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Diffuse midline glioma, including diffuse intrinsic pontine glioma (DIPG), are uniformly fatal high-grade glioma of the midline of the brain, recognized as the leading cause of cancer-related death in children. Other than palliative radiotherapy, it has remained untreatable for more than half a century. To steal the secrets of this insidious cancer, Jackson and colleagues have employed a systems biological approach and identified a combination treatment strategy that targets the unique and emerging biology of DIPG. For details, see article by Jackson and colleagues on page 2421. - PDF Icon PDF LinkTable of Contents
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Cancer Research
Table of Contents
Controversy and Consensus
Review
Immune Checkpoint Inhibitors and the Exposome: Host-Extrinsic Factors Determine Response, Survival, and Toxicity
Cancer Biology
Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants
The p53 DNA binding domain contact mutant p53R245W, but not the structural mutant p53R172H, interacts with KLF15 to drive metastasis in somatic osteosarcoma, providing a potential vulnerability in tumors expressing p53R245W mutation.
Wnt Signaling Stimulates Cooperation between GREB1 and HNF4α to Promote Proliferation in Hepatocellular Carcinoma
GREB1 is a liver cancer–specific Wnt signaling target gene that induces an oncogenic shift of HNF4α, a putative tumor suppressor, and may represent a therapeutic target in Wnt-activated hepatocellular carcinoma.
Cancer Immunology
Ccr2+ Monocyte-Derived Macrophages Influence Trajectories of Acquired Therapy Resistance in Braf-Mutant Melanoma
Ccr2+ melanoma macrophages that are active in tumors during the drug-tolerant persister state following targeted therapy-induced regression are key contributors directing melanoma cell reprogramming toward specific therapeutic resistance trajectories.
The HDAC2-SP1 Axis Orchestrates Protumor Macrophage Polarization
HDAC2 inhibition reverses the protumor phenotype of macrophages mediated by epigenetic modulation induced by the HDAC2–SP1 axis, indicating a therapeutic option to modify the immunosuppressive tumor microenvironment.
Metformin Reprograms Tryptophan Metabolism to Stimulate CD8+ T-cell Function in Colorectal Cancer
Analysis of the impact of metformin on the colorectal cancer immunometabolic landscape at a single-cell resolution shows that metformin alters cancer cell tryptophan metabolism to stimulate CD8+ T-cell antitumor activity.
Cancer Metabolism and Molecular Mechanisms
PTTG1 Reprograms Asparagine Metabolism to Promote Hepatocellular Carcinoma Progression
PTTG1 is upregulated in hepatocellular carcinoma and increases asparagine production to stimulate mTOR activity and promote tumor progression.
Retinol Saturase Mediates Retinoid Metabolism to Impair a Ferroptosis Defense System in Cancer Cells
Retinoids have ferroptosis-protective properties and can be metabolized by RETSAT to promote ferroptosis, suggesting the possibility of targeting retinoid metabolism in cancer as a treatment strategy to trigger ferroptosis.
Therapeutic Development and Chemical Biology
Targeting CD44 Variant 5 with an Antibody–Drug Conjugate Is an Effective Therapeutic Strategy for Intrahepatic Cholangiocarcinoma
Elevated expression of CD44 variant 5 in intrahepatic cholangiocarcinoma confers a targetable vulnerability using the newly developed antibody–drug conjugate H1D8–DC, which induces potent growth suppressive effects without significant toxicity.
Translational Cancer Biology
ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
PI3K/Akt signaling promotes metabolic adaptation to ONC201-mediated disruption of mitochondrial energy homeostasis in diffuse intrinsic pontine glioma, highlighting the utility of a combination treatment strategy using ONC201 and the PI3K/Akt inhibitor paxalisib.
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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