Issues
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Cover Image
Cover Image
Most human colorectal carcinomas (CRCs) generally arise from adenomatous precursors, and mutations in the adenomatous polyposis coli (APC) gene are pivotal in colorectal tumorigenesis. Mouse intestinal tumor models have shown mainly small intestinal lesions; carcinomas are rare. Hinoi and colleagues defined sequences from the human CDX2 gene conferring colon epithelium–preferential transgene expression in the adult mouse, as indicated by the preferential activation of β-galactosidase expression following CDX2P-NLS Cre recombinase–mediated excision of a transcriptional stop element (top right panel; distal esophagus at top right, followed by stomach, small intestine, cecum, colon, and anus at bottom left). CPC;Apc mice carrying a CDX2P-NLS Cre recombinase transgene and a loxP-targeted Apc allele developed mainly colorectal tumors. The excised gastrointestinal tract from a 10-month-old CPC;Apc mouse is shown (top left panel). The location, size, and invasive potential of tumors arising in 18 male and 18 female CPC;Apc mice were defined (bottom right). On average, 5–8 tumors were found in the distal colon of a CPC;Apc mouse, along with 1 cecal and 3 distal small intestinal tumors. Male CPC;Apc mice had roughly 50% more distal lesions than female mice. Invasive carcinomas, similar to the muscularis propria–invasive, β-catenin nuclearpositive staining lesion shown (bottom left panel), were seen in 6 of 36 (17%) mice followed for 300 days. Like human colorectal lesions, the mouse tumors showed biallelic Apc inactivation, β-catenin dysregulation, global DNA hypomethylation, and aneuploidy. The mouse model should facilitate efforts to define novel factors and mechanisms contributing to human CRCs, as well as work on tumor-promoting environmental factors and agents, and strategies for cancer prevention or treatment. For details, see the article by Hinoi and colleagues on page 9721 of this issue. - PDF Icon PDF LinkTable of Contents
Cancer Research
Table of Contents
Reviews
Meeting Report
Eleventh Prouts Neck Meeting on Prostate Cancer: Emerging Strategies in Prostate Cancer Therapy
Priority Reports
Molecular Biology, Pathobiology, and Genetics
Gene Amplification and Overexpression of PRDM14 in Breast Cancers
Casein Kinase 2–Interacting Protein-1, a Novel Akt Pleckstrin Homology Domain-Interacting Protein, Down-regulates PI3K/Akt Signaling and Suppresses Tumor Growth In vivo
Cell, Tumor, and Stem Cell Biology
Tumor Necrosis Factor-α Promotes Malignant Pleural Effusion
Fms-like Tyrosine Kinase 3 Ligand Stimulation Induces MLL-Rearranged Leukemia Cells into Quiescence Resistant to Antileukemic Agents
Experimental Therapeutics, Molecular Targets, and Chemical Biology
Discovery and Pharmacologic Characterization of CP-724,714, a Selective ErbB2 Tyrosine Kinase Inhibitor
A Human CD4 Monoclonal Antibody for the Treatment of T-Cell Lymphoma Combines Inhibition of T-Cell Signaling by a Dual Mechanism with Potent Fc-Dependent Effector Activity
MAGE-A, mMage-b, and MAGE-C Proteins Form Complexes with KAP1 and Suppress p53-Dependent Apoptosis in MAGE-Positive Cell Lines
Thymic Stromal-Derived Lymphopoietin Induces Proliferation of Pre-B Leukemia and Antagonizes mTOR Inhibitors, Suggesting a Role for Interleukin-7Rα Signaling
Immunology
Helper Function of Memory CD8+ T Cells: Heterologous CD8+ T Cells Support the Induction of Therapeutic Cancer Immunity
Adoptively Transferred Tumor-Specific T Cells Stimulated Ex vivo Using Herpes Simplex Virus Amplicons Encoding 4-1BBL Persist in the Host and Show Antitumor Activity In vivo
Live Attenuated Listeria Monocytogenes Effectively Treats Hepatic Colorectal Cancer Metastases and Is Strongly Enhanced by Depletion of Regulatory T Cells
Endocrinology
Control of Androgen Receptor Signaling in Prostate Cancer by the Cochaperone Small Glutamine–Rich Tetratricopeptide Repeat Containing Protein α
Corrections
Journal Archive
Cancer Research
(1941-Present; volumes 1-current)Published twice monthly since 1987. From 1941-1986, published monthly.
(ISSN 0008-5472)
The American Journal of Cancer
(1931-1940; volumes 15-40)Published quarterly in 1931, bimonthly in 1932, and monthly from 1933 to 1940. The journal changed title to Cancer Research in 1941.
(ISSN 0099-7374)
The Journal of Cancer Research
(1916-1930); volumes 1-14)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.
(ISSN 0099-7013)
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