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Pancreatic Carcinoma (pancreatic + carcinoma)
Terms modified by Pancreatic Carcinoma Selected AbstractsPARANEOPLASTIC VASCULITIS AND COEXISTENT TROUSSEAU'S SYNDROME SECONDARY TO PANCREATIC CARCINOMAJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 9 2006Radcliffe Lisk MRCP No abstract is available for this article. [source] ENDOSCOPIC TRANSPAPILLARY CATHETERIZATION INTO THE GALLBLADDER FOR DIAGNOSIS OF GALLBLADDER CARCINOMADIGESTIVE ENDOSCOPY, Issue 2 2006Naohito Uchida It is often difficult to determine the precise nature of lesions in the gallbladder by radiographic, endoscopic and ultrasonographic methods. The approach to the gallbladder by a percutaneous transhepatic route has been reported. However, there is a possibility of seeding tumor cells into the peritoneal cavity and liver in a percutaneous procedure. On the contrary, transpapillary route can be performed without a possibility of seeding. The double-contrast cholecystography, intragallbladder sonography, direct biopsy of gallbladder lesions and cytology using gallbladder bile have been performed by the procedure of the transpapillary catheterization into the gallbladder. Confirming malignancy by histopathological diagnosis is desirous for determining therapeutic strategy in gallbladder carcinoma. Gathering gallbladder bile is comparatively easier than biopsy of the lesion using the transpapillary catheterization into the gallbladder. Examination of telomerase-related molecules is useful for diagnosis of pancreatic carcinoma. Usefulness of combination assay of human telomerase reverse transcriptase mRNA (hTERT mRNA) and cytology using gallbladder bile obtained by transpapillary catheterization is reported here. However, it would appear that hTERT mRNA is less important in the diagnosis of gallbladder carcinoma than in that of pancreatic carcinoma. When the molecular biological substances with higher sensitivity are found, the reliance of the combination assay of the molecular biological substances and cytology will be established. [source] Diagnosis of pancreatic cancerHPB, Issue 5 2006Fumihiko Miura Abstract The ability to diagnose pancreatic carcinoma has been rapidly improving with the recent advances in diagnostic techniques such as contrast-enhanced Doppler ultrasound (US), helical computed tomography (CT), enhanced magnetic resonance imaging (MRI), and endoscopic US (EUS). Each technique has advantages and limitations, making the selection of the proper diagnostic technique, in terms of purpose and characteristics, especially important. Abdominal US is the modality often used first to identify a cause of abdominal pain or jaundice, while the accuracy of conventional US for diagnosing pancreatic tumors is only 50,70%. CT is the most widely used imaging examination for the detection and staging of pancreatic carcinoma. Pancreatic adenocarcinoma is generally depicted as a hypoattenuating area on contrast-enhanced CT. The reported sensitivity of helical CT in revealing pancreatic carcinoma is high, ranging between 89% and 97%. Multi-detector-row (MD) CT may offer an improvement in the early detection and accurate staging of pancreatic carcinoma. It should be taken into consideration that some pancreatic adenocarcinomas are depicted as isoattenuating and that pancreatitis accompanied by pancreatic adenocarcinoma might occasionally result in the overestimation of staging. T1-weighted spin-echo images with fat suppression and dynamic gradient-echo MR images enhanced with gadolinium have been reported to be superior to helical CT for detecting small lesions. However, chronic pancreatitis and pancreatic carcinoma are not distinguished on the basis of degree and time of enhancement on dynamic gadolinium-enhanced MRI. EUS is superior to spiral CT and MRI in the detection of small tumors, and can also localize lymph node metastases or vascular tumor infiltration with high sensitivity. EUS-guided fine-needle aspiration biopsy is a safe and highly accurate method for tissue diagnosis of patients with suspected pancreatic carcinoma. 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) has been suggested as a promising modality for noninvasive differentiation between benign and malignant lesions. Previous studies reported the sensitivity and specificity of FDG-PET for detecting malignant pancreatic tumors as being 71,100% and 64,90%, respectively. FDG-PET does not replace, but is complementary to morphologic imaging, and therefore, in doubtful cases, the method must be combined with other imaging modalities. [source] Antitumor activity of ALK1 in pancreatic carcinoma cellsINTERNATIONAL JOURNAL OF CANCER, Issue 8 2007Hendrik Ungefroren Abstract In this study, the authors investigated the expression of activin receptor-like kinase 1 (ALK1) in pancreatic carcinoma and evaluated its potential role as a tumor suppressor in vitro and in vivo. Endogenous ALK1 expression was demonstrated by immunohistochemistry in both pancreatic tumor tissue and peritumoral normal tissue from 6 patients and by RT-PCR in 8/12 established pancreatic cancer cell lines. Ectopic expression of a constitutively active (ca) ALK1 mutant in TGF-, sensitive PANC-1 and COLO-357 cells augmented transcriptional activation of a Smad2/3 responsive reporter, and slowed down basal growth in vitro. Both effects were further enhanced by TGF-,/ALK5 stimulation, suggesting largely independent nuclear Smad signaling by both type I receptors. Upon orthotopic transplantation of PANC-1-caALK1 into immunodeficient mice, tumor size was strongly reduced and was associated with a lower microvessel density in the PANC-1-caALK1-derived tumors. In vitro, this mutant efficiently blocked TGF-,-induced epithelial-to-mesenchymal transdifferentiation and suppressed TGF-,/ALK5-mediated activation of the p38 MAPK pathway. Mechanistically, caALK1 silenced MyD118, an immediate TGF-, target gene whose protein product, GADD45,, couples Smad signaling to p38 activation. These results show that ALK1 activation in pancreatic tumor cells is antioncogenic by inducing ALK5-independent growth inhibition and by blocking TGF-,/ALK5-mediated epithelial-to-mesenchymal transdifferentiation and, possibly, invasion and metastatic progression. © 2007 Wiley-Liss, Inc. [source] Tolerability of Gemcitabine and Carboplatin Doublet Therapy in Cats with CarcinomasJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 3 2009I. Martinez-Ruzafa Background: This study was performed to determine the toxicity of gemcitabine-carboplatin doublet therapy in cats with carcinomas. Hypothesis: Gemcitabine and carboplatin are safe in tumor-bearing cats. Animals: Twenty cats with spontaneously occurring carcinomas. Methods: A cohort of 6 cats received gemcitabine (2 mg/kg IV) on days 1, 8, and 15 and carboplatin (10 mg/kg IV) immediately after gemcitabine on day 1 of a 21-day cycle. A 2nd cohort of 14 cats received carboplatin 4 hours after gemcitabine on day 1 and gemcitabine on day 8 but not day 15. The cycles were repeated every 21 days. Results: Cats in the 1st cohort received a median of 3.75 cycles per animal (range, 1,6). Two cats (33.3%) developed grade 3 or 4 neutropenia, 1 (16.7%) grade 4 thrombocytopenia, and 1 (16.7%) grade 3 gastrointestinal toxicity. Gemcitabine dose reductions and treatment delays occurred in 1 and 4 cats, respectively. Cats in the 2nd cohort received a median of 2 cycles per animal (range, 0.5,10). Two cats (14.3%) had grade 3 or 4 neutropenia and 1 (7.1%) had grade 3 and 4 gastrointestinal toxicity. One cat required gemcitabine dose reduction and 6 had treatment delays. In the 2nd cohort, of 11 cats with measurable tumors, there was 1 complete response (pancreatic carcinoma) and 1 partial response (squamous cell carcinoma, receiving concurrent nonsteroidal anti-inflammatory drugs). Conclusions and Clinical Importance: Gemcitabine-carboplatin combination appears moderately well tolerated in tumor-bearing cats. Minimal patient benefit suggests that alternative schedules or combinations of gemcitabine with other agents should be explored. [source] Unusual endocrine pancreatic carcinoma (carcinoid tumor) in a 14-year-old girlPEDIATRICS INTERNATIONAL, Issue 6 2008Stefanie Lenze No abstract is available for this article. [source] Combined biliary and gastric bypass procedures as effective palliation for unresectable malignant diseaseANZ JOURNAL OF SURGERY, Issue 6 2009Christopher D. Mann Abstract Background:, Although endoscopic treatment of jaundice is increasingly used in the palliation of unresectable malignant disease, surgical bypass still has a role to play in this setting. This study aimed to reappraise the short-term and long-term results of combined biliary/gastric bypass (hepaticojejunostomy and gastrojejunostomy) as palliation for unresectable malignant disease. Methods:, All patients undergoing simultaneous biliary and gastric bypass procedures for unresectable malignant disease between August 2000 and January 2006 were identified and outcomes reviewed. Results:, One hundred and two patients underwent open surgical biliary drainage procedures for palliation of malignant disease. Underlying malignant disease included pancreatic carcinoma (n = 88), duodenal adenocarcinoma (n = 6) and distal cholangiocarcinoma (n = 3). Thirty-one of the patients underwent a planned palliative bypass procedure, the remainder being carried out after unresectable disease was identified at laparotomy. Postoperative mortality and morbidity rates were higher in the group undergoing planned bypass. During follow up, two patients developed recurrent jaundice that required transhepatic stenting and two patients developed late gastric outlet obstruction requiring refashioning of the gastrojejunostomy. Conclusion:, Combined surgical biliary and gastric bypass achieved effective palliation of jaundice and gastric outlet obstruction until death in >95% of patients in this series. It remains first-line therapy in patients identified as having unresectable disease at laparotomy. [source] IGG4-RELATED SCLEROSING LYMPHOPLASMACYTIC PANCREATITIS AND CHOLANGITIS MIMICKING CARCINOMA OF PANCREAS AND KLATSKIN TUMOURANZ JOURNAL OF SURGERY, Issue 4 2008Moon-Tong Cheung Background: Autoimmune sclerosing pancreatitis is a well-known disease entity for years, particularly recognizing the difficulty in distinguishing it from malignancy. Immunohistochemical study showed that immunoglobulin IgG4 staining was positive in plasma cells of some autoimmune pancreatitis or cholangitis. The term ,autoimmune sclerosing pancreatocholangitis' was used as it was believed that they belonged to a range of disease involving both pancreas and biliary tree. It may also be part of a systemic fibro-inflammatory disease. Patients and Methods: All the patients suffering from immunoglobulin G4 (IgG4)-related pancreatitis and cholangitis from May 2003 to September 2006 in Queen Elizabeth Hospital, Hong Kong were retrospectively studied. Results: A total of five patients with clinical diagnosis of IgG4-related autoimmune pancreatitis or cholangitis were analysed. All presented with jaundice or abdominal pain, mimicking carcinoma. Two patients had major resection, two patients were diagnosed by intraoperative biopsy and one was based on serum IgG4 level. Conclusion: With the growing awareness of this relatively recently characterized clinical entity and its similar presentation to pancreatic carcinoma or bile duct cholangiocarcinoma, it is important for autoimmune sclerosing pancreatocholangitis to be included in the differential diagnosis of pancreaticobiliary disease. The management strategy has shown to be modified , from major resection to intraoperative biopsy and to the assay of serum IgG4 level without the necessity of histology confirmation. [source] Gemcitabine-induced radiation recall in the treatment of pancreatic cancerASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY, Issue 1 2009Wan Mohd Nazri WAN ZAINON Abstract Aim: To evaluate two cases of gemcitabine-induced radiation recall in patients who were treated for localized pancreatic cancer, and review the literature. Methods: The two cases of radiation recall (from a cohort of 80 patients treated for pancreatic carcinoma) were retrospectively identified using patient medical records. Prior publications were identified through an English language literature search of MEDLINE Ovid from January 1966 to October 2006, using the key words gemcitabine and radiation recall. Results: Both the radiation recall reactions were limited to the gastrointestinal system, localized to previous radiotherapy field. No pathology was identified on radiological investigation. The onset of the radiation recall phenomenon was 2 and 10 days, respectively, from the time gemcitabine was initiated. The treatment of radiation recall consisted of the cessation of gemcitabine, initiating steroid therapy and supportive therapy. Both of the patients' symptoms achieved complete resolution. A comprehensive review of the literature found 15 previous cases of radiation recall related to gemcitabine but one reported effect involving the gastrointestinal system. Previously reported sites of recall phenomena included the skin, muscles, brain stem and optic nerve. In the treatment of pancreatic carcinomas, there were only four reported cases, three involving the onset of myositis of abdominal muscle and one case of gastrointestinal bleeding. Conclusion: Radiation recall from gemcitabine chemotherapy is uncommon. It can potentially arise in any site that has been irradiated previously. The treating doctor needs to be aware of this phenomenon to be able to manage this condition appropriately. [source] Radiofrequency field-induced thermal cytotoxicity in cancer cells treated with fluorescent nanoparticles,CANCER, Issue 13 2010Evan S. Glazer MD Abstract BACKGROUND: Nonionizing radiation, such as radiofrequency field and near infrared laser, induces thermal cytotoxicity in cancer cells treated with gold nanoparticles. Quantum dots are fluorescent semiconducting nanoparticles that were hypothesized to induce similar injury after radiofrequency field irradiation. METHODS: Gold nanoparticles and 2 types of quantum dot (cadmium-selenide and indium-gallium-phosphide) conjugated to cetuximab (C225), a monoclonal antibody against human epidermal growth factor receptor (EGFR)-1, demonstrated concentration-dependent heating in a radiofrequency field. The authors investigated the effect of radiofrequency field exposure after targeted nanoparticle treatment in a coculture of 2 human cancer cell lines that have differential EGFR-1 expression (a high-expressing pancreatic carcinoma, Panc-1, and a low-expressing breast carcinoma, Cama-1). RESULTS: Radiofrequency revealed that Panc-1 or Cama-1 cells not containing gold nanoparticles or quantum dots had a viability of >92%. The viability of Panc-1 cells exposed to the radiofrequency field after treatment with 50 nM Au-C225 was 39.4% ± 8.3% without injury to bystander Cama-1 cells (viability was 93.7% ± 1.0%; P , .0006). Panc-1 cells treated with targeted cadmium-selenide quantum dots were only 47.5% viable after radiofrequency field exposure (P<.0001 compared with radiofrequency only Panc-1 control cells). Targeted indium-gallium-phosphide quantum dots decreased Panc-1 viability to 58.2% ± 3.4% after radiofrequency field exposure (P = ,.0004 compared with Cama-1 and Panc-1 controls). CONCLUSIONS: The authors selectively induced radiofrequency field cytotoxicity in Panc-1 cells without injury to bystander Cama-1 cells using EGFR-1,targeted nanoparticles, and demonstrated an interesting bifunctionality of fluorescent nanoparticles as agents for both cancer cell imaging and treatment. Cancer 2010. © 2010 American Cancer Society. [source] Elevated serum heparanase-1 levels in patients with pancreatic carcinoma are associated with poor survivalCANCER, Issue 3 2006Roderick M. Quiros M.D. Abstract BACKGROUND It has previously been shown that heparanase-1 (HPR1), an endoglycosidase, is up-regulated in pancreatic carcinoma. The purpose of this study was to test whether serum HPR1 levels in pancreatic carcinoma patients are elevated, and whether higher serum HPR1 levels are associated with a shortened survival. METHODS Serum HPR1 levels in 40 healthy donors, 31 pancreatic carcinoma patients, and 11 patients treated with gemcitabine were measured by a novel enzyme-linked immunoadsorbent assay. HPR1 expression in tumors was analyzed by immunohistochemical staining. Patient overall survival time was determined according to the Kaplan,Meier method, and their difference was evaluated by the log-rank test. A P value < 0.05 was considered statistically significant. RESULTS The mean serum HPR1 activity in pancreatic carcinoma patients was 439 ± 14 units/mL, compared with 190 ± 4 units/mL in the control serum samples from healthy donors. Serum HPR1 levels were significantly higher in patients with HPR1-positive tumors (660 ± 62 units/mL) compared with those with HPR1-negative tumors (241 ± 14 units/mL). The mean survival of 19 pancreatic carcinoma patients with serum HPR1 activity > 300 units/mL was 7.9 ± 0.2 months, whereas the mean survival of 12 patients with serum HPR1 activity < 300 units/mL was 13.3 ± 0.6 months. A Kaplan,Meier plot of the patient survival curve followed by log-rank test revealed that patients in the high serum HPR1 group had a significantly shorter survival compared with those in the low serum HPR1 group. Mean serum HPR1 activity decreased by 64% in 11 pancreatic carcinoma patients after 2 weeks of treatment with gemcitabine. CONCLUSIONS Serum HPR1 activity in pancreatic carcinoma patients was found to be significantly elevated, in particular in those with HPR1-positive tumors. Increased serum HPR1 activity was associated with a shorter survival in patients with pancreatic carcinoma patients. Cancer 2006. © 2005 American Cancer Society. [source] A highly sensitive and quantitative telomerase activity assay with pancreatic juice is useful for diagnosis of pancreatic carcinoma without problems due to polymerase chain reaction inhibitorsCANCER, Issue 10 2004Analysis of 100 samples of pancreatic juice from consecutive patients Abstract BACKGROUND Early detection of pancreatic carcinoma is difficult even with current diagnostic tools. Novel biomarkers and detection techniques are urgently needed. Telomerase activity is a promising diagnostic marker. However, the conventional telomeric repeat amplification protocol (TRAP) assay is not suitable for clinical application because of its complexity, time-consuming nature, and the effects of polymerase chain reaction (PCR) inhibitors in samples leading to difficulties in quantification. METHODS The authors used a hybridization protection assay in combination with TRAP (TRAP/HPA) to investigate the effects of PCR inhibitors in pancreatic juice on quantification of telomerase activity. They analyzed 117 consecutive samples of pancreatic juice to determine the feasibility of TRAP/HPA for diagnosis of pancreatic carcinoma. RESULTS The authors found that TRAP/HPA was 1000-fold more sensitive than the conventional TRAP assay, and that the effects of PCR inhibitors could be avoided by diluting samples. In a large analysis of pancreatic juice samples with TRAP/HPA, 17 samples were excluded from the final analysis because of insufficient follow-up periods or inadequate treatment of the samples. Relative telomerase activity (RTA) in samples from patients with pancreatic carcinoma was significantly higher in comparison to samples from patients with pancreatitis and 13 (61.9%) of 21 samples from patients with pancreatic carcinoma showed high RTA (> 4 U). Meanwhile, high RTAs were observed in 4 of 35 (11.4%) samples from patients with intraductal papillary mucinous tumor and in 1 of 40 samples (2.5%) fom patients without malignant disease. CONCLUSIONS TRAP/HPA accurately evaluated weak telomerase activity in pancreatic juice samples without the problem due to PCR inhibitors. This large analysis of nonselected pancreatic juice samples suggested that TRAP/HPA is a promising approach for the diagnosis of pancreatic carcinoma. Cancer 2004. © 2004 American Cancer Society. [source] Overexpression of synuclein-, in pancreatic adenocarcinomaCANCER, Issue 1 2004Zhongkui Li Ph.D. Abstract BACKGROUND Currently, pancreatic adenocarcinoma is the fourth leading cause of cancer-related death in the United States. Despite the advances in pancreatic carcinoma research, patients with this devastating disease have a very poor prognosis. To identify the gene expression profile of pancreatic carcinoma, an important step in the process of developing new diagnostic and therapeutic strategies, the authors investigated the alteration of gene expression in this disease. METHODS The authors analyzed a public serial analysis of gene expression (SAGE) database and examined in greater detail the expression of synuclein-, mRNA in several pancreatic carcinoma cell lines and tumor tissue samples by reverse transcriptase,polymerase chain reaction (RT-PCR) analysis and Northern blot analysis. The expression of synuclein-, protein was investigated further by immunohistochemical and Western blot analyses using tumor cell lines, tumor tissue, and serum samples. RESULTS Synuclein-, mRNA was overexpressed in 11 of 12 pancreatic carcinoma cell lines, including AsPc-1, MDAPanc28, Capan-1, Capan-2, PANC-1, HS766T, MDAPanc3, MDAPanc48, Colo357FG, MiaPaCa2, CFPac1, and BxPc3. The expression of synuclein-, protein was detectable in 8 of 12 pancreatic carcinoma cell lines (67%) and in 22 of 32 pancreatic tumor tissue samples (69%) by Western blot analysis. On immunohistochemical staining, synuclein-, protein was present in 61% of the tumor tissue samples examined from patients with Stage I and II pancreatic carcinoma. The overexpression of synuclein-, is correlated with perineural and lymph node invasion. Synuclein-, protein also was detectable by Western blot in serum samples from 21 of 56 patients (38%) with pancreatic carcinoma. CONCLUSIONS Synuclein-,, which initially was described as a breast carcinoma,specific gene involved in invasion, metastasis, and chemotherapy resistance, was frequently overexpressed in pancreatic carcinoma. Overexpression of synuclein-, may play a role in pancreatic carcinoma invasion. Further studies will be necessary to determine the role of synuclein-, in pancreatic carcinoma. Cancer 2004. © 2004 American Cancer Society. [source] Linear IgA bullous dermatosis in a patient with advanced pancreatic carcinomaCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 4 2008M. Adami No abstract is available for this article. [source] Expression of the CXCR6 on polymorphonuclear neutrophils in pancreatic carcinoma and in acute, localized bacterial infectionsCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2008M. M. Gaida Summary The chemokine receptor CXCR6 has been described on lymphoid cells and is thought to participate in the homing of activated T-cells to non-lymphoid tissue. We now provide evidence that the chemokine receptor CXCR6 is also expressed by activated polymorphonuclear neutrophils (PMN) in vivo: Examination of biopsies derived from patients with pancreatic carcinoma by confocal laser scan microscopy revealed a massive infiltration of PMN that expressed CXCR6, while PMN of the peripheral blood of these patients did not. To answer the question whether CXCR6 expression is a property of infiltrated and activated PMN, leucocytes were collected from patients with localized soft tissue infections in the course of the wound debridement. By cytofluorometry, the majority of these cells were identified as PMN. Up to 50% of these PMN were also positive for CXCR6. Again, PMN from the peripheral blood of these patients were nearly negative for CXCR6, as were PMN of healthy donors. In a series of in vitro experiments, up-regulation of CXCR6 on PMN of healthy donors by a variety of cytokines was tested. So far, a minor, although reproducible, effect of tumour necrosis factor (TNF,) was seen: brief exposure with low-dose TNF, induced expression of CXCR6 on the surface of PMN. Furthermore, we could show an increased migration of PMN induced by the axis CXCL16 and CXCR6. In summary, our data provide evidence that CXCR6 is not constitutively expressed on PMN, but is up-regulated under inflammatory conditions and mediates migration of CXCR6-positive PMN. [source] Diagnosis of metastatic pancreatic mesenchymal tumors by endoscopic ultrasound-guided fine-needle aspiration,DIAGNOSTIC CYTOPATHOLOGY, Issue 11 2009Linda Varghese M.D. Abstract Involvement of the pancreas by metastatic sarcoma is rare, and can prove challenging to differentiate from sarcomatoid carcinomas which occur more commonly. The endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) technique has been successfully used for the diagnosis of pancreatic carcinomas whether primary or metastatic, and is now considered the most effective noninvasive method for the identification of pancreatic metastases. However, to date very few reports detail the diagnosis of mesenchymal neoplasms by EUS-FNA. Herein, we report a series of four patients who underwent EUS-FNA of the pancreas, where the diagnosis of metastatic sarcoma was made based on morphology and ancillary studies. The cases include metastases of leiomyosarcoma, liposarcoma, alveolar rhabdomyosarcoma, and solitary fibrous tumor. The history of a primary sarcoma of the chest wall, mediastinum, and respectively lower extremity was known for the first three of these patients while in the case of the solitary fibrous tumor a remote history of a paraspinal "hemangiopericytoma" was only elicited after the EUS-FNA diagnosis was made. We conclude that EUS-FNA is efficient and accurate in providing a diagnosis of sarcoma, even in patients without a known primary sarcoma, thus allowing institution of therapy without additional biopsies. Diagn. Cytopathol. 2009. © 2009 Wiley-Liss, Inc. [source] Contrast-enhanced power Doppler sonography of ductal pancreatic adenocarcinomas: Correlation with digital subtraction angiography findingsJOURNAL OF CLINICAL ULTRASOUND, Issue 4 2004Chien-Hua Chen MD Abstract Purpose The purpose of this prospective study was to utilize contrast-enhanced power Doppler sonography to evaluate the enhancement characteristics of ductal pancreatic adenocarcinomas and correlate them with the tumor vascularity observed on digital subtraction angiography (DSA). Methods Twenty consecutive patients with ductal pancreatic adenocarcinoma underwent power Doppler sonography and DSA. Tumor vascularity was assessed using unenhanced and contrast-enhanced power Doppler sonography. The contrast agent Levovist was administered intravenously by bolus injection of a dose of 2.5 g at a concentration of 350 mg/mL; saline was administered immediately thereafter. The patients were asked to hold their breath for 30 seconds (for the period 15,45 seconds after saline injection) while the early phase of enhancement was studied; the delayed phase of enhancement was observed between 60 and 120 seconds after saline administration, while patients breathed gently. Results None of the 20 pancreatic carcinomas showed any color signals on power Doppler sonography before administration of the contrast medium. Seventeen (85%) of the 20 pancreatic carcinomas also showed no enhancement in the early and delayed phases of contrast-enhanced power Doppler sonography. However, in the early phase of contrast-enhanced power Doppler sonography; 1 lesion showed pronounced enhancement and 2 showed mild enhancement. On DSA, the 17 carcinomas showing no enhancement on power Doppler sonography were found to be hypovascular, whereas the remaining 3 carcinomas with contrast enhancement on power Doppler sonography were found to be hypervascular. Conclusions The enhancement characteristics of the ductal pancreatic adenocarcinomas correlated well with the tumor vascularity observed on DSA. However, further study is needed to determine the accuracy of contrast-enhanced sonography in the diagnosis of pancreatic masses. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:179,185, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/jcu.20018 [source] Differential expression of insulin-like growth factor binding protein-5 in pancreatic adenocarcinomas: Identification using DNA microarrayMOLECULAR CARCINOGENESIS, Issue 11 2006Sarah K. Johnson Abstract Pancreatic ductal adenocarcinoma (PDAC) is characterized by its aggressiveness and resistance to both radiation and chemotherapeutic treatment. To better understand the molecular pathogenesis of pancreatic cancer, DNA array technology was employed to identify genes differentially expressed in pancreatic tumors when compared to non-malignant pancreatic tissues. RNA isolated from 11 PDACs and 14 non-malignant bulk pancreatic duct specimens was used to probe Affymetrix U95A DNA arrays. Genes that displayed at least a fourfold differential expression were identified and real-time quantitative PCR was used to verify the differential expression of selected upregulated genes. Interrogation of the DNA array revealed that 73 genes were upregulated in PDACs and 77 genes were downregulated. The majority of the 150 genes identified have not been previously reported to be differentially expressed in pancreatic tumors, although a number of the upregulated transcripts have been reported previously. Immunohistochemistry was used to correlate calponin and insulin-like growth factor binding protein-5 (IGFBP-5) RNA levels with protein expression in PDACs and revealed peritumoral calponin staining in the reactive stroma and intense focal staining of islets cells expressing IGFBP-5 at the edge of tumors; thus implicating the interplay of various cell types to promote neoplastic cell growth within pancreatic carcinomas. As a potential modulator of cell proliferation, the overexpression of IGFBP-5 may, therefore, play a significant role in the malignant transformation of normal pancreatic epithelial cells. © 2006 Wiley-Liss, Inc. [source] Microarray: an instrument for cancer surgeons of the future?ANZ JOURNAL OF SURGERY, Issue 7-8 2010Matthew L. Broadhead Abstract Microarray enables the study of thousands of genes simultaneously. While still in its infancy as a technique and with a number of barriers to be overcome, microarray is allowing scientists to thoroughly examine the molecular pathways of cancer pathogenesis. However, the adoption of microarray as a clinically applicable technique has been slow coming. Current literature suggests roles in the diagnosis of tumours of unknown origin, in the evaluation of prognostic markers, and in guiding treatment for recurrent and resistant malignancy. This review outlines the science of microarray and draws on clinical examples, including osteosarcoma, breast, prostate and pancreatic carcinomas, to highlight the potential of microarray as a technique of surgical importance. [source] Gemcitabine-induced radiation recall in the treatment of pancreatic cancerASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY, Issue 1 2009Wan Mohd Nazri WAN ZAINON Abstract Aim: To evaluate two cases of gemcitabine-induced radiation recall in patients who were treated for localized pancreatic cancer, and review the literature. Methods: The two cases of radiation recall (from a cohort of 80 patients treated for pancreatic carcinoma) were retrospectively identified using patient medical records. Prior publications were identified through an English language literature search of MEDLINE Ovid from January 1966 to October 2006, using the key words gemcitabine and radiation recall. Results: Both the radiation recall reactions were limited to the gastrointestinal system, localized to previous radiotherapy field. No pathology was identified on radiological investigation. The onset of the radiation recall phenomenon was 2 and 10 days, respectively, from the time gemcitabine was initiated. The treatment of radiation recall consisted of the cessation of gemcitabine, initiating steroid therapy and supportive therapy. Both of the patients' symptoms achieved complete resolution. A comprehensive review of the literature found 15 previous cases of radiation recall related to gemcitabine but one reported effect involving the gastrointestinal system. Previously reported sites of recall phenomena included the skin, muscles, brain stem and optic nerve. In the treatment of pancreatic carcinomas, there were only four reported cases, three involving the onset of myositis of abdominal muscle and one case of gastrointestinal bleeding. Conclusion: Radiation recall from gemcitabine chemotherapy is uncommon. It can potentially arise in any site that has been irradiated previously. The treating doctor needs to be aware of this phenomenon to be able to manage this condition appropriately. [source] | |||||||||||||||||||||||||