Issues
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Cover Image
Cover Image
Glioblastomas are routinely treated with ionizing radiation. During treatment, the tissue surrounding tumors is also irradiated, which can induce senescence of normal brain cells including astrocytes. Senescent astrocytes promote glioblastoma aggressiveness and recurrence via release of SASP factors, and this can be ameliorated by senolytic therapy. The cover shows an image of a mouse brain stained for nuclei (blue), GFAP (green; marker for astrocytes), and Lamin B1 (red; loss of which is a marker for senescence). For details, see the article by Fletcher-Sananikone and colleagues on page 5935. - PDF Icon PDF LinkTable of Contents
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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
Breaking Insights
Editorial
Review
Cancer Research Landmarks
Controversy and Consensus
Resource Report
The Mutational Signature Comprehensive Analysis Toolkit (musicatk) for the Discovery, Prediction, and Exploration of Mutational Signatures
The musicatk package empowers researchers to characterize mutational signatures and tumor heterogeneity with a comprehensive set of preprocessing utilities, discovery and prediction tools, and multiple functions for downstream analysis and visualization.
Genome and Epigenome
Genomic and Transcriptomic Analysis of Relapsed and Refractory Childhood Solid Tumors Reveals a Diverse Molecular Landscape and Mechanisms of Immune Evasion
Antisense RNAs Influence Promoter Usage of Their Counterpart Sense Genes in Cancer
This study characterizes a previously unexplored role of ncNATs in regulation of isoform expression of associated sense genes, highlighting a mechanism of alternative promoter usage in cancer.
Metabolism and Chemical Biology
Patterns of Carbon-Bound Exogenous Compounds in Patients with Lung Cancer and Association with Disease Pathophysiology
Molecular Cell Biology
ALKBH5 Facilitates Hypoxia-Induced Paraspeckle Assembly and IL8 Secretion to Generate an Immunosuppressive Tumor Microenvironment
A PLCB1–PI3K–AKT Signaling Axis Activates EMT to Promote Cholangiocarcinoma Progression
PLCB1 functions as an oncogenic driver in cholangiocarcinoma development that confers an actionable therapeutic vulnerability to AKT inhibition.
The HNF4α-BC200-FMR1–Positive Feedback Loop Promotes Growth and Metastasis in Invasive Mucinous Lung Adenocarcinoma
ALDH1A1 Activity in Tumor-Initiating Cells Remodels Myeloid-Derived Suppressor Cells to Promote Breast Cancer Progression
Tumor Biology and Immunology
Elimination of Radiation-Induced Senescence in the Brain Tumor Microenvironment Attenuates Glioblastoma Recurrence
Supraphysiologic Testosterone Induces Ferroptosis and Activates Immune Pathways through Nucleophagy in Prostate Cancer
Hypoxia Drives Dihydropyrimidine Dehydrogenase Expression in Macrophages and Confers Chemoresistance in Colorectal Cancer
Hypoxia induces HIF2α-mediated overexpression of dihydropyrimidine dehydrogenase in TAMs, leading to chemoresistance to 5-FU in colon cancers.
Myeloid-Derived Suppressive Cell Expansion Promotes Melanoma Growth and Autoimmunity by Inhibiting CD40/IL27 Regulation in Macrophages
Translational Science
Hyperpolarized Carbon-13 MRI for Early Response Assessment of Neoadjuvant Chemotherapy in Breast Cancer Patients
Hyperpolarized carbon-13 MRI allows response assessment in patients with breast cancer after 7–11 days of neoadjuvant chemotherapy and outperformed state-of-the-art and research quantitative proton MRI techniques.
Targeting an Inducible SALL4-Mediated Cancer Vulnerability with Sequential Therapy
Inhibition of PIM Kinases in DLBCL Targets MYC Transcriptional Program and Augments the Efficacy of Anti-CD20 Antibodies
Specific Activation of the CD271 Intracellular Domain in Combination with Chemotherapy or Targeted Therapy Inhibits Melanoma Progression
The discovery of a means to specifically activate the CD271 death domain reveals unknown pathways mediated by the receptor and highlights new treatment possibilities for melanoma.
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