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Issues

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

Review

Cancer Biology

Systematic investigation of the influence of post-transcriptional regulation on cancer cell motility established a connection between P-body–mediated translational control and EMT, which could be therapeutically exploited to attenuate metastasis formation.

Nuclear AXL and WRNIP1 interact and mediate replication stress response, promote therapy resistance, and support metastatic progression, indicating that targeting the AXL/WRNIP1 axis is a potentially viable therapeutic strategy for breast cancer.

DNA-PK is a cytoplasmic DNA sensor that activates ZAK/AKT/mTOR signaling and boosts glycolysis to enhance malignancy and chemoresistance of lung squamous cell carcinoma.

Cancer Metabolism and Molecular Mechanisms

ATGL promotes prostate cancer metabolic plasticity and progression through both lipase-dependent and lipase-independent activity, informing strategies to target ATGL and lipid metabolism for cancer treatment.

Translational Cancer Biology

Acquired resistance to FGFR inhibition can be rapidly promoted by paracrine activation of the NRG1/HER3 axis mediated by adipocyte precursors and can be overcome by the combination of pertuzumab and erdafitinib treatment.

Cancer Landscapes

Standard treatments are related to loss of DNA methylation in IDHmut glioma, resulting in epigenetic activation of genes associated with tumor progression and alterations in the microenvironment that resemble treatment-naïve IDHwt glioma.

Elucidation of the complex interplay between body weight and the molecular landscape of cancer could potentially guide tailored therapies and improve patient management amid the global obesity crisis.

Convergence Science

Chronic stress stimulates cancer stemness by reducing the intestinal abundance of L. johnsonii and its metabolite PCA to enhance β-catenin signaling, forming a basis for potential strategies to circumvent stress-induced cancer aggressiveness.

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