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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 Hallmarks Review

Resource Report

Comprehensive characterization of tumor-associated nonimmune stromal cells provides a robust resource for dissecting tumor microenvironment complexity and guiding stroma-targeted therapy development across multiple human cancer types.

Cancer Biology

Ring sideroblast isolation combined with state-of-the-art multiomics identifies survival mechanisms underlying SF3B1-mutant erythropoiesis and establishes an active role for erythroid differentiation and ring sideroblasts themselves in SF3B1-mutant myelodysplastic syndrome pathogenesis.

Small cell lung cancer cells overcome deficiency of the prometastatic oncogene NFIB to gain metastatic potential through various molecular mechanisms, which may represent targets to block progression of this fatal cancer type.

CRISPR/Cas9 screening in Ewing sarcoma identifies a dependency on CHD4, which is crucial for maintenance of chromatin architecture to suppress DNA damage and a promising therapeutic target for DNA damage repair-deficient malignancies.

Cancer Immunology

Spatial analysis identifies IFN-induced MHC-IhiGal9+ CAFs that form a trap for CD8+ T cells, providing insights into the complex networks in the tumor microenvironment that regulate T-cell infiltration and function.

The stress-responsive transcription factor HSF1 reduces CD8+ T-cell infiltration in breast tumors to prevent immune-mediated killing, indicating that cellular stress responses affect tumor-immune interactions and that targeting HSF1 could improve immunotherapies.

Cancer Metabolism and Molecular Mechanisms

Increased fatty acid oxidation induced by endocrine therapy activates Src signaling to promote endocrine resistance in breast cancer, which can be overcome using clinically approved therapies targeting FAO and Src.

Epigenetic adaptation allows cancer cells to overcome the tumor-suppressive effects of glucose restriction by inducing de-differentiation and an aggressive phenotype, which could help design better metabolic treatments.

Upregulation of bone-remodeling factors S100A4 and LGALS3 mediated by a circMMP2(6,7)/β-catenin/PRMT5 complex generates a niche that supports breast cancer bone metastasis, identifying PRMT5 as a promising target for treating metastasis.

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