Issues
-
Cover Image
Cover Image
Matrix stiffness promotes the proliferation and metastasis of tumors, while hindering the infiltration of immune cells. In colorectal cancer with obstruction, the content of collagen fibers and proteoglycans in the extracellular matrix is significantly increased and cross-linked compared to those without obstruction, indicating a further progression of matrix fibrosis during obstruction development. Given the higher incidence of obstruction in hyperlipidemic populations, palmitic acid accumulates in the tumor, stimulating tumor cells and activating the matrix type of cancer-associated fibroblasts (mCAF), which leads to the progression of matrix stiffness. The cover image highlights the stimulation of matrix stiffness by fatty acid accumulation. In the presence of fatty acid droplets, matrix fibers become thicker and more interwoven, contracting cells and tightening the tumor. This progression of matrix stiffness underlies the clinical development of obstruction. For details, see article by Deng and colleagues on page 1784. - PDF Icon PDF LinkTable of Contents
- PDF Icon PDF LinkEditorial Board
Cancer Research
Table of Contents
In the Spotlight
Review
Resource Report
The Lung Cancer Autochthonous Model Gene Expression Database Enables Cross-Study Comparisons of the Transcriptomic Landscapes Across Mouse Models
The Lung Cancer Autochthonous Model Gene Expression Database (LCAMGDB) provides a comprehensive and accessible resource for the research community to investigate lung cancer biology in mouse models.
Cancer Biology
Palmitic Acid Accumulation Activates Fibroblasts and Promotes Matrix Stiffness in Colorectal Cancer
Palmitic acid accumulation activates the NF-κB pathway in colorectal cancer cells to promote cytokine secretion that facilitates the generation of matrix cancer-associated fibroblasts, driving extracellular matrix remodeling and development of obstructions.
SMARCA4 Inhibits Breast Cancer Progression and Metastasis through RHOA Suppression
CRISPR-knockout screen in 3D tumor spheroid revealed that SMARCA4, a SWI/SNF ATPase subunit, suppresses triple-negative breast cancer growth and metastasis by increasing ARHGAP29 transcription and inhibiting the RHOA signaling pathway.
Intratumoral Fusobacterium nucleatum Recruits Tumor-Associated Neutrophils to Promote Gastric Cancer Progression and Immune Evasion
Intratumoral F. nucleatum activates NF-κB signaling to facilitate gastric cancer immune evasion by promoting tumor-associated neutrophil recruitment that sensitizes tumors to immune checkpoint blockade therapy.
Cancer Immunology
Macrophage-Derived Itaconate Suppresses Dendritic Cell Function to Promote Acquired Resistance to Anti–PD-1 Immunotherapy
Elevated itaconate production by macrophages induced by IFNγ is a critical negative feedback immunoregulatory metabolic response to anti-PD-1 immunotherapy that inhibits the cross-priming function of dendritic cells and confers immunotherapy resistance.
Cancer Metabolism and Molecular Mechanisms
De Novo Serine Synthesis Is a Metabolic Vulnerability That Can Be Exploited to Overcome Sunitinib Resistance in Advanced Renal Cell Carcinoma
Sunitinib treatment induces metabolic reprogramming to provide essential metabolite building blocks for tumor survival, resistance, and progression by upregulating serine biosynthesis, which represents a targetable dependency to enhance therapeutic efficacy.
Therapeutic Development and Chemical Biology
Engineered SH3-Derived Sherpabodies Function as a Modular Platform for Targeted T-cell Immunotherapy
Sherpabodies represent a biological targeting technology that could help extend the success of CAR T-cell therapy from treating leukemias and lymphomas to the treatment of solid cancers.
Translational Cancer Biology
Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
PARP inhibitor sensitivity is associated with cGAS–STING–IFN signaling, which can be harnessed by combining PARP inhibitors with STING agonists to overcome acquired resistance and requires NK cells to mediate antitumor immunity.
FADD Functions as an Oncogene in Chr11q13.3-Amplified Head and Neck Squamous Cell Carcinoma
FADD promotes progression of tumors with chr11q13.3 amplification by binding to the DNA helicase complex, which can be targeted in combination with cyclin D1 as a viable therapeutic strategy for HNSCC patients.
Cancer Landscapes
Colorectal Tumors in Diverse Patient Populations Feature a Spectrum of Somatic Mutational Profiles
Analysis of tumors from various populations can broadly characterize genomic landscapes and enhance precision medicine strategies.
Editor’s Note
Retractions
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)
Advertisement
Email alerts
NOTICE: This notice serves to inform the reader that, in 2023, AACR received a donation by Pfizer of the rights to royalties from the sale—within the United States—of Bavencio® (avelumab), a pharmaceutical owned by Merck. None of these funds are being, or will be, used to directly support any specific publication or author. If an individual article is published that deals with this particular drug, such article will include standard financial disclosures per AACR journal policy. For more detail regarding AACR’s established policies for authors, please go to https://aacrjournals.org/pages/editorial-policies#coi.
RSS Feeds