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  • 1
    Call number: QZ365WI650:16
    Keywords: Rectal Neoplasms / diagnosis ; Rectal Neoplasms / therapy
    Pages: vii,276 p. : ill.
    ISBN: 3-540-23341-5
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    QZ365WI650:16 available
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  • 2
    Keywords: Medicine ; Oncology ; Endocrinology ; Biomedicine ; Cancer Research ; Oncology ; Endocrinology ; Springer eBooks
    Pages: : digital
    ISBN: 9780387774985
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  • 3
    Call number: 05-MED-17:17
    Keywords: Inflammation / Mediators ; Phospholipase A2 / Pathophysiology ; Phospholipase A2 / Inhibitors ; Inflammation / physiopathology ; Phospholipases A / physiology ; Phospholipases A / antagonists & inhibitors
    Pages: xi, 250 p. : ill.
    ISBN: 3805564414
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    05-MED-17:17 departmental collection or stack – please contact the library
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  • 4
    Call number: QZ365WI810:28
    Keywords: Pancreatic Neoplasms
    Pages: 165 p. : ill.
    ISBN: 3895997072
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  • 5
    Keywords: Oncology ; Oncology   ; Endocrinology ; Cancer Research ; Oncology ; Endocrinology ; Springer Nature Living Reference
    Description / Table of Contents: Epidemiology: world overview, risk factors, prospects for prevention -- Development and structure of pancreas -- Pathologic classification and biological behaviour of pancreatic neoplasia -- Developmental molecular biology of the pancreas -- Molecular pathology of precursor lesions of pancreatic cancer, pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), and mucinous cystic neoplasm (MCN) -- Epigenetics: its fundamentals and applications to a revised comprehensive progression model for pancreatic cancer -- Molecular pathology of pancreatic neuroendocrine tumours MEN-1: gastrinomas, insulinoma, Non-Functioning Tumours, VIPoma, glucagonoma, Von Hippel-Lindau, Neurofibromatosis -- Sporadic neuroendocrine pancreatic tumours -- Molecular pathology of non-pancreatic cancer lesions: Ampullary cancer, intra-pancreatic bile duct cancer, and duodenal cancer -- Miscellaneous non-pancreatic non-endocrine tumours -- Novel molecular relationships between chronic pancreatitis and cancer -- Pancreatic cancer stem cells -- Cell cycle control: signalling pathways in pancreatic pathogenesis -- Apoptosis: signalling pathways in pancreatic pathogenesis -- EGFR: signalling pathways in pancreatic pathogenesis Pl3, Akt, lKK, Ras, Raf, MAPKK, ERK -- Hedgehog: signalling pathways in pancreatic pathogenesis -- Smad4/TGF-ß pathway: signalling pathways in pancreatic pathogenesis -- Notch signalling in pancreatic morphogenesis and pancreatic cancer -- Molecular characterization of pancreatic cell lines -- Mouse models of exocrine pancreatic cancer -- Principles and applications of microarray gene expression in pancreatic cancer -- Principles and applications of proteomics in pancreatic cancer -- Tumour-stromal interaction: invasion and metastases -- Genetic susceptibility, high risk groups, chronic and hereditary pancreatitis, familial pancreatic cancer syndromes -- Inherited endocrine pancreatic tumors associated with Multiple Endocrine Neoplasia Type 1 Von-Hippel-Lindau Syndrome, and Neurofibromatosis Type 1 -- Clinical decision making in pancreatic cancer -- Paraneoplastic syndromes -- Diagnostic and therapeutic response markers -- CT and fusion PET-CT Diagnosis, staging, and follow-up -- MRI and MRCP: diagnosis and staging of pancreatic cancer -- EUS Diagnosis and staging -- Laparoscopy and laparoscopic ultrasound: diagnosis and staging -- Overview of palliative management for pancreatic cancer -- Endoscopy -- Interventional radiology -- Role of palliative surgery in advanced pancreatic cancer -- Chemotherapy for advanced pancreatic cancer -- Developments in chemoradiation in advanced pancreatic cancer -- Surgical resection for pancreatic cancer -- Role of venous resection in pancreatic cancer surgery -- Pathological reporting and staging following resection -- Japanese Pancreas Society staging for pancreatic cancer -- Adjuvant chemotherapy in pancreatic cancer -- Case for adjuvant chemoradiation therapy for pancreatic cancer -- Case for neoadjuvant treatment in pancreatic cancer -- Borderline resectable disease -- Management of cystic neoplasms serous cystic neoplasms mucinous, cystic neoplasms, intraductal paillary mucinous neoplasms -- Laparoscopic surgery for pancreatic neoplasm -- Modern Japanese approach to pancreas cancer -- Development of novel biomarkers -- Inherited genetics of pancreatic cancer and secondary screening -- Gene therapy for pancreatic cancer -- Vaccine therapy and immunotherapy -- Emerging targets in pancreatic cancer.-
    Abstract: Worldwide, there are an estimated 232, 000 new cases of pancreatic cancer annually. In the United States, it is the fourth leading cause of cancer death, and approximately 30,000 people die of pancreatic cancer each year. The disease is difficult to diagnose in its early stages, and most patients have incurable disease by the time they present with symptoms. The overall 5-year survival rate for this disease is less than 5%. In organizing this handbook, Dr. Neoptolemos and his co-editors will produce a distinguished Major Reference Work devoted to pancreatic cancer. This handbook will have widespread appeal among clinicians, pathologists and basic scientists who are now struggling to understand this complex and rapidly expanding field. Because of the recent and vast growth in both the clinical and scientific research being done in pancreatic cancer (there is currently an unprecedented investment by academia and industry in this field), each researcher’s knowledge of other specialty areas outside his or her own is now often quite limited. The aim of this book is to place these the tangible advances—those that are indispensable to all working on pancreatic cancer—readily at hand. The book will focus on advances that will not become dated, and the editors will choose authors who are the very best in each area
    Pages: 208 illus., 60 illus. in color. : online resource.
    ISBN: 9781493966318
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  • 6
    Keywords: Medicine ; Cancer Research ; Endocrinology ; Oncology ; Biomedicine ; Cancer Research ; Oncology ; Endocrinology ; Springer eBooks
    Description / Table of Contents: Section: The Nature of Pancreatic Cancer -- Cell Cycle Machinery and Its Alterations in Pancreatic Cancer -- Animal modelling of Pancreatitis-to-Cancer Progression -- Stromal Inflammation in Pancreatic Cancer: Mechanisms and Translational Applications -- Familial Pancreatic Cancer -- Section: Clinical Management of Pancreatic Cancer -- Therapeutic Endoscopy in the Management of Pancreatic Cancer -- Controversies in Pathology Reporting and Staging -- Staging and Postoperative Outcomes Using the International Study Group of Pancreatic Surgery (ISGPS) Classifications -- Borderline Respectable Pancreatic Cancer -- New Japanese Classification of Pancreatic Cancer -- Arterial Resection in Pancreatic Cancer -- Treatment of Recurrent Pancreatic Cancer After Surgery -- Neoadjuvant Chemotherapy in Pancreatic Cancer -- Differential Therapy Based on Tumor Heterogeneity in Pancreatic Cancer -- Neoadjuvant Chemoradiation for Operable Pancreatic Cancer: the Importance of Local Disease Control -- Section: New Directions -- Development of Novel Therapeutic Response Biomarkers -- Clinical Applications of Genomics and Proteomics in Pancreatic Cancer -- Approaching Pancreatic Cancer Phenotypes via Metabolomics -- Circulating Tumour Cells -- Cancer Exosomes for Early Pancreatic Cancer Diagnosis and Role Metastasis -- Metabolism in Pancreatic Cancer -- Secondary Screening for Inherited Pancreatic Ductal Adenocarcinoma -- Role of Radiotherapy in Locally Advanced Pancreatic Cancer -- Evolution of Pancreatic Cancer Surgery -- Multiparameter Modalities for the Study of Patients in the Setting of Individualized Medicine -- Epigenetic Pharmacology -- Precision Medicine Based on Next Generation Sequencing and Master Controllers
    Abstract: In organizing the second edition of this renowned Handbook, Dr. Neoptolemos and his co-editors have produced and updated a revised edition to the distinguished Major Reference Work devoted to pancreatic cancer. Like its preceding edition, the second edition continues to have a widespread appeal among clinicians, pathologists and basic scientists, who are now struggling to understand this complex and rapidly expanding field. Because of the recent and vast growth in both the clinical and scientific research being done in pancreatic cancer, (there is currently an unprecedented investment by academia and industry in this field), each research’s knowledge of other specialty areas outside his or her own is often quite limited. The aim of the new edition is to place the tangible advances, including new developments in surgical approaches with regards to resection techniques, the state of laparoscopic approaches, the growing impact of surgical approaches in the management of recurrent pancreatic cancer, controversies in the management of IMPN as the precursor lesion for PDAC and others – readily at hand. The second edition focuses on advances that will not become dated, and the editors have chosen authors, who are the very best in each area
    Pages: 244 illus., 177 illus. in color. eReference. : online resource.
    Edition: 2nd ed. 2018.
    ISBN: 9781493971930
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  • 7
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    German Medical Science; Düsseldorf, Köln
    In:  121. Kongress der Deutschen Gesellschaft für Chirurgie; 20040427-20040430; Berlin; DOC04dgch1489 /20041007/
    Publication Date: 2004-10-07
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 8
    Keywords: APOPTOSIS ; CELLS ; carcinoma ; Germany ; LUNG ; THERAPY ; TOOL ; TIME ; resistance ; INITIATION ; pancreas ; RE ; pancreatic ; rectum ; viability ; MOLECULAR ANALYSIS ; tumour specimen ; surgical resection ; rectum carcinoma
    Abstract: Surgical resected tumours are often stored for hours in the clinic upon transfer to the bench leading to apoptosis of tumour cells making them no longer suitable for molecular analysis and diagnostic procedures. The way out of this problem may be a new oxygen-enriched solution (OES). We tested this agent using surgical resections of carcinomas of lung, rectum and pancreas. Immediately after resection, one part of each individual tumour was stored in PBS and the other part in OES, and the content of viable or dead cells was determined by trypan blue exclusion and MTT-assay. We found that OES keeps tumour cells up to 3 days and longer more viable than PBS and reduces the percentage of dead cells without inducing therapy resistance and affecting the outcome of experimental procedures. Thus, storing freshly resected tumours in OES may save time for tumour transfer and initiation of experiments
    Type of Publication: Journal article published
    PubMed ID: 16596178
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  • 9
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; carcinoma ; Germany ; IN-VIVO ; INHIBITION ; THERAPY ; VITRO ; GENE ; GENES ; LINES ; MICE ; PATIENT ; IMPACT ; INDUCTION ; treatment ; 5-FLUOROURACIL ; prevention ; resistance ; AGE ; NUDE-MICE ; CELL-LINE ; chemotherapy ; LINE ; CARCINOMAS ; specificity ; CISPLATIN ; pancreatic cancer ; CANCER-THERAPY ; CYTOTOXICITY ; signaling ; GEMCITABINE ; RE ; PANCREATIC-CANCER ; cancer therapy ; pancreatic ; GENDER ; dexamethasone ; GLUCOCORTICOID-INDUCED APOPTOSIS ; NAUSEA ; HISTOLOGY ; in vivo ; surgical resection
    Abstract: Background: Chemotherapy for pancreatic carcinoma often has severe side effects that limit its efficacy. The glucocorticoid (GC) dexamethasone (DEX) is frequently used as co-treatment to prevent side effects of chemotherapy such as nausea, for palliative purposes and to treat allergic reactions. While the potent pro-apoptotic properties and the supportive effects of GCs to tumour therapy in lymphoid cells are well studied, the impact of GCs to cytotoxic treatment of pancreatic carcinoma is unknown. Methods: A prospective study of DEX-mediated resistance was performed using a pancreatic carcinoma xenografted to nude mice, 20 surgical resections and 10 established pancreatic carcinoma cell lines. Antiapoptotic signaling in response to DEX was examined by Western blot analysis. Results: In vitro, DEX inhibited drug-induced apoptosis and promoted the growth in all of 10 examined malignant cells. Ex vivo, DEX used in physiological concentrations significantly prevented the cytotoxic effect of gemcitabine and cisplatin in 18 of 20 freshly isolated cell lines from resected pancreatic tumours. No correlation with age, gender, histology, TNM and induction of therapy resistance by DEX co-treatment could be detected. In vivo, DEX totally prevented cytotoxicity of chemotherapy to pancreatic carcinoma cells xenografted to nude mice. Mechanistically, DEX upregulated pro-survival factors and anti-apoptotic genes in established pancreatic carcinoma cells. Conclusion: These data show that DEX induces therapy resistance in pancreatic carcinoma cells and raise the question whether GC-mediated protection of tumour cells from cancer therapy may be dangerous for patients
    Type of Publication: Journal article published
    PubMed ID: 16539710
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  • 10
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; CELLS ; IN-VITRO ; tumor ; AGENTS ; carcinoma ; CELL ; Germany ; IN-VIVO ; INHIBITION ; THERAPY ; VITRO ; VIVO ; SAMPLES ; TUMORS ; TIME ; PATIENT ; INDUCTION ; cell cycle ; CELL-CYCLE ; CYCLE ; treatment ; PROGRESSION ; resistance ; INDUCED APOPTOSIS ; PLASMA ; prostate cancer ; PROSTATE-CANCER ; chemotherapy ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; DERIVATIVES ; HEPATOMA-CELLS ; EPITHELIAL-CELLS ; CARCINOMAS ; PHARMACOKINETICS ; AGENT ; SINGLE ; ONCOLOGY ; RE ; EX-VIVO ; SOLID TUMORS ; MEDIATED APOPTOSIS ; MOLECULAR-MECHANISMS ; LEVEL ; analysis ; methods ; PLASMA-LEVELS ; dexamethasone ; PROMOTION ; USA ; GLUCOCORTICOIDS ; prospective ; in vivo ; clinical study
    Abstract: Background: Glucocorticoids have been used widely in conjunction with cancer therapy due to their ability to induce apoptosis in hematological cells and to prevent nausea and emesis. However, recent data including ours, suggest induction of therapy resistance by glucocorticoids in solid tumors, although it is unclear whether this happens only in few carcinomas or is a more common cell type specific phenomenon. Material and Methods: We performed an overall statistical analysis of our new and recent data obtained with 157 tumor probes evaluated in vitro, ex vivo and in vivo. The effect of glucocorticoids on apoptosis, viability and cell cycle progression under diverse clinically important questions was examined. Results: New in vivo results demonstrate glucocorticoid - induced chemotherapy resistance in xenografted prostate cancer. In an overall statistical analysis we found glucocorticoid - induced resistance in 89% of 157 analysed tumor samples. Resistance is common for several cytotoxic treatments and for several glucocorticoid - derivatives and due to an inhibition of apoptosis, promotion of viability and cell cycle progression. Resistance occurred at clinically achievable peak plasma levels of patients under anti - emetic glucocorticoid therapy and below, lasted for a long time, after one single dose, but was reversible upon removal of glucocorticoids. Two nonsteroidal alternative anti - emetic agents did not counteract anticancer treatment and may be sufficient to replace gluco corticoids in cotreatment of carcinoma patients. Conclusion: These data demonstrate the need for prospective clinical studies as well as for detailed mechanistic studies of GC - induced cell - type specific pro - and anti - apoptotic signalling
    Type of Publication: Journal article published
    PubMed ID: 17224649
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