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125 results on '"Dumon, K."'

12. Bariatric Surgery for Congestive Heart Failure Patients Improves Access to Transplantation and Long-term Survival

Author

Choudhury, Rashikh A., primary, Foster, M., additional, Hoeltzel, G., additional, Moore, H. B., additional, Yaffe, H., additional, Yoeli, D., additional, Prins, K., additional, Ghincea, C., additional, Vigneshwar, N., additional, Dumon, K. R., additional, Rame, J. E., additional, Conzen, K. D., additional, Pomposelli, J. J., additional, Pomfret, E. A., additional, and Nydam, T. L., additional

Published
2020
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16. A two arm phase II study of FOLFIRI in combination with standard or escalating dose of cetuximab as first line treatment for metastatic colorectal cancer: Everest 2 final results

Author

UCL - SSS/IREC/MIRO - Pôle d'imagerie moléculaire, radiothérapie et oncologie, UCL - (SLuc) Unité d'oncologie médicale, Chiritescu, G, Dumon, K, Mercadé, T Macarulla, Lang, I, Vivas, C Santos, Papai, Z, Janssens, J, Hendrickx, K, Pracht, M, Van den Eynde, Marc, Taïeb, J, Moons, V, Geboes, K, Van Laethem, J, Greil, R, Cervantes, A, Vergauwe, P, Ferrante, M, Vanderstraeten, E, Fridrik, M, Wöll, E, Limón, M, Rivera, F, Sagaert, X, Tejpar, S, Van Cutsem, E, ESMO 20th World Congress on Gastrointestinal Cancer, UCL - SSS/IREC/MIRO - Pôle d'imagerie moléculaire, radiothérapie et oncologie, UCL - (SLuc) Unité d'oncologie médicale, Chiritescu, G, Dumon, K, Mercadé, T Macarulla, Lang, I, Vivas, C Santos, Papai, Z, Janssens, J, Hendrickx, K, Pracht, M, Van den Eynde, Marc, Taïeb, J, Moons, V, Geboes, K, Van Laethem, J, Greil, R, Cervantes, A, Vergauwe, P, Ferrante, M, Vanderstraeten, E, Fridrik, M, Wöll, E, Limón, M, Rivera, F, Sagaert, X, Tejpar, S, Van Cutsem, E, and ESMO 20th World Congress on Gastrointestinal Cancer

Published
2018

17. Final results of a phase II quality of life (QOL) randomized, cross-over (CO) study with gemcitabine (Gem) and nab-paclitaxel (n-P) in locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC): QOLINPAC

Author

Chiritescu, G., primary, Dumon, K., additional, Verslype, C., additional, Houbiers, G., additional, Peeters, M., additional, Janssens, J., additional, van Daele, D., additional, Laurent, S., additional, Arts, J., additional, Hendrickx, K., additional, Borbath, I., additional, Ferrante, M., additional, Bastin, F.M., additional, Goeminne, J.-C., additional, van Laethem, J.-L., additional, Vanderstraeten, E., additional, Decaestecker, J., additional, van Vaerenbergh, W., additional, Delhougne, B., additional, and Van Cutsem, E., additional

Published
2018
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18. Gemcitabine with nab-paclitaxel in patients with locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC): A quality of life randomized cross-over study (QOLINPAC)

Author

Chiritescu, G., primary, Dumon, K., additional, Verslype, C., additional, Prenen, H., additional, Houbiers, G., additional, Peeters, M., additional, Janssens, J., additional, Van Daele, D., additional, Laurent, S., additional, Arts, J., additional, Hendrickx, K., additional, Borbath, I., additional, Ferrante, M., additional, Bastin, F., additional, Goeminne, J., additional, Van Laethem, J., additional, Vanderstraeten, E., additional, Decaestecker, J., additional, Van Vaerenbergh, W., additional, Delhougne, B., additional, and Van Cutsem, E., additional

Published
2018
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19. A two arm phase II study of FOLFIRI in combination with standard or escalating dose of cetuximab as first line treatment for metastatic colorectal cancer: Everest 2 final results

Author

Chiritescu, G., primary, Dumon, K., additional, Mercadé, T. Macarulla, additional, Lang, I., additional, Vivas, C. Santos, additional, Papai, Z., additional, Janssens, J., additional, Hendrickx, K., additional, Pracht, M., additional, Van den Eynde, M., additional, Taïeb, J., additional, Moons, V., additional, Geboes, K., additional, Van Laethem, J., additional, Greil, R., additional, Cervantes, A., additional, Vergauwe, P., additional, Ferrante, M., additional, Vanderstraeten, E., additional, Fridrik, M., additional, Wöll, E., additional, Limón, M., additional, Rivera, F., additional, Sagaert, X., additional, Tejpar, S., additional, and Van Cutsem, E., additional

Published
2018
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20. 740P - Final results of a phase II quality of life (QOL) randomized, cross-over (CO) study with gemcitabine (Gem) and nab-paclitaxel (n-P) in locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC): QOLINPAC

Author

Chiritescu, G., Dumon, K., Verslype, C., Houbiers, G., Peeters, M., Janssens, J., van Daele, D., Laurent, S., Arts, J., Hendrickx, K., Borbath, I., Ferrante, M., Bastin, F.M., Goeminne, J.-C., van Laethem, J.-L., Vanderstraeten, E., Decaestecker, J., van Vaerenbergh, W., Delhougne, B., and Van Cutsem, E.

Published
2018
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21. O-015 - A two arm phase II study of FOLFIRI in combination with standard or escalating dose of cetuximab as first line treatment for metastatic colorectal cancer: Everest 2 final results

Author

Chiritescu, G., Dumon, K., Mercadé, T. Macarulla, Lang, I., Vivas, C. Santos, Papai, Z., Janssens, J., Hendrickx, K., Pracht, M., Van den Eynde, M., Taïeb, J., Moons, V., Geboes, K., Van Laethem, J., Greil, R., Cervantes, A., Vergauwe, P., Ferrante, M., Vanderstraeten, E., Fridrik, M., Wöll, E., Limón, M., Rivera, F., Sagaert, X., Tejpar, S., and Van Cutsem, E.

Published
2018
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22. O-003 - Gemcitabine with nab-paclitaxel in patients with locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC): A quality of life randomized cross-over study (QOLINPAC)

Author

Chiritescu, G., Dumon, K., Verslype, C., Prenen, H., Houbiers, G., Peeters, M., Janssens, J., Van Daele, D., Laurent, S., Arts, J., Hendrickx, K., Borbath, I., Ferrante, M., Bastin, F., Goeminne, J., Van Laethem, J., Vanderstraeten, E., Decaestecker, J., Van Vaerenbergh, W., Delhougne, B., and Van Cutsem, E.

Published
2018
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27. Final Results of a Randomized Phase Ii Study with Neo-Adjuvant Triplet or Doublet Therapy, Radiation and Total Mesorectal Excision for Locally Advanced Rectal Cancer: Axe Beam

Author

Chiritescu, G., primary, Dumon, K., additional, Vergauwe, P., additional, Arts, J., additional, Verbeke, L., additional, Polus, M., additional, Humblet, Y., additional, van Laethem, J., additional, Daisne, J., additional, Decaestecker, J., additional, D'Hoore, A., additional, Mardjuadi, F., additional, Debucquoy, A., additional, Verstraete, M., additional, Sagaert, X., additional, Haustermans, K., additional, and Van Cutsem, E., additional

Published
2014
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28. AXE Beam: Neo-Adjuvant Triplet Versus Doublet Therapy with Radiation and Total Mesorectal Excision for Locally Advanced Rectal Cancer – A Randomized Phase II Study at the End of Recruitment

Author

Chiritescu, G., primary, Dumon, K., additional, Vergauwe, P., additional, Arts, J., additional, Verbeke, L., additional, Polus, M., additional, Humblet, Y., additional, Van Laethem, J.L., additional, Daisne, J.F., additional, Decaestecker, J., additional, D'Hoore, A., additional, Mardjuadi, F., additional, Debucquoy, A., additional, Verstraete, M., additional, Sagaert, X., additional, Haustermans, K., additional, and Van Cutsem, E., additional

Published
2014
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30. An adenovirus carrying the rat protein tyrosine phosphatase eta suppresses the growth of human thyroid carcinoma cell lines in vitro and in vivo

Author

Iuliano, R., Trapasso, F., Le Pera, I., filippo schepis, Sama, I., Clodomiro, A., Dumon, K. R., Santoro, M., Chiariotti, L., Viglietto, G., Fusco, A., Iuliano, R, Trapasso, F, LE PERA, I, Schepis, F, Sama, I, Clodomiro, A, Dumon, Kr, Santoro, Massimo, Chiariotti, Lorenzo, Viglietto, G, and Fusco, Alfredo

Subjects
EXPRESSION, PHOSPHOLIPASE C-GAMMA, Genetic Vectors, Mice, Nude, Cell Cycle Proteins, THERAPY, Adenoviridae, Mice, Adenocarcinoma, Follicular, Animals, Cell Division, Cyclin-Dependent Kinase Inhibitor p27, Gene Therapy, Humans, Isoenzymes, Nude, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinases, Phospholipase C gamma, Phosphorylation, Protein Tyrosine Phosphatases, Rats, Thyroid Neoplasms, Transduction, Genetic, Tumor Cells, Cultured, Tumor Suppressor Proteins, Type C Phospholipases, Xenograft Model Antitumor Assays, Transduction, Genetic, Adenocarcinoma, Follicular, Tumor Cells, Cultured, DEP-1, Genetic Therapy
Abstract

We demonstrated previously that rat tyrosine phosphatase r-PTPeta expression was suppressed in rat and human thyroid neoplastic cells, and that restoration of r-PTPeta expression reverted the malignant phenotype. To investigate the potential of this gene for cancer therapy, we generated an adenovirus carrying the r-PTPeta cDNA (Ad-r-PTPeta). This virus infected human thyroid carcinoma cells and overexpressed the r-PTPeta protein. Overexpression of r-PTPeta significantly inhibited the growth of four thyroid carcinoma cell lines. Cell growth inhibition was associated with down-regulation of extracellular signal-regulated kinase 1/2 activity, with increased levels of the cell-cycle inhibitor p27(kip1) protein and with dephosphorylation of PLCgamma1, a substrate of DEP-1, the human homologue of r-PTPeta. Finally, the growth of xenograft tumors induced in athymic mice by anaplastic thyroid carcinoma ARO cells transduced with the Ad-r-PTPeta virus was drastically reduced. These data suggest that gene therapy based on restoration of PTPeta function has potential in the treatment of human thyroid malignant neoplasias.

Published
2003

36. O-0010 - AXE Beam: Neo-Adjuvant Triplet Versus Doublet Therapy with Radiation and Total Mesorectal Excision for Locally Advanced Rectal Cancer – A Randomized Phase II Study at the End of Recruitment

Author

Chiritescu, G., Dumon, K., Vergauwe, P., Arts, J., Verbeke, L., Polus, M., Humblet, Y., Van Laethem, J.L., Daisne, J.F., Decaestecker, J., D'Hoore, A., Mardjuadi, F., Debucquoy, A., Verstraete, M., Sagaert, X., Haustermans, K., and Van Cutsem, E.

Published
2014
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42. Potential cancer therapy with the fragile histidine triad gene: review of the preclinical studies.

Author

Ishii H, Dumon KR, Vecchione A, Fong LYY, Baffa R, Huebner K, Croce CM, Ishii, H, Dumon, K R, Vecchione, A, Fong, L Y, Baffa, R, Huebner, K, and Croce, C M

Abstract

Context: The fragile histidine triad gene (FHIT) encompasses a human common fragile site, FRA3B, that is susceptible to environmental carcinogens. Deletion and inactivation of FHIT have been seen in a number of human premalignant and malignant lesions.Objective: To review and evaluate preclinical studies of cancer therapy using the FHIT tumor suppressor gene and related studies involving Fhit protein expression.Data Sources: A MEDLINE search of articles published from 1996 to June 2001 was performed; article reference lists were used to retrieve additional relevant articles.Study Selection: Immunohistochemical studies of primary tumors or relevant lesions were selected to evaluate Fhit expression in premalignant or malignant stages. Preclinical studies on antitumorigenic or therapeutic introduction of FHIT were reviewed for the effects of exogenous Fhit expression. For the immunohistochemical analyses, 26 studies were included that analyzed at least 15 cases of a single type of tumor. For precancerous lesions, 9 studies were included that analyzed at least 4 cases. For studies of FHIT introduction, 9 published studies were included.Data Extraction: Using primary data from each of the studies, we assessed the rationale and potential contribution of FHIT cancer therapy. Data was independently abstracted by 2 authors and study quality was assessed by 2 other authors.Data Synthesis: Overall, 60% (1162/1948 cases) of primary tumors showed absent or markedly reduced Fhit protein expression in cancer cells. Studies of preneoplastic lesions or early-stage cancer showed absence or marked reduction of Fhit protein expression in 0% to 93% of samples (overall, 31% [127/408 cases]). Preclinical studies using 26 cancer-derived cell lines from human lung, head and neck, esophageal, gastric, cervical, pancreatic, and kidney cancers, showed that reintroduction of FHIT resulted in inhibition of in vitro tumor cell growth or of in vivo tumorigenicity in 17 (57%) of 30 cell line experiments. Model systems for human preventive cancer therapy suggested that oral introduction of viral vector-mediated FHIT into Fhit-deficient mice may prevent carcinogen-induced tumor development in some cases.Conclusion: These findings show that FHIT gene therapy may potentially be clinically useful for treatment of cancer and also prevention of carcinogen-induced tumor development, suggesting a rationale for further research involving FHIT introduction. [ABSTRACT FROM AUTHOR]

Published
2001
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47. Restoration of receptor-type protein tyrosine phosphatase function inhibits human pancreatic carcinoma cell growth in vitro and in vivo

Author

Rossano Cesari, Francesco Trapasso, Luisa Infante, Hideshi Ishii, Robin Seto, Byron Feig, Matthew J. During, Andrea Vecchione, Sai Yendamuri, Rodolfo Iuliano, Carlo M. Croce, Kristoffel R. Dumon, Alfredo Fusco, Trapasso, F., Yendamuri, S., Dumon, K. R., Iuliano, R., Cesari, R., Feig, B., Seto, R., Infante, L., Ishii, H., Vecchione, A., During, M. J., Croce, C. M., and Fusco, Alfredo

Subjects
Cancer Research, Pancreatic disease, Genotype, tumor suppressor, Protein tyrosine phosphatase, Biology, Transfection, Polymerase Chain Reaction, Cell Line, Tumor, Pancreatic cancer, human pancreatic carcinoma cell, medicine, Animals, Humans, Genes, Tumor Suppressor, DNA Primers, DEP-1/HPTPeta, Reverse Transcriptase Polymerase Chain Reaction, Cell growth, Receptor-Like Protein Tyrosine Phosphatases, Class 3, Exons, General Medicine, Cell cycle, medicine.disease, Candidate Tumor Suppressor Gene, Rats, Pancreatic Neoplasms, Kinetics, medicine.anatomical_structure, Cell culture, Cancer research, Protein Tyrosine Phosphatases, Pancreas, Cell Division
Abstract

DEP-1/HPTPeta, a receptor-type protein tyrosine phosphatase, is a candidate tumor suppressor gene because its expression was blocked in rat and human thyroid transformed cells, and its restoration reverted their neoplastic phenotype. In addition, loss of DEP-1/HPTPeta heterozygosity has been described in mammary, lung and colon primary tumors. We now show that DEP-1/HPTPeta is drastically reduced in several cell lines originating from human epithelial pancreatic carcinomas compared with normal pancreatic tissue. We also show that the infection of AsPC1 and PSN1 cells with a recombinant adenovirus carrying r-PTPeta cDNA (the rat homolog of DEP-1/HPTPeta) inhibits their proliferation. Flow cytometric analysis of the infected cells demonstrated that restoration of r-PTPeta activity disrupts their cell cycle and leads to apoptosis. Finally, the growth of PSN1 xenograft tumors was blocked by the intratumoral injection of a recombinant adeno-associated virus carrying r-PTPeta. The data suggest that restoration of DEP-1/HPTPeta expression could be a useful tool for the gene therapy of human pancreatic cancers.

Published
2004

48. Tumor suppressor functions of ARLTS1 in lung cancers

Author

Tamotsu Kuroki, Carlo M. Croce, Manuela Ferracin, Masayoshi Shimizu, Kristoffel R. Dumon, Florencia Bullrich, Larry R. Kaiser, Sai Yendamuri, Cinzia Sevignani, Chang Gong Liu, Massimo Negrini, Shashi Rattan, George A. Calin, Noel N. Williams, Francesco Trapasso, Rossano Cesari, YENDAMURI S, TRAPASSO F, FERRACIN M, CESARI R, SEVIGNANI C, SHIMIZU M, RATTAN S, KUROKI T, DUMON K. R, BULLRICH F, LIU C. G, M. NEGRINI, WILLIAMS N. N, KAISER L. R, CROCE C. M, and CALIN G. A

Subjects
Cancer Research, Lung Neoplasms, Tumor suppressor gene, Molecular Sequence Data, Down-Regulation, Mice, Nude, Apoptosis, Cell Growth Processes, Biology, Adenoviridae, Mice, Cell Line, Tumor, medicine, Animals, Humans, Genes, Tumor Suppressor, Amino Acid Sequence, Lung cancer, Promoter Regions, Genetic, Conserved Sequence, A549 cell, Cell Growth Processe, Animal, Cell growth, ADP-Ribosylation Factors, Apoptosi, ADP-Ribosylation Factor, Promoter, Gene Therapy, Genetic Therapy, DNA Methylation, medicine.disease, Lung Neoplasm, Oncology, Cell culture, DNA methylation, Cancer research, Promoter Regions (Genetics), Sequence Alignment, Human
Abstract

ARLTS1 is a newly characterized tumor suppressor gene located at chromosome 13q14.3 and involved in the pathogenesis of various types of tumors: two single-nucleotide polymorphisms, one of them responsible for protein truncation, were found statistically associated with familial malignancies, whereas DNA hypermethylation and genomic deletions have been identified as a mechanism of ARLTS1 down-regulation in sporadic cancers. We found that in a large portion of lung carcinomas (37%) and in all analyzed lung cancer cell lines, ARLTS1 is strongly down-regulated due to DNA methylation in its promoter region. After its restoration by adenoviral transduction, ARLTS1-negative A549 and H1299 cells underwent apoptosis and inhibition of cell growth. Furthermore, ARLTS1 reexpression significantly reduced the ability of A549 and H1299 to form tumors in nude mice. Finally, we identified ∼650 transcripts differentially expressed after restoration of ARLTS1 expression in A549 cells, suggesting that various pathways involved in cell survival, proliferation, signaling, and development mediate the effects of wild-type ARLTS1 in a lung cancer system. [Cancer Res 2007;67(16):7738–45]

Published
2007

49. Therapy of human pancreatic carcinoma based on suppression of HMGA1 protein synthesis in preclinical models

Author

Francesca Pentimalli, Giuseppe Viglietto, Takashi Watanabe, Hansjuerg Alder, Francesco Trapasso, Rami I. Aqeilan, Rossano Cesari, Alfredo Fusco, Kristoffel R. Dumon, Carlo M. Croce, Sai Yendamuri, Manuela Sarti, Nobutsugu Abe, Luisa Infante, Trapasso, F., Sarti, M., Cesari, R., Yendamuri, S., Dumon, K. R., Aqeilan, R. I., Pentimalli, Francesca, Infante, L., Alder, H., Abe, N., Watanabe, T., Viglietto, G., Croce, C. M., and Fusco, Alfredo

Subjects
Male, Cancer Research, HMGA1, adenoviru, Green Fluorescent Proteins, Transplantation, Heterologous, Down-Regulation, Mice, Nude, medicine.disease_cause, Adenoviridae, Mice, Downregulation and upregulation, Pancreatic cancer, Tumor Cells, Cultured, medicine, Animals, Humans, HMGA1a Protein, Molecular Biology, Cell Proliferation, biology, pancreatic carcinoma, apoptosis, Oligonucleotides, Antisense, medicine.disease, Pancreatic Neoplasms, Transplantation, Apoptosis, Cell culture, Models, Animal, biology.protein, Cancer research, Molecular Medicine, CA19-9, Carcinogenesis
Abstract

Pancreatic carcinoma is one of the most aggressive tumors, and, being refractory to conventional therapies, is an excellent target for new therapeutic approaches. Based on our previous finding of high HMGA1 expression in pancreatic cancer cells compared to normal pancreatic tissue, we evaluated whether suppression of HMGA1 protein expression could be a treatment option for patients affected by pancreatic cancer. Here we report that HMGA1 proteins are overexpressed in pancreatic carcinoma cell lines, and their downregulation through an adenovirus carrying the HMGA1 gene in an antisense orientation (Ad Yas-GFP) results in the death of three human pancreatic carcinoma cell lines (PANC1, Hs766T and PSN1). Pretreatment of PANC1 and PSN1 cells with Ad Yas-GFP suppressed and reduced, respectively, their ability to form xenograft tumors in nude mice. To further verify the role of HMGA1 in pancreatic tumorigenesis, we used a HMGA1 antisense phosphorothioate oligodeoxynucleotide (ODN); its addition induced a decrease in HMGA1 protein levels and a significant reduction of the proliferation rate of PANC1-, Hs766T- and PSN1-treated cells. Therefore, suppression of HMGA1 protein synthesis by an HMGA1 antisense approach seems to be a feasible treatment strategy in pancreatic carcinomas.

Published
2004

50. Trends in bariatric surgery training: bariatric operations performed by Fellowship Council trainees from 2012 to 2019.

Author

Jog A, Baldwin D, Wernsing D, Gershuni V, Hashimoto DA, Williams N, Dumon K, and Altieri MS

Subjects
Humans, Retrospective Studies, United States, Education, Medical, Graduate trends, Laparoscopy education, Laparoscopy statistics & numerical data, Laparoscopy trends, Female, Gastrectomy education, Gastrectomy trends, Gastrectomy statistics & numerical data, Male, Obesity, Morbid surgery, Bariatric Surgery education, Bariatric Surgery statistics & numerical data, Bariatric Surgery trends, Fellowships and Scholarships statistics & numerical data, Fellowships and Scholarships trends
Abstract

Background: The American Society for Metabolic and Bariatric Surgery (ASMBS) Fellowship Certificate was created to ensure satisfactory training and requires a minimum number of anastomotic cases. With laparoscopic sleeve gastrectomy becoming the most common bariatric procedure in the United States, this may present a challenge for fellows to obtain adequate numbers for ASMBS certification., Objectives: To investigate bariatric fellowship trends from 2012 to 2019, the types, numbers, and approaches of surgical procedures performed by fellows were examined., Setting: Academic training centers in the United States., Methods: Data were obtained from Fellowship Council records of all cases performed by fellows in ASMBS-accredited bariatric surgery training programs between 2012 and 2019. A retrospective analysis using standard descriptive statistical methods was performed to investigate trends in total case volume and cases per fellow for common bariatric procedures., Results: From 2012 to 2019, sleeve gastrectomy cases performed by all Fellowship Council fellows nearly doubled from 6,514 to 12,398, compared with a slight increase for gastric bypass, from 8,486 to 9,204. Looking specifically at bariatric fellowships, the mean number of gastric bypass cases per fellow dropped over time, from 91.1 cases (SD = 46.8) in 2012-2013 to 52.6 (SD = 62.1) in 2018-2019. Mean sleeve gastrectomy cases per fellow increased from 54.7 (SD = 31.5) in 2012-2013 to a peak of 98.6 (SD = 64.3) in 2015-2016. Robotic gastric bypasses also increased from 4% of all cases performed in 2012-2013 to 13.3% in 2018-2019., Conclusions: Bariatric fellowship training has seen a decrease in gastric bypasses, an increase in sleeve gastrectomies, and an increase in robotic surgery completed by each fellow from 2012 to 2019., (Copyright © 2023 American Society for Metabolic and Bariatric Surgery. Published by Elsevier Inc. All rights reserved.)

Published
2024
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