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Your search keyword '"Nijman LE"' showing total 2 results
Start Over Author "Nijman LE" Journal nature communications
2 results on '"Nijman LE"'

1. Molecular characterization of colorectal cancer related peritoneal metastatic disease.

Author

Lenos KJ, Bach S, Ferreira Moreno L, Ten Hoorn S, Sluiter NR, Bootsma S, Vieira Braga FA, Nijman LE, van den Bosch T, Miedema DM, van Dijk E, Ylstra B, Kulicke R, Davis FP, Stransky N, Smolen GA, Coebergh van den Braak RRJ, IJzermans JNM, Martens JWM, Hallam S, Beggs AD, Kops GJPL, Lansu N, Bastiaenen VP, Klaver CEL, Lecca MC, El Makrini K, Elbers CC, Dings MPG, van Noesel CJM, Kranenburg O, Medema JP, Koster J, Koens L, Punt CJA, Tanis PJ, de Hingh IH, Bijlsma MF, Tuynman JB, and Vermeulen L

Subjects
Humans, Peritoneum metabolism, Quality of Life, Colorectal Neoplasms pathology, Neoplasms, Second Primary, Peritoneal Neoplasms genetics, Peritoneal Neoplasms secondary
Abstract

A significant proportion of colorectal cancer (CRC) patients develop peritoneal metastases (PM) in the course of their disease. PMs are associated with a poor quality of life, significant morbidity and dismal disease outcome. To improve care for this patient group, a better understanding of the molecular characteristics of CRC-PM is required. Here we present a comprehensive molecular characterization of a cohort of 52 patients. This reveals that CRC-PM represent a distinct CRC molecular subtype, CMS4, but can be further divided in three separate categories, each presenting with unique features. We uncover that the CMS4-associated structural protein Moesin plays a key role in peritoneal dissemination. Finally, we define specific evolutionary features of CRC-PM which indicate that polyclonal metastatic seeding underlies these lesions. Together our results suggest that CRC-PM should be perceived as a distinct disease entity., (© 2022. The Author(s).)

Published
2022
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2. Chromosomal copy number heterogeneity predicts survival rates across cancers.

Author

van Dijk E, van den Bosch T, Lenos KJ, El Makrini K, Nijman LE, van Essen HFB, Lansu N, Boekhout M, Hageman JH, Fitzgerald RC, Punt CJA, Tuynman JB, Snippert HJG, Kops GJPL, Medema JP, Ylstra B, Vermeulen L, and Miedema DM

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Child, Computer Simulation, Datasets as Topic, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genomics, Humans, Male, Middle Aged, Mutation, Neoplasms genetics, Neoplasms pathology, Prognosis, Progression-Free Survival, Risk Assessment methods, Survival Rate, Young Adult, DNA Copy Number Variations, Genetic Heterogeneity, Models, Genetic, Neoplasms mortality, Tumor Microenvironment genetics
Abstract

Survival rates of cancer patients vary widely within and between malignancies. While genetic aberrations are at the root of all cancers, individual genomic features cannot explain these distinct disease outcomes. In contrast, intra-tumour heterogeneity (ITH) has the potential to elucidate pan-cancer survival rates and the biology that drives cancer prognosis. Unfortunately, a comprehensive and effective framework to measure ITH across cancers is missing. Here, we introduce a scalable measure of chromosomal copy number heterogeneity (CNH) that predicts patient survival across cancers. We show that the level of ITH can be derived from a single-sample copy number profile. Using gene-expression data and live cell imaging we demonstrate that ongoing chromosomal instability underlies the observed heterogeneity. Analysing 11,534 primary cancer samples from 37 different malignancies, we find that copy number heterogeneity can be accurately deduced and predicts cancer survival across tissues of origin and stages of disease. Our results provide a unifying molecular explanation for the different survival rates observed between cancer types.

Published
2021
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