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1 February 2008
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Cover Image
Breast cancer is made of various molecular subtypes with different prognosis. Using whole-genome oligonucleotide microarrays, Finetti and colleagues studied the expression of kinase genes in 80 luminal A and 58 basal breast cancers. The expression (measured by a kinase score) of 16 genes encoding serine/threonine kinases involved in mitosis distinguished two subgroups of luminal A tumors: Aa, of good prognosis, and Ab, of poor prognosis (top image). This classification and its prognostic impact were validated in 276 luminal A cases from three independent series (bottom image). Among 1222 breast cancer samples (middle image), most of the luminal A (dark blue for Aa and black for Ab) and normal-like (green) tumors had negative kinase scores, while most of the basal (red ) and luminal B (light blue) tumors had positive kinase scores. ERBB2-overexpressing (pink) samples were equally distributed with respect to their kinase scores. This mitotickinase signature reveals a continuum of luminal cases from the more proliferative (luminal B) to the less proliferative (luminal Aa). For details, see the article by Finetti and colleagues on page 767 of this issue.Close Modal - PDF Icon PDF LinkTable of Contents
ISSN 0008-5472
EISSN 1538-7445
Journal Archive
Cancer Research (1941-Present; volumes 1-current)
(ISSN 0008-5472) Published twice monthly since 1987. From 1941-1986, published monthly.The American Journal of Cancer (1931-1940; volumes 15-40)
(ISSN 0099-7374) Published quarterly in 1931, bimonthly in 1932, and monthly from 1933 to 1940. The journal changed title to Cancer Research in 1941.The Journal of Cancer Research (1916-1930); volumes 1-14)
(ISSN 0099-7013) Published quarterly from 1916 through 1930 (publication was suspended from November 1922 to March 1924). The journal changed title to The American Journal of Cancer in 1931.Table of Contents
Reviews
Meeting Report
Priority Reports
Molecular Biology, Pathobiology, and Genetics
Multiple Alternative Splicing Markers for Ovarian Cancer
Roscoe Klinck; Anne Bramard; Lyna Inkel; Geneviève Dufresne-Martin; Julien Gervais-Bird; Richard Madden; Éric R. Paquet; ChuShin Koh; Julian P. Venables; Panagiotis Prinos; Manuela Jilaveanu-Pelmus; Raymund Wellinger; Claudine Rancourt; Benoit Chabot; Sherif Abou Elela
Modeling Genomic Diversity and Tumor Dependency in Malignant Melanoma
William M. Lin; Alissa C. Baker; Rameen Beroukhim; Wendy Winckler; Whei Feng; Jennifer M. Marmion; Elisabeth Laine; Heidi Greulich; Hsiuyi Tseng; Casey Gates; F. Stephen Hodi; Glenn Dranoff; William R. Sellers; Roman K. Thomas; Matthew Meyerson; Todd R. Golub; Reinhard Dummer; Meenhard Herlyn; Gad Getz; Levi A. Garraway
Cell, Tumor, and Stem Cell Biology
Enhanced Activation of Epidermal Growth Factor Receptor Caused by Tumor-Derived E-Cadherin Mutations
Anja Bremm; Axel Walch; Margit Fuchs; Jörg Mages; Justus Duyster; Gisela Keller; Christine Hermannstädter; Karl-Friedrich Becker; Sandra Rauser; Rupert Langer; Claus Hann von Weyhern; Heinz Höfler; Birgit Luber
CCN3/Nephroblastoma Overexpressed Matricellular Protein Regulates Integrin Expression, Adhesion, and Dissemination in Melanoma
Viviana Vallacchi; Maria Daniotti; Francesca Ratti; Delia Di Stasi; Paola Deho; Annamaria De Filippo; Gabrina Tragni; Andrea Balsari; Antonino Carbone; Licia Rivoltini; Giorgio Parmiani; Noureddine Lazar; Bernard Perbal; Monica Rodolfo
The Human Trithorax Protein hASH2 Functions as an Oncoprotein
Juliane Lüscher-Firzlaff; Isabella Gawlista; Jörg Vervoorts; Karsten Kapelle; Till Braunschweig; Gesa Walsemann; Chantal Rodgarkia-Schamberger; Henning Schuchlautz; Stephan Dreschers; Elisabeth Kremmer; Richard Lilischkis; Christa Cerni; Axel Wellmann; Bernhard Lüscher
CD43, but not P-Selectin Glycoprotein Ligand-1, Functions as an E-Selectin Counter-Receptor in Human Pre-B–Cell Leukemia NALL-1
Chizu Nonomura; Jiro Kikuchi; Nobutaka Kiyokawa; Hidenori Ozaki; Kanae Mitsunaga; Hidenobu Ando; Akiko Kanamori; Reiji Kannagi; Junichiro Fujimoto; Kazuo Muroi; Yusuke Furukawa; Mitsuru Nakamura
Experimental Therapeutics, Molecular Targets, and Chemical Biology
Aggravated Endoplasmic Reticulum Stress as a Basis for Enhanced Glioblastoma Cell Killing by Bortezomib in Combination with Celecoxib or Its Non-Coxib Analogue, 2,5-Dimethyl-Celecoxib
Adel Kardosh; Encouse B. Golden; Peter Pyrko; Jasim Uddin; Florence M. Hofman; Thomas C. Chen; Stan G. Louie; Nicos A. Petasis; Axel H. Schönthal
Immunology
Endocrinology
Clinical Research
Epidemiology
Prevention
Corrections
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