Search

Your search keyword '"Jacobs, Rutger J."' showing total 36 results
Start Over Author "Jacobs, Rutger J."
36 results on '"Jacobs, Rutger J."'

2. Deficits in Geriatric Assessment Associate With Disease Activity and Burden in Older Patients With Inflammatory Bowel Disease

Author

Asscher, Vera E.R., Waars, Sanne N., van der Meulen-de Jong, Andrea E., Stuyt, Rogier J.L., Baven-Pronk, A. Martine C., van der Marel, Sander, Jacobs, Rutger J., Haans, Jeoffrey J.L., Meijer, Lennart J., Klijnsma-Slagboom, Jacqueline D., Duin, Marijn H., Peters, Milou E.R., Lee-Kong, Felicia V.Y.L., Provoost, Nanda E., Tijdeman, Femke, van Dijk, Kenan T., Wieland, Monse W.M., Verstegen, Mirre G.M., van der Meijs, Melissa E., Maan, Annemijn D.I., van Deudekom, Floor J., Mooijaart, Simon P., and Maljaars, P.W. Jeroen

Published
2022
Full Text
View/download PDF

6. Frailty Screening is Associated with Hospitalization and Decline in Quality of Life and Functional Status in Older Patients with Inflammatory Bowel Disease.

Author

Asscher, Vera E R, Gírondo, Mar Rodriguez, Fens, Jesse, Waars, Sanne N, Stuyt, Rogier J L, Baven-Pronk, A Martine C, Srivastava, Nidhi, Jacobs, Rutger J, Haans, Jeoffrey J L, Meijer, Lennart J, Klijnsma-Slagboom, Jacqueline D, Duin, Marijn H, Peters, Milou E R, Lee-Kong, Felicia V Y L, Provoost, Nanda E, Tijdeman, Femke, Dijk, Kenan T van, Wieland, Monse W M, Verstegen, Mirre G M, and Meijs, Melissa E van der

Abstract

Background and Aims Our goals were to study frailty screening in association with hospitalization and decline in quality of life [QoL] and functional status in older patients with inflammatory bowel diseases [IBD]. Methods This was a prospective multicentre cohort study in IBD patients ≥65 years old using frailty screening [G8 Questionnaire]. Outcomes were all-cause, acute, and IBD-related hospitalization, any infection, any malignancy, QoL [EQ5D-3L], and functional decline (Instrumental Activities of Daily Living [IADL]) during 18 months of follow-up. Confounders were age, IBD type, biochemical disease activity [C-reactive protein ≥10 mg/L and/or faecal calprotectin ≥250 µg/g], and comorbidity [Charlson Comorbidity Index]. Results Of 405 patients, with a median age of 70 years, 196 [48%] were screened as being at risk for frailty. All-cause hospitalizations occurred 136 times in 96 patients [23.7%], and acute hospitalizations 103 times in 74 patients [18.3%]. Risk of frailty was not associated with all-cause (adjusted hazard ratio [aHR] 1.5, 95% confidence interval [CI] 0.9–2.4), but was associated with acute hospitalizations [aHR 2.2, 95% CI 1.3–3.8]. Infections occurred in 86 patients [21.2%] and these were not associated with frailty. A decline in QoL was experienced by 108 [30.6%] patients, and a decline in functional status by 46 patients [13.3%]. Frailty screening was associated with a decline in QoL (adjusted odds ratio [aOR] 2.1, 95% CI 1.3–3.6) and functional status [aOR 3.7, 95% CI 1.7–8.1]. Conclusions Frailty screening is associated with worse health outcomes in older patients with IBD. Further studies are needed to assess the feasibility and effectiveness of its implementation in routine care. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

7. Frailty Screening is Associated with Hospitalization and Decline in Quality of Life and Functional Status in Older Patients with Inflammatory Bowel Disease

Author

Asscher, Vera E R, primary, Rodriguez Gírondo, Mar, additional, Fens, Jesse, additional, Waars, Sanne N, additional, Stuyt, Rogier J L, additional, Baven-Pronk, A Martine C, additional, Srivastava, Nidhi, additional, Jacobs, Rutger J, additional, Haans, Jeoffrey J L, additional, Meijer, Lennart J, additional, Klijnsma-Slagboom, Jacqueline D, additional, Duin, Marijn H, additional, Peters, Milou E R, additional, Lee-Kong, Felicia V Y L, additional, Provoost, Nanda E, additional, Tijdeman, Femke, additional, van Dijk, Kenan T, additional, Wieland, Monse W M, additional, Verstegen, Mirre G M, additional, van der Meijs, Melissa E, additional, Maan, Annemijn D I, additional, van Deudekom, Floor J, additional, van der Meulen-de Jong, Andrea E, additional, Mooijaart, Simon P, additional, and Maljaars, P W Jeroen, additional

Published
2023
Full Text
View/download PDF

8. Intestinal tumorigenesis is not affected by progesterone signaling in rodent models.

Author

Heijmans, Jarom, Muncan, Vanesa, Jacobs, Rutger J, de Jonge-Muller, Eveline SM, Graven, Laura, Biemond, Izak, Ederveen, Antwan G, Groothuis, Patrick G, Mosselman, Sietse, Hardwick, James C, Hommes, Daniel W, and van den Brink, Gijs R

Subjects
Intestinal Mucosa, Colon, Intestine, Small, Animals, Mice, Rats, Intestinal Neoplasms, Cell Transformation, Neoplastic, Intestinal Polyposis, Disease Models, Animal, Progesterone, Receptors, Progesterone, Progestins, Immunohistochemistry, Signal Transduction, Cell Proliferation, Cell Transformation, Neoplastic, Disease Models, Animal, Intestine, Small, Receptors, General Science & Technology
Abstract

Clinical data suggest that progestins have chemopreventive properties in the development of colorectal cancer. We set out to examine a potential protective effect of progestins and progesterone signaling on colon cancer development. In normal and neoplastic intestinal tissue, we found that the progesterone receptor (PR) is not expressed. Expression was confined to sporadic mesenchymal cells. To analyze the influence of systemic progesterone receptor signaling, we crossed mice that lacked the progesterone receptor (PRKO) to the Apc(Min/+) mouse, a model for spontaneous intestinal polyposis. PRKO-Apc(Min/+) mice exhibited no change in polyp number, size or localization compared to Apc(Min/+). To examine effects of progestins on the intestinal epithelium that are independent of the PR, we treated mice with MPA. We found no effects of either progesterone or MPA on gross intestinal morphology or epithelial proliferation. Also, in rats treated with MPA, injection with the carcinogen azoxymethane did not result in a difference in the number or size of aberrant crypt foci, a surrogate end-point for adenoma development. We conclude that expression of the progesterone receptor is limited to cells in the intestinal mesenchyme. We did not observe any effect of progesterone receptor signaling or of progestin treatment in rodent models of intestinal tumorigenesis.

Published
2011

9. The role of EZH2 and DNA methylation in the silencing of the tumour suppressor RUNX3 in colorectal cancer.

Author

Kodach, Liudmila L, Jacobs, Rutger J, Heijmans, Jarom, van Noesel, Carel JM, Langers, Alexandra MJ, Verspaget, Hein W, Hommes, Daniel W, Offerhaus, G Johan A, van den Brink, Gijs R, and Hardwick, James CH

Subjects
Humans, Colorectal Neoplasms, DNA-Binding Proteins, Transcription Factors, RNA, Messenger, Blotting, Western, Immunoenzyme Techniques, Enzyme-Linked Immunosorbent Assay, Electrophoretic Mobility Shift Assay, Tissue Array Analysis, Chromatin Immunoprecipitation, Reverse Transcriptase Polymerase Chain Reaction, DNA Methylation, Gene Expression Regulation, Neoplastic, Gene Silencing, Regulatory Sequences, Nucleic Acid, Genes, Tumor Suppressor, Core Binding Factor Alpha 3 Subunit, Promoter Regions, Genetic, Enhancer of Zeste Homolog 2 Protein, Polycomb Repressive Complex 2, Blotting, Western, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Promoter Regions, Genetic, RNA, Messenger, Regulatory Sequences, Nucleic Acid, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract

In gastric cancer, a new epigenetic mechanism of tumour suppressor loss has been suggested where the histone methyltransferase enhancer of zeste homolog 2 (EZH2) is responsible for loss of expression of RUNX3. This is consistent with EZH2 upregulation in multiple cancer types being associated with poor prognosis. We investigated whether EZH2 influences the expression of RUNX3 in colorectal cancer (CRC) and whether this is independent of methylation. We determined protein and messenger RNA (mRNA) levels of EZH2 and RUNX3 and assessed RUNX3 methylation with methylation-specific polymerase chain reaction using 72 human CRCs and 8 CRC cell lines. We assessed the effect of efficient RNA interference-mediated knockdown of EZH2 on RUNX3 levels, cell viability and H3K27 trimethylation of the RUNX3 promoter using chromatin immunoprecipitation. Despite higher levels of EZH2 and lower levels of RUNX3 in CRC specimens in general, no inverse correlation between EZH2 and RUNX3 in paired samples was found arguing against a major role for histone methylation in silencing RUNX3 in CRC. Conversely, downregulation of RUNX3 mRNA in the same tumours was associated with RUNX3 DNA methylation (P < 0.05). In cell lines, knockdown of EZH2 removed the repressive chromatin marks from RUNX3 but did not result in RUNX3 re-expression. However, it prevented the re-silencing of RUNX3 after the removal of demethylating agents. In conclusion, DNA methylation is primarily responsible for the transcriptional silencing of RUNX3 in CRC, but EZH2 and histone methylation are necessary for its methylation-dependent re-silencing after the removal of demethylating agents. These results would predict that inhibitors of EZH2 and histone methylation would enhance the effects of demethylating agents in cancer therapy.

Published
2010

13. Statin use is associated with a reduced incidence of colorectal cancer expressing SMAD4

Author

Ouahoud, Sarah, primary, Jacobs, Rutger J., additional, Kodach, Ludmilla L., additional, Voorneveld, Philip W., additional, Hawinkels, Lukas J. A. C., additional, Weil, Nikki L., additional, van Vliet, Britt, additional, Herings, Ron M., additional, van der Burg, Lennart R. A., additional, van Wezel, Tom, additional, Morreau, Hans, additional, Slingerland, Marije, additional, Bastiaannet, Esther, additional, Putter, Hein, additional, and Hardwick, James C. H., additional

Published
2021
Full Text
View/download PDF

14. Healthy Cotwins Share Gut Microbiome Signatures With Their Inflammatory Bowel Disease Twins and Unrelated Patients

Author

Brand, Eelco C., primary, Klaassen, Marjolein A.Y., additional, Gacesa, Ranko, additional, Vich Vila, Arnau, additional, Ghosh, Hiren, additional, de Zoete, Marcel R., additional, Boomsma, Dorret I., additional, Hoentjen, Frank, additional, Horjus Talabur Horje, Carmen S., additional, van de Meeberg, Paul C., additional, Willemsen, Gonneke, additional, Fu, Jingyuan, additional, Wijmenga, Cisca, additional, van Wijk, Femke, additional, Zhernakova, Alexandra, additional, Oldenburg, Bas, additional, Weersma, Rinse K., additional, Brand, Eelco C., additional, Honkoop, Pieter, additional, Jacobs, Rutger J., additional, Ponsioen, Cyriel Y., additional, de Boer, Nanne K.H., additional, Alderlieste, Yasser A., additional, van Herwaarden, Margot A., additional, van Tuyl, Sebastiaan A.C., additional, Lutgens, Maurice W., additional, Janneke van der Woude, C., additional, Mares, Wout G.M., additional, de Koning, Daan B., additional, Bosman, Joukje H., additional, Vecht, Juda, additional, de Schryver, Anneke M.P., additional, van der Meulen-de Jong, Andrea E., additional, Pierik, Marieke J., additional, Boekema, Paul J., additional, Verburg, Robert J., additional, Jharap, Bindia, additional, Jansen, Jeroen M., additional, Stokkers, Pieter C.F., additional, Quispel, Rutger, additional, Mahmmod, Nofel, additional, West, Rachel L., additional, Willems, Marleen, additional, Minderhoud, Itta M., additional, Fidder, Herma H., additional, van Schaik, Fiona D.M., additional, Hirdes, Meike M.C., additional, Boontje, Nynke A., additional, Müskens, Bart L.M., additional, and Romberg-Camps, Marielle J.L., additional

Published
2021
Full Text
View/download PDF

18. Statin Use After Diagnosis of Colon Cancer and Patient Survival

Author

Voorneveld, Philip W., primary, Reimers, Marlies S., additional, Bastiaannet, Esther, additional, Jacobs, Rutger J., additional, van Eijk, Ronald, additional, Zanders, Marjolein M.J., additional, Herings, Ron M.C., additional, van Herk-Sukel, Myrthe P.P., additional, Kodach, Liudmila L., additional, van Wezel, Tom, additional, Kuppen, Peter J.K., additional, Morreau, Hans, additional, van de Velde, Cornelis J.H., additional, Hardwick, James C.H., additional, and Liefers, Gerrit Jan, additional

Published
2017
Full Text
View/download PDF

20. Tu1976 Statin Use After Diagnosis Improves Survival in Colorectal Cancer Patients

Author

Voorneveld, Philip, primary, Reimers, Marlies S., additional, Jacobs, Rutger J., additional, Bastiaannet, Esther, additional, Van Eijk, Ronald, additional, Kodach, Liudmila L., additional, van Wezel, Tom, additional, Kuppen, Peter J., additional, Morreau, Hans, additional, van de Velde, Cornelis J., additional, Liefers, Gerrit Jan, additional, and Hardwick, James C., additional

Published
2015
Full Text
View/download PDF

21. Tu1230 Integrated Care Pathways for Inflammatory Bowel Disease Surgery: Design and First Analysis

Author

Jacobs, Rutger J., primary, Reardon, Sarah, additional, Sagar, Dipti, additional, Hommes, Tijmen J., additional, Margolis, Daniel J., additional, Kane, Ellen, additional, van Deen, Welmoed K., additional, Eimers, Laurin, additional, Inserra, Elizabeth K., additional, Duran, Natalie, additional, Choi, Jennifer M., additional, Ha, Christina, additional, Roth, Bennett E., additional, Ho, Andrew D., additional, Esrailian, Eric, additional, Sack, Jonathan, additional, and Hommes, Daniel W., additional

Published
2015
Full Text
View/download PDF

23. Loss of SMAD4 Alters BMP Signaling to Promote Colorectal Cancer Cell Metastasis via Activation of Rho and ROCK

Author

Voorneveld, Philip W., primary, Kodach, Liudmila L., additional, Jacobs, Rutger J., additional, Liv, Nalan, additional, Zonnevylle, A. Christiaan, additional, Hoogenboom, Jacob P., additional, Biemond, Izak, additional, Verspaget, Hein W., additional, Hommes, Daniel W., additional, de Rooij, Karien, additional, van Noesel, Carel J.M., additional, Morreau, Hans, additional, van Wezel, Tom, additional, Offerhaus, G. Johan A., additional, van den Brink, Gijs R., additional, Peppelenbosch, Maikel P., additional, ten Dijke, Peter, additional, and Hardwick, James C.H., additional

Published
2014
Full Text
View/download PDF

26. Correction: Intestinal Tumorigenesis Is Not Affected by Progesterone Signaling in Rodent Models

Author

Heijmans, Jarom, primary, Muncan, Vanesa, additional, Jacobs, Rutger J., additional, de Jonge-Muller, Eveline S. M., additional, Graven, Laura, additional, Biemond, Izak, additional, Ederveen, Antwan G., additional, Groothuis, Patrick G., additional, Mosselman, Sietse, additional, Hardwick, James C., additional, Hommes, Daniel W., additional, and van den Brink, Gijs R., additional

Published
2013
Full Text
View/download PDF

34. T1179 Estrogens Promote Both Tumor Initiation and Progression in a Mouse Model of Colitis Associated Cancer

Author

Heijmans, Jarom, primary, Jacobs, Rutger J., additional, van Dop, Willemijn A., additional, van der Zon, Johanna, additional, Hommes, Daniel W., additional, Hardwick, James C., additional, Biemond, Izak, additional, Edevireen, Twan A.G., additional, Groothuis, Patrick G., additional, Muncan, Vanesa, additional, and van den Brink, Gijs R., additional

Published
2010
Full Text
View/download PDF

36. The potential of statins for individualized colorectal cancer chemoprevention.

Author

Jacobs RJ, Kodach LL, and Hardwick JC

Subjects
Animals, Bone Morphogenetic Proteins genetics, Bone Morphogenetic Proteins metabolism, Bone Morphogenetic Proteins physiology, Chemoprevention methods, Colorectal Neoplasms epidemiology, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors pharmacology, Mice, Rats, Risk Assessment, Chemoprevention trends, Colorectal Neoplasms prevention & control, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Precision Medicine
Abstract

Colorectal cancer is a leading cause of death by cancer in the western world. Despite major progress, even new chemotherapeutic regimens have had relatively little impact on long term survival in the approximately 50% of patients with advanced disease at presentation meaning that prevention is the only realistic way to reduce the burden of this disease. Many countries have implemented population-based screening methods to prevent colorectal cancer by the physical removal of its precursor lesion the adenoma, or to detect cancer at an earlier stage when it is amenable to surgical cure. However these programs have only been shown to reduce colorectal cancer deaths by 30% in those screened and therefore new or complimentary approaches are needed. One such approach is chemoprevention. A number of compounds have shown potential in reducing the incidence of colorectal cancer. Most widely known are NSAIDs but recently inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, also known as statins, commonly prescribed medications that lower serum cholesterol, have been shown to reduce colorectal cancer incidence. A critical issue in chemoprevention is the weighing of benefits against risks. In chemoprevention this balance is likely to be unfavourable when used in a wide unselected population even for the safest of compounds. Therapy should therefore be tailored to the individual patient. The balance will be more favourable in high risk groups such as individuals especially susceptible to neoplasia because of environmental risk factors, patients with inflammatory bowel disease, those with a hereditary predisposition and patients with a previous history of colorectal cancer or polyps. Furthermore colorectal cancer is not one disease but a heterogeneous group of diseases with different underlying molecular mechanisms. It is likely that both prevention and therapy will need to be tailored to the molecular subtype of the cancer in question. This may explain why studies of colorectal cancer in statin users do not show consistent protective effects. Evidence in vitro has shown a dichotomous effect of statins with either a cancer inhibiting or cancer promoting effect depending on their molecular subtype. Further studies are needed to determine in which patient groups statins can be used to prevent colorectal cancer and whether in other patients groups they should be avoided.

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results