Issues
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Cover Image
Cover Image
Mutant KRAS drives pancreatic ductal adenocarcinoma (PDAC) initiation and progression. The receptor tyrosine kinase FGFR2 supports mutant KRAS signaling in the early phases of pancreatic tumorigenesis and the inactivation of FGFR2 intercepts disease development. The cover image depicts a murine precancerous lesion expressing FGFR2 (green), acquiring invasive features (p53 accumulation in orange and increased CDKN2A/ARF transcriptional expression in cyan), and progressing to PDAC. For details, see article by Tonelli and colleagues on page 1960. - PDF Icon PDF LinkTable of Contents
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Cancer Research
Table of Contents
In the Spotlight
Cancer Biology
FGFR2 Abrogation Intercepts Pancreatic Ductal Adenocarcinoma Development
FGFR2 inhibition reduces mutant KRAS signaling, which can impair mutant KRAS-expressing pancreatic cancer precursor lesions that are prevalent in the average healthy adult and delay pancreatic ductal adenocarcinoma progression.
The Prolonged Half-Life of the p53 Missense Variant R248Q Promotes Accumulation and Heterotetramer Formation with Wild-Type p53 to Exert the Dominant-Negative Effect
Heterotetramerization between R248Q mutant and wild-type p53 in conjunction with supraphysiologic p53R248Q accumulation underlies the dominant-negative effect, highlighting the need to develop pharmacologic strategies to decrease the elevated R248Q:WT ratio.
Cancer Immunology
Mutation of SMARCA4 Induces Cancer Cell–Intrinsic Defects in the Enhancer Landscape and Resistance to Immunotherapy
Epigenetic reprogramming in SMARCA4-mutant cancer cells alters immune infiltration and limits immunotherapy efficacy by downregulating immunostimulatory gene expression, which could potentially be targeted to overcome immunotherapy resistance in SMARCA4-deficient tumors.
Blocking the TCA Cycle in Cancer Cells Potentiates CD36+ T-cell–Mediated Antitumor Immunity by Suppressing ER Stress–Associated THBS2 Signaling
The immunomodulatory role of the TCA cycle in cancer cells provides a therapeutic opportunity to enhance antitumor immunity by targeting tumor cell metabolism.
Cancer Metabolism and Molecular Mechanisms
SMYD3 Activates Fatty Acid β-Oxidation to Promote Self-Renewal of Leukemia Stem Cells
The epigenetic modulator SMYD3 promotes leukemogenesis and self-renewal of leukemia stem cells by upregulating FABP5 to stimulate fatty acid β-oxidation, which can be targeted to treat chronic myeloid leukemia.
CRTC2 Forms Co-Condensates with YTHDF2 That Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance
CRTC2 hijacks the YTHDF2–m6A pathway to increase translation of c-Jun and promote hepatocellular carcinoma development and lenvatinib resistance, indicating that CRTC2 is a promising biomarker and therapeutic target.
Therapeutic Development and Chemical Biology
An Anti-EGFR Antibody–Drug Radioconjugate Labeled with Actinium-225 Elicits Durable Antitumor Responses in KRAS- and BRAF-Mutant Colorectal Cancer
Radiolabeling with [225Ac]Ac improves the efficacy of an anti-EGFR antibody-drug conjugate in KRAS- and BRAFV600E-mutant colorectal cancer, providing hope for patients with these mutations who do not qualify for EGFR-targeted therapies.
Translational Cancer Biology
Perivascular Niche–Resident Alveolar Macrophages Promote Interstitial Pneumonitis Related to Trastuzumab Deruxtecan Treatment
Preconditioning the perivascular niche can prevent lung inflammation induced by antibody-drug conjugate phagocytosis by alveolar macrophages and subsequent SPP1high macrophage differentiation, providing a clinically viable strategy for mitigating interstitial lung disease.
Targeting the SP/KLF Transcriptional Regulatory Network Synergizes with HDAC Inhibition to Impede Progression of H3K27M Diffuse Intrinsic Pontine Glioma
The SP/KLF transcriptional regulatory network is activated in H3K27M-mutated diffuse intrinsic pontine glioma and represents a promising therapeutic target in combination with HDAC inhibitors for combating these lethal pediatric brain tumors.
Combining Apatinib and Oxaliplatin Remodels the Immunosuppressive Tumor Microenvironment and Sensitizes Desert-Type Gastric Cancer to Immunotherapy
Apatinib combined with oxaliplatin reprograms the tumor immune microenvironment in desert-type gastric cancer, enhancing the efficacy of immune checkpoint blockade and paving the way for optimized combination immunotherapeutic strategies.
Editor’s Notes
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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