Search

Your search keyword '"Offerhaus, G.J.A"' showing total 295 results
Start Over Author "Offerhaus, G.J.A"
295 results on '"Offerhaus, G.J.A"'

51. Misclassification of Dysplasia in Patients with Inflammatory Bowel Disease: Consequences for Progression Rates to Advanced Neoplasia

Author

Schaik, F.D.M. van, Kate, F.J.W. ten, Offerhaus, G.J.A., Schipper, M.E.I., Vleggaar, F.P., Woude, C.J. van der, Stokkers, P.C.F., Jong, D.J. de, Hommes, D.W., Bodegraven, A.A. van, Siersema, P.D., Oldenburg, B., Dutch Initiative Crohn Colitis, Amsterdam Gastroenterology Endocrinology Metabolism, Cancer Center Amsterdam, Pathology, Other departments, Gastroenterology and hepatology, CCA - Innovative therapy, Internal Medicine, and Gastroenterology & Hepatology

Subjects
Adult, Male, medicine.medical_specialty, Adolescent, Databases, Factual, Colorectal cancer, inflammatory bowel disease dysplasia colorectal cancer low-grade dysplasia ulcerative-colitis colorectal-cancer risk-factor follow-up surveillance guidelines, education, Kaplan-Meier Estimate, Molecular gastro-enterology and hepatology Pathogenesis and modulation of inflammation [IGMD 2], Inflammatory bowel disease, Gastroenterology, Young Adult, SDG 3 - Good Health and Well-being, Crohn Disease, Risk Factors, Internal medicine, Humans, Immunology and Allergy, Medicine, University medical, In patient, Young adult, Child, Aged, Crohn disease, business.industry, Middle Aged, biochemical phenomena, metabolism, and nutrition, medicine.disease, Dysplasia, Disease Progression, Colitis, Ulcerative, Female, Progression rate, Colorectal Neoplasms, business, Precancerous Conditions
Abstract

Background: The natural behavior of flat low-grade (LGD) and indefinite dysplasia (IND) in patients with inflammatory bowel disease (IBD) remains uncertain and seems to be dependent on the interpretation of the pathologist. We studied the progression rate of flat LGD and IND to advanced neoplasia (high-grade dysplasia [HGD] or colorectal cancer [CRC]) before and after histopathological review by a panel of gastrointestinal expert pathologists. Methods: A nationwide pathology database was used to identify IBD patients with dysplasia in six Dutch university medical centers between 1990 and 2006. Medical charts of patients with recorded flat LGD or IND were reviewed. Histological slides from three university medical centers were reviewed by a panel of three expert gastrointestinal pathologists. Results: We identified 113 flat LGD patients and 26 flat IND patients. Advanced neoplasia was found in 18 flat LGD patients (16%) after a median follow-up of 48 months, resulting in a 5-year progression rate of 12%. Five IND patients (19%) developed advanced neoplasia after a median follow-up of 24 months, resulting in a 5-year progression rate of 21%. Review of 1547 histological slides from 87 patients resulted in an increase of the 5-year progression rate of flat LGD to advanced neoplasia to 37%, whereas the progression rate of IND decreased to 5%. Conclusions: A diagnosis of flat LGD that is confirmed by a panel of expert gastrointestinal pathologists is associated with a substantial risk of progression to advanced neoplasia, while confirmed IND is associated with a low risk of progression. (Inflamm Bowel Dis 2011;17:1108-1116)

Published
2011
Full Text
View/download PDF

55. Impact of centralization of pancreatoduodenectomy on reported radical resections rates in a nationwide pathology database

Author

Onete, V.G. (Veronica G.), Besselink, M.G. (Marc), Salsbach, C.M. (Chanielle M.), Eijck, C.H.J. (Casper) van, Busch, O.R.C. (Olivier), Gouma, D.J. (Dirk), Hingh, I.H.J.T. (Ignace) de, Sieders, E. (Egbert), Dejong, C.H. (Cees), Offerhaus, G.J.A. (Johan), Molenaar, I.Q. (I. Quintus), Onete, V.G. (Veronica G.), Besselink, M.G. (Marc), Salsbach, C.M. (Chanielle M.), Eijck, C.H.J. (Casper) van, Busch, O.R.C. (Olivier), Gouma, D.J. (Dirk), Hingh, I.H.J.T. (Ignace) de, Sieders, E. (Egbert), Dejong, C.H. (Cees), Offerhaus, G.J.A. (Johan), and Molenaar, I.Q. (I. Quintus)

Abstract

Background Centralization of a pancreatoduodenectomy (PD) leads to a lower post-operative mortality, but is unclear whether it also leads to improved radical (R0) or overall resection rates. Methods Between 2004 and 2009, pathology reports of 1736 PDs for pancreatic and peri-ampullary neoplasms from a nationwide pathology database were analysed. Pre-malignant lesions were excluded. High-volume hospitals were defined as performing ≥ 20 PDs annually. The relationship between R0 resections, PD-volume trends, quality of pathology reports and hospital volume was analysed. Results During the study period, the number of hospitals performing PDs decreased from 39 to 23. High-volume hospitals reported more R0 resections in the pancreatic head and distal bile duct tumours than low-volume hospitals (60% versus 54%, P = 0.035) although they operated on more advanced (T3/T4) tumours (72% versus 58%, P < 0.001). The number of PDs increased from 258 in 2004 to 394 in 2009 which was partly explained by increased overall resection rates of pancreatic head and distal bile duct tumours (11.2% in 2004 versus 17.5% in 2009, P < 0.001). The overall reported R0 resection rate of pancreatic head and distal bile duct tumours increased (6% in 2004 versus 11% in 2009, P < 0.001). Pathology reports of low-volume hospitals lacked more data including tumour stage (25% versus 15%, P < 0.001). Conclusions Centralization of PD was associated with both higher resection rates and more reported R0 resections. The impact of this finding on overall survival should be further assessed.

Published
2015
Full Text
View/download PDF

56. Peutz-Jeghers syndrome polyps are polyclonal with expanded progenitor cell compartment

Author

de Leng, W.W.J., Jansen, M., Keller, J.J., de Gijsel, M., Milne, A.N.A., Morsink, F.H.M., Weterman, M.A.J., Iacobuzio-Donahue, C.A., Clevers, H.C., Giardiello, F.M., and Offerhaus, G.J.A.

Subjects
Peutz-Jeghers syndrome -- Genetic aspects, Peutz-Jeghers syndrome -- Development and progression, Peutz-Jeghers syndrome -- Risk factors, Health
Published
2007

57. Adenomatous polyposis coli-deficient zebrafish are susceptible to digestive tract neoplasia

Author

Haramis, A.-P.G., Hurlstone, A., Velden, Y. van der, Begthel, H., Born, M. van den, Offerhaus, G.J.A., Clevers, J.C., and Hubrecht Institute for Developmental Biology and Stem Cell Research

Abstract

Truncation of the tumour suppressor adenomatous polyposis coli (APC) constitutively activates the Wnt/beta-catenin signalling pathway. This event constitutes the primary transforming event in sporadic colorectal cancer in humans. Moreover, humans or mice carrying germline truncating mutations in APC develop large numbers of intestinal adenomas. Here, we report that zebrafish that are heterozygous for a truncating APC mutation spontaneously develop intestinal, hepatic and pancreatic neoplasias that are highly proliferative, accumulate beta-catenin and express Wnt target genes. Treatment with the chemical carcinogen 7,12-dimethylbenz[a]anthracene accelerates the induction of these lesions. These observations establish apc-mutant zebrafish as a bona fide model for the study of digestive tract cancer.

Published
2006

62. International Cancer of the Pancreas Screening (CAPS) Consortium summit on the management of patients with increased risk for familial pancreatic cancer.

Author

Canto, M.I., Harinck, F., Hruban, R.H., Offerhaus, G.J.A., Poley, J.W., Kamel, I., Nio, Y., Schulick, R.S., Bassi, C., Kluijt, I., Levy, M.J., Chak, A., Fockens, P., Goggins, M., CAPS Consortium, x, Bruno, M., Canto, M.I., Harinck, F., Hruban, R.H., Offerhaus, G.J.A., Poley, J.W., Kamel, I., Nio, Y., Schulick, R.S., Bassi, C., Kluijt, I., Levy, M.J., Chak, A., Fockens, P., Goggins, M., CAPS Consortium, x, and Bruno, M.

Published
2013

63. Pancreatic cancer risk in Peutz-Jeghers syndrome patients: A large cohort study and implications for surveillance

Author

Korsse, S.E. (Susanne), Harinck, F. (Femme), Lier, M.G.F. (Margot) van, Biermann, K. (Katharina), Offerhaus, G.J.A. (Johan), Krak, N.C. (Nanda), Looman, C.W.N. (Caspar), Veelen, W. (Wendy) van, Kuipers, E.J. (Ernst), Wagner, A. (Anja), Dekker, E. (Evelien), Mathus-Vliegen, E.M.H. (Elisabeth), Fockens, P. (Paul), Leerdam, M.E. (Monique) van, Bruno, M.J. (Marco), Korsse, S.E. (Susanne), Harinck, F. (Femme), Lier, M.G.F. (Margot) van, Biermann, K. (Katharina), Offerhaus, G.J.A. (Johan), Krak, N.C. (Nanda), Looman, C.W.N. (Caspar), Veelen, W. (Wendy) van, Kuipers, E.J. (Ernst), Wagner, A. (Anja), Dekker, E. (Evelien), Mathus-Vliegen, E.M.H. (Elisabeth), Fockens, P. (Paul), Leerdam, M.E. (Monique) van, and Bruno, M.J. (Marco)

Abstract

Background Although Peutz-Jeghers syndrome (PJS) is known to be associated with pancreatic cancer (PC), estimates of this risk differ widely. This hampers counselling of patients and implementation of surveillance strategies. We therefore aimed to determine the PC risk in a large cohort of Dutch PJS patients. Methods PJS was defined by diagnostic criteria recommended by the WHO, a proven LKB1 mutation, or both. All patients with a presumptive diagnosis of pancreatic, ampullary or distal bile duct cancer were identified. Cases were reviewed clinically, radiologically and immunohistochemically. Cumulative PC risks were calculated by Kaplan-Meier analysis and relative risks by Poisson regression analysis. Results We included 144 PJS patients (49% mal

Published
2013
Full Text
View/download PDF

64. International cancer of the pancreas screening (CAPS) consortium summit on the management of patients with increased risk for familial pancreatic cancer

Author

Canto, M.I. (Marcia Irene), Harinck, F. (Femme), Hruban, R.H. (Ralph), Offerhaus, G.J.A. (Johan), Poley, J.-W. (Jan-Werner), Kamel, M.S. (Mohamed), Nio, C.Y. (Yung), Schulick, R. (Richard), Bassi, C. (Claudio), Kluijt, I. (Irma), Levy, M.L. (Michael), Chak, A. (Amitabh), Fockens, P. (Paul), Goggins, M. (Michael), Bruno, M.J. (Marco), Canto, M.I. (Marcia Irene), Harinck, F. (Femme), Hruban, R.H. (Ralph), Offerhaus, G.J.A. (Johan), Poley, J.-W. (Jan-Werner), Kamel, M.S. (Mohamed), Nio, C.Y. (Yung), Schulick, R. (Richard), Bassi, C. (Claudio), Kluijt, I. (Irma), Levy, M.L. (Michael), Chak, A. (Amitabh), Fockens, P. (Paul), Goggins, M. (Michael), and Bruno, M.J. (Marco)

Abstract

Background Screening individuals at increased risk for pancreatic cancer (PC) detects early, potentially curable, pancreatic neoplasia. Objective To develop consortium statements on screening, surveillance and management of high-risk individuals with an inherited predisposition to PC. Methods A 49-expert multidisciplinary international consortium met to discuss pancreatic screening and vote on statements. Consensus was considered reached if ≥75% agreed or disagreed. Results There was excellent agreement that, to be successful, a screening programme should detect and treat T1N0M0 margin-negative PC and high-grade dysplastic precursor lesions (pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasm). It was agreed that the following were candidates for screening: first-degree relatives (FDRs) of patients with PC from a familial PC kindred with at least two affected FDRs; patients with Peutz–Jeghers syndrome; and p16, BRCA2 and hereditary non-polyposis colorectal cancer (HNPCC) mutation carriers with ≥1 affected FDR. Consensus was not reached for the age to initiate screening or stop surveillance. It was agreed that initial screening should include endoscopic ultrasonography (EUS) and/or MRI/magnetic resonance cholangiopancreatography not CT or endoscopic retrograde cholangiopancreatography. There was no consensus on the need for EUS fine-needle aspiration to evaluate cysts. There was disagreement on optimal screening modalities and intervals for follow-up imaging. When surgery is recommended it should be performed at a high-volume centre. There was great disagreement as to which screenin

Published
2013
Full Text
View/download PDF

65. International Cancer of the Pancreas Screening (CAPS) Consortium summit on the management of patients with increased risk for familial pancreatic cancer

Author

Cancer, Pathologie, Canto, M.I., Harinck, F., Hruban, R.H., Offerhaus, G.J.A., Poley, J.W., Kamel, I., Nio, Y., Schulick, R.S., Bassi, C., Kluijt, I., Levy, M.J., Chak, A., Fockens, P., Goggins, M., CAPS Consortium, x, Bruno, M., Cancer, Pathologie, Canto, M.I., Harinck, F., Hruban, R.H., Offerhaus, G.J.A., Poley, J.W., Kamel, I., Nio, Y., Schulick, R.S., Bassi, C., Kluijt, I., Levy, M.J., Chak, A., Fockens, P., Goggins, M., CAPS Consortium, x, and Bruno, M.

Published
2013

66. Hemochromatosis (HFE) gene mutations and risk of gastric cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

Author

JC Overig onderzoek, Other research (not in main researchprogram), Cancer, MS MDL 1, General Practice & Nursing Science, Pathologie, Agudo, A, Bonet, C., et al, X, Bueno de Mesquita, H.B., Siersema, P.D., Numans, M.E., Offerhaus, G.J.A., Jakszyn, P., JC Overig onderzoek, Other research (not in main researchprogram), Cancer, MS MDL 1, General Practice & Nursing Science, Pathologie, Agudo, A, Bonet, C., et al, X, Bueno de Mesquita, H.B., Siersema, P.D., Numans, M.E., Offerhaus, G.J.A., and Jakszyn, P.

Published
2013

67. Prostate stem-cell antigen gene is associated with diffuse and intestinal gastric cancer in Caucasians: Results from the EPIC-EURGAST study

Author

Sala, N. Muñoz, X. Travier, N. Agudo, A. Duell, E.J. Moreno, V. Overvad, K. Tjonneland, A. Boutron-Ruault, M.C. Clavel-Chapelon, F. Canzian, F. Kaaks, R. Boeing, H. Meidtner, K. Trichopoulos, A. Tsiotas, K. Zylis, D. Vineis, P. Panico, S. Palli, D. Krogh, V. Tumino, R. Lund, E. Bueno-De-Mesquita, H.B. Numans, M.E. Peeters, P.H.M. Quirós, J.R. Sánchez, M.-J. Navarro, C. Ardanaz, E. Dorronsoro, M. Hallmans, G. Stenling, R. Manjer, J. Allen, N.E. Travis, R.C. Khaw, K.-T. Jenab, M. Offerhaus, G.J.A. Riboli, E. González, C.A. and Sala, N. Muñoz, X. Travier, N. Agudo, A. Duell, E.J. Moreno, V. Overvad, K. Tjonneland, A. Boutron-Ruault, M.C. Clavel-Chapelon, F. Canzian, F. Kaaks, R. Boeing, H. Meidtner, K. Trichopoulos, A. Tsiotas, K. Zylis, D. Vineis, P. Panico, S. Palli, D. Krogh, V. Tumino, R. Lund, E. Bueno-De-Mesquita, H.B. Numans, M.E. Peeters, P.H.M. Quirós, J.R. Sánchez, M.-J. Navarro, C. Ardanaz, E. Dorronsoro, M. Hallmans, G. Stenling, R. Manjer, J. Allen, N.E. Travis, R.C. Khaw, K.-T. Jenab, M. Offerhaus, G.J.A. Riboli, E. González, C.A.

Abstract

A genome-wide study performed in a Japanese population identified a strong association between SNP rs2294008 (Met1Thr) in the Prostate Stem Cell Antigen gene (PSCA) and diffuse-type gastric cancer (GC). This association was validated in different Asian populations, and, very recently, a study has been published in Caucasians. In this study, we analyzed the association between PSCA variation and GC risk in Caucasians from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Six tagSNPs covering the PSCA gene region were genotyped in 411 incident gastric adenocarcinoma cases and 1530 matched controls from a nested case-control study in the EPIC cohort. Associations were analyzed by unconditional logistic regression, adjusting for age, sex and country. The T allele of rs2294008 in PSCA was found to be a highly significant risk factor for GC (per allele OR = 1.42, 95% CI: 1.23-1.66, p-value = 6.5 × 10 -6), particularly of the noncardia-type (per allele OR = 1.47, 95% CI: 1.19-1.81, p-value = 3 × 10 -4). At contrast with previous studies, no significant differences were observed between the diffuse (per allele OR = 1.54, 95% CI: 1.20-1.96, p-value = 5 × 10 -4) and the intestinal (per allele OR = 1.52, 95% CI: 1.20-1.93, p-value = 5 × 10 -4) GC histological subtypes. Although rs12155758 and rs9297976 were also found associated with GC, this association appeared to be due to linkage disequilibrium with rs2294008. Haplotype analysis did not provide additional information. These results confirm the association between variation in the promoter region of PSCA and GC risk in Caucasians and also indicate that the rs2294008 variant is a similar risk factor for both the diffuse and intestinal-types of GC. © 2011 UICC.

Published
2012

77. Molecular characteristics of pancreatic ductal adenocarcinoma.

Author

Other research (not in main researchprogram), Cancer, Pathologie, Ottenhof, N.A., de Wilde, R.F., Maitra, A., Hruban, R.H., Offerhaus, G.J.A., Other research (not in main researchprogram), Cancer, Pathologie, Ottenhof, N.A., de Wilde, R.F., Maitra, A., Hruban, R.H., and Offerhaus, G.J.A.

Published
2011

86. Mutations in CCBE1 cause generalized lymph vessel dysplasia in humans.

Author

Alders, M., Hogan, B.M., Gjini, E., Salehi, F., Al-Gazali, L., Hennekam, E.A., Holmberg, E.E., Mannens, M.M., Mulder, M.F., Offerhaus, G.J.A., Prescott, T.E., Schroor, E.J., Verheij, J.B., de Witte, M., Zwijnenburg, P.J., Vikkula, M., Schulte-Merker, S., Hennekam, R., Alders, M., Hogan, B.M., Gjini, E., Salehi, F., Al-Gazali, L., Hennekam, E.A., Holmberg, E.E., Mannens, M.M., Mulder, M.F., Offerhaus, G.J.A., Prescott, T.E., Schroor, E.J., Verheij, J.B., de Witte, M., Zwijnenburg, P.J., Vikkula, M., Schulte-Merker, S., and Hennekam, R.

Abstract

Lymphedema, lymphangiectasias, mental retardation and unusual facial characteristics define the autosomal recessive Hennekam syndrome. Homozygosity mapping identified a critical chromosomal region containing CCBE1, the human ortholog of a gene essential for lymphangiogenesis in zebrafish. Homozygous and compound heterozygous mutations in seven subjects paired with functional analysis in a zebrafish model identify CCBE1 as one of few genes causing primary generalized lymph-vessel dysplasia in humans., Lymphedema, lymphangiectasias, mental retardation and unusual facial characteristics define the autosomal recessive Hennekam syndrome. Homozygosity mapping identified a critical chromosomal region containing CCBE1, the human ortholog of a gene essential for lymphangiogenesis in zebrafish. Homozygous and compound heterozygous mutations in seven subjects paired with functional analysis in a zebrafish model identify CCBE1 as one of few genes causing primary generalized lymph-vessel dysplasia in humans.

Published
2009

87. LKB1 and AMPK family signaling: the intimate link between cell polarity and energy metabolism.

Author

Jansen, M., ten Klooster, J.P., Offerhaus, G.J.A., Clevers, H., Jansen, M., ten Klooster, J.P., Offerhaus, G.J.A., and Clevers, H.

Abstract

Research on the LKB1 tumor suppressor protein mutated in cancer-prone Peutz-Jeghers patients has continued at a feverish pace following exciting developments linking energy metabolism and cancer development. This review summarizes the current state of research on the LKB1 tumor suppressor. The weight of the evidence currently indicates an evolutionary conserved role for the protein in the regulation of various aspects of cellular polarity and energy metabolism. We focus on studies examining the concept that both cellular polarity and energy metabolism are regulated through the conserved LKB1-AMPK signal transduction pathway. Recent studies from a variety of model organisms have given new insight into the mechanism of polyp development and cancer formation in Peutz-Jeghers patients and the role of LKB1 mutation in sporadic tumorigenesis. Conditional LKB1 mouse models have outlined a tissue-dependent context for pathway activation and suggest that LKB1 may affect different AMPK isoforms independently. Elucidation of the molecular mechanism responsible for Peutz-Jeghers syndrome will undoubtedly reveal important insight into cancer development in the larger population., Research on the LKB1 tumor suppressor protein mutated in cancer-prone Peutz-Jeghers patients has continued at a feverish pace following exciting developments linking energy metabolism and cancer development. This review summarizes the current state of research on the LKB1 tumor suppressor. The weight of the evidence currently indicates an evolutionary conserved role for the protein in the regulation of various aspects of cellular polarity and energy metabolism. We focus on studies examining the concept that both cellular polarity and energy metabolism are regulated through the conserved LKB1-AMPK signal transduction pathway. Recent studies from a variety of model organisms have given new insight into the mechanism of polyp development and cancer formation in Peutz-Jeghers patients and the role of LKB1 mutation in sporadic tumorigenesis. Conditional LKB1 mouse models have outlined a tissue-dependent context for pathway activation and suggest that LKB1 may affect different AMPK isoforms independently. Elucidation of the molecular mechanism responsible for Peutz-Jeghers syndrome will undoubtedly reveal important insight into cancer development in the larger population.

Published
2009

88. Immunophenotyping of hereditary breast cancer

Author

Cancer, Pathologie, van der Wall, E, Offerhaus, G.J.A., van der Groep, P., Cancer, Pathologie, van der Wall, E, Offerhaus, G.J.A., and van der Groep, P.

Published
2009

89. Molecular and pro-inflammatory genetic profile in gastric carcinomas

Author

Infection & Immunity, Pathologie, Offerhaus, G.J.A., Maciejewski, R., Polkowski, W.P., Milne - Blaney, A.N.A., de Leng, WW, Sitarz, R., Infection & Immunity, Pathologie, Offerhaus, G.J.A., Maciejewski, R., Polkowski, W.P., Milne - Blaney, A.N.A., de Leng, WW, and Sitarz, R.

Published
2009

90. Barrett esophagus and cancer: pathogenesis, carcinogenesis, and diagnostic dilemmas

Author

Polkowski, W., Van Lanschot, J.J.B., and Offerhaus, G.J.A.

Subjects
6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología [CDU], Pathogenesis, Adenocarcinoma
Abstract

A metaplastic process, in which native squamous epithelium of the distal esophagus is replaced by columnar epithelium, is known as Barrett esophagus (BE). Over the past years, intestinal metaplasia was recognized as a marker for BE. The risk for the development of esophageal adenocarcinoma in a patients with BE is much hi"gh er when com~aredto the normal population. Duodeno-gastro-esophageal reflux is supposed to play a role in the pathogenesis of BE and rising incidence of adenocarcinoma of the esophagus. With current therapeutic options, when clinical manifestation of this cancer occurs, it is too late for cure in the majority of patients. Therefore, attention should be focused on early diagnosis, for which molecular genetic techniques might become available. Current data on genetic alterations involved in carcinogenesis of BE are discussed. Grading of dysplasia in BE carries important clinical consequences for the individual patient: intensification of endoscopic surveillance or 'prophylactic esophagectomy'. Several morpho- andlor cytometric parameters may be used for discrimination between different grades of dysplasia in BE. Therefore, a new and original algorythm for the potential application of quantitative pathology in grading of dysplasia in patients with BE has been proposed. Molecular biology together with image analysis of histological spectrum of BE enable better understanding of the mechanisms of malignant degeneration and might ultimately lead to targeted cancer prevention andlor therapeutic interventions.

Published
1999

91. Clinical applications of detecting dysfunctional p53 tumor suppressor protein

Author

Baas, I.O., Hruban, R.H., and Offerhaus, G.J.A.

Subjects
Neoplasia, 6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología [CDU], Cell cycle
Abstract

The p53 gene encodes for a protein, p53, which plays a critical role in controlling the cell cycle, in DNA repair and in programed cell death (apoptosis). p53 is one of the most frequently mutated genes in human neoplasms and a variety of techniques have been developed to detect these mutations. These range from advanced molecular-genetic analyses to immunohistochemical staining for the p53 protein. This review will summarize our current understanding of the function of p53 as well as current methods to detect dysfunctional p53 and the clinical value of such analyses.

Published
1999

Catalog

Books, media, physical & digital resources
See catalog results