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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

In the Spotlight

Cancer Biology

CRISPR screening reveals topoisomerase 1 as an immediately actionable vulnerability in cancers harboring MYC as a driver oncoprotein that can be targeted with clinically approved inhibitors.

Cancer Immunology

Metabolic reprogramming of bladder cancer cells driven by mutant FGFR3 increases serine synthesis that suppresses macrophage immunostimulatory functions to generate an immunosuppressive TME, which can be overcome by targeting PI3K.

LILRB3 regulates differentiation and proliferation in acute myeloid leukemia and can be targeted with monoclonal antibodies and CAR T cells to suppress leukemia growth.

Cancer Metabolism and Molecular Mechanisms

Fructose activates AMPK–mTORC1 signaling to inhibit autophagy-mediated cell death in pancreatic cancer cells caused by glucose deficiency, facilitating metabolic adaptation to the tumor microenvironment and supporting tumor growth.

LINC01089 is a super enhancer–driven long noncoding RNA that induces ERK signaling and epithelial–mesenchymal transition by regulating DIAPH3 alternative splicing that blocks N6-methyladenosine–mediated mRNA stabilization, establishing an epigenetic network that promotes hepatocellular carcinoma metastasis.

Translational Cancer Biology

Identification of synthetic lethal genes with KRASG12Ci using genome-wide CRISPR/Cas9 screening and credentialing of the ability of TEAD inhibition to enhance KRASG12Ci efficacy provides a roadmap for combination strategies.

YAP1/TAZ-TEAD activation compensates for loss of KRAS effector signaling, establishing a mechanistic basis for concurrent inhibition of TEAD to enhance the efficacy of KRASG12C-selective inhibitor treatment of KRASG12C-mutant cancers.

Identification of resistance mechanisms to KRASG12C/SHP2 coinhibition highlights the need for additional combination therapies for lung cancer beyond on-pathway combinations and offers the basis for development of more effective combination approaches.

The poorly characterized protein kinase citron kinase is a therapeutic target in prostate cancer that drives tumor growth by regulating diverse substrates, which control several hallmarks of aggressive prostate cancer progression.

The molecular-guided therapeutic strategy of combining cabozantinib and sapanisertib restrains ERK activity to effectively suppress growth of renal cell carcinomas, including those unresponsive to immune checkpoint inhibitors.


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