Solitary pancreatic tuberculous abscess mimicking prancreatic cystadenocarcinoma: a case report.
(17/165)
BACKGROUND: The incidence of pancreatic tuberculosis is extremely rare, and it frequently misdiagnosed as pancreatic neoplasms. The nonsurgical diagnosis of this entity continues to be a challenge. CASE PRESENTATION: A 33 year old male with six-month history of intermittent right epigastric vague pain and weight lost had found a solitary pancreatic cystic mass and diagnosed as pancreatic cystadenocarcinoma. The chest X-ray film and physical examination revealed no abnormalities. Abdominal ultrasound (US) examination showed an irregular hypoechoic lesion of 6.6 cm x 4.4 cm in the head of pancreas, and color Doppler flow imaging did not demonstrate blood stream in the mass. The attempts to obtain pathological evidence of the lesion by US-guided percutaneous fine needle aspiration failed, an exploratory laparotomy and incisional biopsy revealed a caseous abscess of the head of pancreas without typical changes of tuberculous granuloma, but acid-fast stain was positive. CONCLUSIONS: Pancreatic tuberculosis should be considered in the differential diagnosis of focal pancreatic lesions, especially for young people in developing countries. (+info)
Immuno-histological characterization of OVS1 and OVS2 monoclonal antibodies recognizing human ovarian mucinous cystadenocarcinoma.
(18/165)
OVS1 and OVS2 monoclonal antibodies (MAbs) were established by fusing murine myeloma cell line NS1/1-Ag4-1 with mouse spleen cells immunized with fresh human ovarian mucinous-cystadenocarcinoma tissue. The selection of the MAbs was assayed by an immuno-histological (streptavidin-biotin) staining of the specific antigen antibody reaction localized on frozen sections of the same tumor. Other paraffin sections and established cell lines were also screened by immuno-histological staining in order to characterize the specificity and sensitivity of these two MAbs. OVS1 MAb showed 96% specificity and 67% sensitivity to mucinous cystadenocarcinoma with no cross reactions to normal tissue, benign tissue, other cancers, or any established cell lines. OVS2 MAb revealed only 8% specificity but 78% sensitivity to mucinous cystadenocarcinoma, however, a cross reaction to some normal and benign tissues or other cancers was shown. The data suggested that OVS1 and OVS2 MAbs could be used in combination to detect ovarian mucinous cystadenocarcinoma. (+info)
Modulation of cisplatin sensitivity and growth rate of an ovarian carcinoma cell line by bombesin and tumor necrosis factor-alpha.
(19/165)
A twofold change in the cisplatin (DDP) sensitivity of 2008 human ovarian carcinoma cells is sufficient to reduce tumor response in vivo. The DDP sensitivity of these cells can be enhanced by activation of the epidermal growth factor and protein kinase C signal transduction pathways. We report here that two endogenous growth factors, bombesin and tumor necrosis factor alpha (TNF alpha), enhanced DDP sensitivity by factors of 1.7 +/- 0.1 (SD)-fold and 1.8 +/- 0.1 (SD)-fold, respectively. Both agents also produced sensitization in an 11-fold DDP-resistant 2008 subline. Neither bombesin nor TNF alpha changed the accumulation of DDP, glutathione content, or glutathione-S-transferase activity in 2008 cells. However, a 2-h exposure to both bombesin and TNF alpha was sufficient to increase 2008 cloning efficiency by up to 2.6 +/- 0.1 (SD)-fold and 2.2 +/- 0.1 (SD)-fold, and it increased average colony size by 1.35 +/- 0.1 (SD)-fold and 1.55 +/- 0.1 (SD)-fold, respectively. Bombesin increased intracellular free calcium, and this was blocked by the bombesin receptor-specific antagonist SC196, demonstrating that 2008 cells have functional bombesin receptors. These results indicate that bombesin and TNF alpha can enhance sensitivity to DDP in both DDP sensitive and resistant variants of a human ovarian carcinoma and that both agents serve as growth factors for this tumor. (+info)
Cystadenoma and cystadenocarcinoma of the pancreas.
(20/165)
The pathological findings in 14 cases of cystadenoma and three cases of cystadenocarcinoma of the pancreas have been studied in relation to the clinical effects. All the patients were women, and their ages ranged from 13 to 90 years. Four tumours measuring 2 to 4 cm. in diameter had not caused symptoms or signs. Tumours from 7 to 12 cm. in diameter had been felt in the upper abdomen and half the patients with such tumours had complained of pain. In two cases with large tumours there was severe bleeding into the alimentary canal. THE CYSTADENOMAS WERE OF TWO TYPES: 1 Tumours with small loculi lined by cubical epithelium, in which there was little secretion of mucus by the epithelium but abundant mucoid stroma. There were six of these tumours and we have no evidence of malignant change in this type. 2 Tumours with relatively large cystic spaces filled with mucus and lined by tall, mucus-secreting epithelium. There were eight of these, and the possibility of malignant transformation in this type of tumour is indicated by the finding that in three cases of cystadenocarcinoma two appeared to have been preceded by simple mucus-secreting cystadenomas. Signs of recent or old haemorrhage were common in both types of cystadenoma and also in the cystadenocarcinomas. (+info)
A mutation in the canine BHD gene is associated with hereditary multifocal renal cystadenocarcinoma and nodular dermatofibrosis in the German Shepherd dog.
(21/165)
Hereditary multifocal renal cystadenocarcinoma and nodular dermatofibrosis (RCND) is a naturally occurring canine kidney cancer syndrome that was originally described in German Shepherd dogs. The disease is characterized by bilateral, multifocal tumors in the kidneys, uterine leiomyomas and nodules in the skin consisting of dense collagen fibers. We previously mapped RCND to canine chromosome 5 (CFA5) with a highly significant LOD score of 16.7 (theta=0.016). We have since narrowed the RCND interval following selection and RH mapping of canine genes from the 1.3 x canine genome sequence. These sequences also allowed for the isolation of gene-associated BACs and the characterization of new microsatellite markers. Ordering of newly defined markers and genes with regard to recombinants localizes RCND to a small chromosomal region that overlaps the human Birt-Hogg-Dube locus, suggesting the same gene may be responsible for both the dog and the phenotypically similar human disease. We herein describe a disease-associated mutation in exon 7 of canine BHD that leads to the mutation of a highly conserved amino acid of the encoded protein. The absence of recombinants between the disease locus and the mutation in US and Norwegian dogs separated by several generations is consistent with this mutation being the disease-causing mutation. Strong evidence is provided that the RCND mutation may have a homozygous lethal effect (P<0.01). (+info)
Cystadenocarcinoma of the appendix: an incidental imaging finding in a patient with adenocarcinomas of the ascending and the sigmoid colon.
(22/165)
BACKGROUND: Primary adenocarcinomas of the appendix are uncommon. Mucoceles that result from mucinous adenocarcinomas of the appendix may be incidentally detected on imaging. CASE PRESENTATION: A case of a mucocele of the appendix, due to cystadenocarcinoma, is presented as an incidental imaging finding in a female, 86-year-old patient. The patient was admitted due to rectal hemorrhage and underwent colonoscopy, x-ray, US and CT. Adenocarcinoma of the ascending colon, adenomatous polyp of the sigmoid colon and a cystic lesion in the right iliac fossa were diagnosed. The cystic lesion was characterized as mucocele. The patient underwent right hemicolectomy, excision of the mucocele and sigmoidectomy. She recovered well and in two-year follow-up is free from cancer. CONCLUSIONS: Preoperative diagnosis of an underlying malignancy in a mucocele is important for patient management, but it is difficult on imaging studies. Small lymph nodes or soft tissue stranding in the surrounding fat on computed tomography examination may suggest the possibility of malignancy. (+info)
Feasibility of reinstitution of CAPD after partial hepatectomy in patients with malignant hepatic tumors.
(23/165)
OBJECTIVE: To determine the feasibility of reinstitution of continuous ambulatory peritoneal dialysis (CAPD) in patients with malignant hepatic tumors after partial hepatectomy. DESIGN: Retrospective analysis of 2 CAPD patients. SETTING: Dialysis unit of a university teaching hospital. PATIENTS: Two CAPD patients with malignant hepatic tumors who had undergone partial hepatectomy. MAIN OUTCOME MEASURES: Serum biochemistry, Kt/V, peritoneal equilibration test (PET) results before and after hepatectomy. RESULTS: One patient was able to resume CAPD 4 weeks after partial hepatectomy. The other patient was successfully resumed on CAPD after resting the peritoneum for 3 months following partial hepatectomy. The serum biochemistry, Kt/V, and PET results of the 2 patients did not change significantly before and after partial hepatectomy. CONCLUSIONS: Reinstitution of CAPD after partial hepatectomy in patients with malignant hepatic tumors is feasible. (+info)
The c-myc and PyMT oncogenes induce different tumor types in a somatic mouse model for pancreatic cancer.
(24/165)
We have generated a mouse model for pancreatic cancer through the somatic delivery of oncogene-bearing avian retroviruses to mice that express TVA, the receptor for avian leukosis sarcoma virus subgroup A (ALSV-A), under the control of the elastase promoter. Delivery of ALSV-A-based RCAS vectors encoding either mouse polyoma virus middle T antigen (PyMT) or c-Myc to elastase-tv-a transgenic, Ink4a/Arf null mice induced the formation of pancreatic tumors. RCAS-PyMT induced pancreatic tumors with the histologic features of acinar or ductal carcinomas. The induced pancreatic lesions express Pdx1, a marker for pancreas progenitor cells, and many tumors express markers for both exocrine and endocrine cell lineages, suggesting that the tumors may be derived from progenitor cells. In contrast, RCAS-c-myc induced endocrine tumors exclusively, as determined by histology and detection of differentiation markers. Thus, specific oncogenes can induce the formation of different pancreatic tumor types in a single transgenic line, most likely from one or more types of multipotential progenitor cells. Our model appears to be useful for elucidating the genetic alterations, target cells, and signaling pathways that are important in the genesis of different types of pancreatic cancer. (+info)