the time of diagnosis of pancreatic cancer. 5 (6.5%) developed one or more deep vein thrombosis (DVTs) after the diagnosis of PC. Diabetes was present in 15 (19.7%) for an average duration of 19 months. Only 4(26.6%) out of 15 patients were on insulin therapy before the diagnosis of pancreatic cancer. Six additional patients (an increase of 7.93%) developed diabetes after the diagnosis of pancreatic cancer. 13 (61.9%) of the 21 patients required insulin therapy after the diagnosis of pancreatic cancer. As many as 27 (35%) patients opted for hospice care after the diagnosis of pancreatic cancer. Whipple’s procedure or exploratory debulking surgery of the tumor was performed in 33 (43%) patients. 29 (38.1%) patients received Gemcitabine/carboplatin/5 FU based chemotherapy. Conclusion: We found that the Incidence of Insulin-dependent diabetes increased in patients diagnosed with pancreatic cancer.

Tumor markers such as beta Human Chorionic Gonadotropin (bHCG) and Carboxyhydrate Antigen 19-9 (CA19-9) have long been associated with bladder cancer and although their expression is associated with poorer oncological outcomes, they have little role in the routine clinical management of this disease. Recent advances in engineered antibody technology have lead to renewed interest in these markers as potential targets for new therapeutics. Here we report the case of a patient with locally advanced bladder cancer and the response of serum bHCG and CA19-9 to endoscopic resection and then radical cystectomy and serves to highlight how these tumor markers might be used to measure treatment effect.

C-Jun N-terminal kinase (JNK) represents a group of mitogen-activated protein kinases (MAPKs) involved in many cellular responses including apoptosis. We have previously reported that taxol, a microtubule-interfering therapeutic agent widely used against various cancers, induces caspase-independent but apoptotic inducing factor (AIF)-dependent apoptosis in human ovarian cancer cell line SKOV3 cells. In the present study, we add to this report a detailed analysis of the taxol-induced apoptotic mechanisms in SKOV3 cells, particularly focusing on JNK and p53. In line with the previous report, we found that taxol induced caspase-independent apoptosis with concurrent activation of JNK, phosphorylation of Bcl-2, Bax translocation to the mitochondria, and AIF release from the mitochondria. Restoration of p53 functionality into SKOV3 cells, which are p53-null cells, by transfection of wild-type p53, however, induced caspase-dependent apoptosis in response to taxol treatment as evidenced by increasing PARP cleavage and the emergence of processed, active caspase-3 and -7. More to the point, treatment with a JNK inhibitor SP600125 blocked taxol-induced apoptotic cell death in both parental SKOV3 cells (p53-deficient) and p53-transfectant cells. Collectively, the aforementioned findings lend support to the view that taxol-induced apoptotic cell death in SKOV3 cells is executed by different mechanisms depending on the presence of p53 but commonly mediated by ASK1-JNK and/or -p38 axes.