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Results from the Reproducibility Project: Cancer Biology provide a picture of the rate of false positives in cancer preclinical research, but it is still not clear if research in this field is less reproducible than it should be.

A project to repeat experiments from high-impact papers in cancer biology did not complete all replications, with challenges ranging from mundane reasons to unexpected methodological issues.

A project to repeat experiments from high-impact papers in cancer biology encountered a series of challenges, many of which were caused by a lack of detail in the original papers.

Using IGF2BP1-PLK1 axis as an example, targeting oncogenic signaling represents a direction treatment for HCC patients with high FBXO45 expression.

Hexosamine salvage through the enzyme N-acetylglucosamine kinase is stimulated in nutrient-limited conditions and supports pancreatic tumor growth.

Oncogenic BRAF causes genome duplication and reversible growth arrest in human melanocytes that is conditional on microRNA expression and differentiation state.

Specific localization of KRAS downstream target ARL4C with its novel interacting proteins was the active site of invasion of pancreatic cancer cell and induced metastasis.

Tumor-infiltrating regulatory T cells are regulated by the immunoreceptor CD300a, which suppresses signals from tumor-derived extracellular vesicles.

Biochemical analysis shows that muscle-invasive-bladder-cancer cells are deficient in DNA repair and hypermutable, non-muscle-invasive-bladder-cancer cells are proficient in DNA repair, DNA repair capacity is regulated by tumor suppressor TAp63g, and cell invasions are regulated by TAp63g and p53.

Deletion and small-molecule inhibition of ubiquitin-specific protease 28 destabilizes the oncogenes c-MYC, c-JUN, and Δp63, and elicits regression of squamous cell lung carcinoma, a major cancer type with currently limited treatment options.