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Pancreatic Neoplasms: HELP
Articles by Christoph Mamot
Based on 2 articles published since 2009
(Why 2 articles?)
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Between 2009 and 2019, Christoph Mamot wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial "HEATPAC" - a phase II randomized study of concurrent thermochemoradiotherapy versus chemoradiotherapy alone in locally advanced pancreatic cancer. 2017

Datta, Niloy Ranjan / Pestalozzi, Bernhard / Clavien, Pierre-Alain / Siebenhüner, Alexander / Puric, Emsad / Khan, Shaka / Mamot, Christoph / Riesterer, Oliver / Knuchel, Jürg / Reiner, Cäcilia Sophie / Bodis, Stephan / Anonymous8980927. ·Centre for Radiation Oncology KSA-KSB, Kantonsspital Aarau AG, Tellstrasse, CH-5001, Aarau, Switzerland. niloyranjan.datta@ksa.ch. · Centre for Hematology and Oncology, University Hospital Zurich, Zürich, Switzerland. · Department of Surgery and Transplantation, University Hospital Zurich, Zürich, Switzerland. · Centre for Radiation Oncology KSA-KSB, Kantonsspital Aarau AG, Tellstrasse, CH-5001, Aarau, Switzerland. · Centre for Medical Oncology / Hematology, Kantonsspital, Aarau, Switzerland. · Department of Radiation Oncology, University Hospital Zurich, Zürich, Switzerland. · Department of Gastroenterology and Hepatology, Kantonsspital, Aarau, Switzerland. · Institute for Diagnostic and Interventional Radiology, University Hospital Zurich, Zürich, Switzerland. ·Radiat Oncol · Pubmed #29162142.

ABSTRACT: BACKGROUND: Pancreatic cancer has a dismal prognosis with 5-year overall survival rate of around 5%. Although surgery is still the best option in operable cases, majority of the patients who present in locally advanced stages are deemed inoperable. Novel approaches are therefore needed for the management of around 80% of these inoperable locally advanced pancreatic cancers (LAPC). Hyperthermia (39-43 °C) is a potent radiosensitizer and further enhances the action of gemcitabine, also a known radiosensitizer. Thus through triple sensitization, a combination of hyperthermia, radiotherapy and gemcitabine could be expected to improve the therapeutic outcomes in LAPC. METHODS: This phase II randomized trial, HEATPAC in unresectable LAPC, explores the feasibility and efficacy of concurrent thermochemoradiotherapy (HTCTRT) over chemoradiotherapy (CTRT) alone with pre- and post-intervention FOLFIRINOX at standard dosage and schedule. Following 4 cycles of neoadjuvant FOLFIRINOX, patients with no metastasis and absence of gross peritoneal carcinomatosis would be randomized to either (a) control arm: concurrent CTRT with gemcitabine (400 mg/m DISCUSSION: The expected 1-year baseline overall survival with CTRT alone is considered as 40%. With HTCTRT, a survival advantage of +20% is expected. Considering α = 0.05 and β = 0.80 for sample size computation, a total of 86 patients would be equally randomized into the two treatment groups. This phase II study if found to be safe and effective, would form the basis of a future phase III randomized study. TRIAL REGISTRATION: The trial has been registered with the ClinicalTrials.gov ( NCT02439593 ). The study has been approved by the Ethical Commissions of Basel and Zurich and is open for patient recruitment.

2 Article Targeting tumor-associated endothelial cells: anti-VEGFR2 immunoliposomes mediate tumor vessel disruption and inhibit tumor growth. 2012

Wicki, Andreas / Rochlitz, Christoph / Orleth, Annette / Ritschard, Reto / Albrecht, Imke / Herrmann, Richard / Christofori, Gerhard / Mamot, Christoph. ·Division of Oncology, University Hospital, Petersgraben 4, CH-4031 Basel, Switzerland. ·Clin Cancer Res · Pubmed #22065082.

ABSTRACT: PURPOSE: Angiogenesis is a key process in tumor progression. By binding VEGF, VEGF receptor-2 (VEGFR2) is a main signaling transducer in tumor-associated angiogenesis. Accordingly, therapeutic approaches against the VEGF/VEGFR2 signaling axis have been designed. However, an efficient and specific chemotherapeutic targeting of tumor-associated endothelial cells has not yet been achieved. EXPERIMENTAL DESIGN: We have employed anti-VEGFR2 antibodies covalently linked to pegylated liposomal doxorubicin (PLD) to specifically ablate tumor-associated endothelial cells in the Rip1Tag2 mouse model of insulinoma, in the MMTV-PyMT mouse model of breast cancer, and in the HT-29 human colon cancer xenograft transplantation model. RESULTS: In each model, anti-VEGFR2-targeted immunoliposomes (ILs) loaded with doxorubicin (anti-VEGFR2-ILs-dox) were superior in therapeutic efficacy to empty liposomes, empty anti-VEGFR2-ILs, antibodies alone, and PLD. Efficacy was similar to that of the oral VEGFR1, -2, and -3 inhibitor PTK787. Detailed histopathologic and molecular analysis revealed a strong antiangiogenic effect of anti-VEGFR2-ILs-dox, and the observed antiangiogenic therapy was significantly more efficient in reducing tumor burden in well-vascularized transgenic mouse models as compared with the less-vascularized xenograft model. CONCLUSIONS: Anti-VEGFR2 ILs provide a highly efficient approach to selectively deplete VEGFR2-expressing tumor vasculature. They offer a novel and promising anticancer strategy.