Supervised risk predictor of breast cancer based on intrinsic subtypes.
D diagnosis by intrinsic subtype adds significant prognostic and predictive information to standard parameters for patients with breast cancer.
Integrated genomic characterization of endometrial carcinoma
- D. Levine, Gad Stacey B. Kristian Eric Andrey Carrie Mike Cyriac Getz Gabriel Cibulskis Lander Sivachenko Sougnez L, H. Sofia
- Biology, MedicineNature
- 1 May 2013
The genomic features of endometrial carcinomas permit a reclassification that may affect post-surgical adjuvant treatment for women with aggressive tumours, and these features are classified into four categories: POLE ultramutated, microsatellite instability hypermutated, copy- number low, and copy-number high.
Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer
It is confirmed that a prognostically relevant differentiation hierarchy exists across all breast cancers in which the claudin-low subtype most closely resembles the mammary epithelial stem cell.
The Immune Landscape of Cancer
Ki67 Index, HER2 Status, and Prognosis of Patients With Luminal B Breast Cancer
Luminal B and luminal–HER2-positive breast cancers were statistically significantly associated with poor breast cancer recurrence-free and disease-specific survival in all adjuvant systemic treatment categories.
Comprehensive Molecular Portraits of Invasive Lobular Breast Cancer
Comprehensive, Integrative Genomic Analysis of Diffuse Lower-Grade Gliomas.
The integration of genomewide data from multiple platforms delineated three molecular classes of lower-grade gliomas that were more concordant with IDH, 1p/19q, and TP53 status than with histologic class.
Molecular Profiling Reveals Biologically Discrete Subsets and Pathways of Progression in Diffuse Glioma
Comprehensive genomic characterization of head and neck squamous cell carcinomas
It is shown that human-papillomavirus-associated tumours are dominated by helical domain mutations of the oncogene PIK3CA, novel alterations involving loss of TRAF3, and amplification of the cell cycle gene E2F1.