Mucins are multi-domain high-molecular-weight glycoproteins encoded by large multi-exon genes that are aberrantly overexpressed in inflammation and cancer. Alternative splicing, high mutational rates, and polymorphisms in mucin genes in cancer and inflammation can potentially generate a large repertoire of functionally diverse, disease-specific mucin gene products that can serve as potential biomarkers and therapeutic targets. This review summarizes the current understanding of the genetic variants of mucins in cancer and inflammation, identifies the gaps in our knowledge and discusses the future course of research to discern their functional role and exploit their diagnostic and therapeutic potential.

Aromatic adducts in DNA from leukocytes were measured by means of the ³²P-post-labeling technique in a case-cohort study including 305 breast cancer cases, Doubling the DNA adduct concentrations resulted in a 61% increase in the risk of breast cancer.

Copper and zinc play important roles in inflammatory and oxidative pathways. We show that higher copper levels and copper/zinc ratio are associated with an increased CRC risk, which is more apparent for the 2 years prior to diagnosis.

This study demonstrates the role of BM-MSCs’ microvesicles on MM cells’ phenotype and translation initiation status (TI). MVs from MM patients’ BM-MSCs elevate MM cells’ TI and consequently their proliferation, migration, invasion, and autophagy whereas normal donors’ BM-MSCs MVs do not.

We have extended characterization of our novel GSTA3 knockout mice toward better understanding human liver cancer. Our results demonstrate extensive oval cell proliferation, numerous pathological changes, tumor formation and increased female susceptibility following aflatoxin and CCl₄ exposure in GSTA3 knockouts.

In this manuscript, we report the role of LTA4H in skin cancer development. LTA4H regulates cell cycle at the G0/G1 phase by negatively regulating p27 ubiquitination, which is associated with decreased phosphorylation of CDK2 and inhibition of the CDK2/cyclin E complex.

Tumor suppressor proteins protect liver from development of cancer. We have found that the tumor suppressor proteins are eliminated in hepatoblastoma by a small subunit of proteasome Gankyrin. This elimination of TSPs causes a failure of stem cells to differentiate into hepatocytes leading to development of hepatoblastoma.

PPARδ directly targeted SLC1-A5 and Glut1 gene transcription resulting in influx of amino acid and glucose, activation of mTOR signaling and tumor progression. This was reversed by silenced PPARδ or antagonist treatment.