Globally, there is an increasing prevalence of vitamin D deficiency, including in Southeast Asia, which ranges from 6% to 70%. Vitamin D plays an important role in calcium metabolism and bone health. Melanin is one factor that contributes to vitamin D deficiency. It has photoprotective properties that inhibit vitamin D synthesis, but the mechanism has not been fully understood. To determine the mechanism of the association between melanin and vitamin D, this systematic review was conducted on 11 articles, including cross-sectional studies, cohort studies, and randomised controlled trials published from 2010 to 2020. The search included Pubmed, EBSCO, and Proquest databases, and data were synthesised from 11 studies. This critical review found nine of the 11 studies reported a significant association between melanin and vitamin D, while two reported non-significant results. Of the nine significant studies, eight reported that people with higher melanin have lower vitamin D levels, while one study suggested that melanin levels do not necessarily associate with lower vitamin D levels. In conclusion, the review establishes a significant association between melanin and vitamin D.

The incidence of obesity, type II diabetes mellitus, and metabolic syndrome in children and adults show an alarming increase worldwide. This increase was supported by one factor: the increasing availability of high-calorie foods and beverages, thus increasing the need for sweeteners. Researchers are driven to find a sweetener that can replace sugar. One of the natural sweeteners that can be used is the Stevia plant. Stevia contains stevioside, which is a natural sweetener with 300 times sweetness compared to sucrose. Besides, stevioside can reduce blood sugar levels and show benefits for people with diabetes.

Overall, triple negative breast cancers (TNBCs) constitute 12% of all breast cancers, and is approximately twice more prevalent in African-American populations. Louisiana has a high proportion of African-American residents (32.5% in 2015), and thus hosts a higher population of TNBC patients. TNBCs have an aggressive phenotype that is elusive to the targeted therapeutics used to treat other breast cancer subtypes. Certain kinase families have been extensively studied as regulators of epithelial-mesenchymal transition (EMT), a process involved in the initiation of cancer metastasis. Discovery of novel kinase targets within the subset of uncharacterized kinases could provide important insight into future targeted therapies. However, current models utilized in target discovery research are limited by the inability to accurately recapitulate the complex stromal architecture and heterogenous genetic and molecular composition of breast cancer. Furthermore, immortalized cell lines are limited to a 2D environment and over time acquire mutations that may not reflect the primary tumor. Recently, our laboratory has successfully established two TNBC patient-derived xenograft (PDX) models derived from African-American patients, and generated cell lines (TU-BCx-2K1, TU-BCx-2O0) and mammospheres. One of these models, 2O0, presents tumor architecture, cellular composition, genomic (qRT-PCR) and protein (western blot) expressions that are concordant with a claudin-low subtype, which has higher rates of metastasis and recurrence. Furthermore, we show that both TNBC models metastasize to the lungs, and exhibit molecular characteristics consistent with mesenchymal phenotypes. We utilized these translational PDX models to screen a library of small molecule inhibitors that represent a variety of kinase pathways to identify novel therapeutic targets and/or pathways that are specific to TNBC subtypes. We found in a preliminary cell morphology screen using three TNBC cell lines (MDA-MB-231, BT549, MDA-MB-157), two small molecule inhibitors that increased epithelial marker (CDH1) gene expression, suppressed mesenchymal (VIM, c-FOS, SNAI1, ZEB1) expression and/or suppressed cellular motility in transwell migration assays. We observed after ex vivo treatments with our PDX tumors the two compounds increase the epithelial marker CDH1 expression, and suppress mesenchymal markers (VIM, MMP2, c-FOS, SNAI1, ZEB1) expressions. We confirm these findings in the TU-BCx-2K1 cell line. Kinase array data revealed candidate kinases responsible for the observed EMT changes in the two compounds of interest (NEK5, NEK9, NEK1 potentially affect cell motility; SRC-family kinases, TAOK2, STK10 potentially affect EMT gene changes); we plan to utilize the PDX cell lines to characterize these kinases in EMT. We aim to ultimately discover novel therapeutic targets specific to different TNBC molecular subtypes. Citation Format: Matossian M, Burks H, Bowles A, Sabol R, Hoang V, Elliott S, Bunnell B, Zuercher W, Drewry D, Wells C, Alfortish A, Lee S, Hartono A, Jones S, Moroz K, Zea A, Burow M, Collins-Burow B. Patient-derived triple negative breast cancer xenografts as a translational model to screen for novel kinase pathways [abstract]. In: Proceedings of the 2017 San Antonio Breast Cancer Symposium; 2017 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2018;78(4 Suppl):Abstract nr P5-05-05.

Colorectal cancer (CRC) is still a health problem with a high incidence worldwide. Genetic factors and environmental factors are the etiology of colorectal cancer. Eating habits are one of the environmental factors that can be regulated so as to prevent colorectal cancer. Diet food in the development of colorectal cancer has an important role. Several studies in the last decade have shown an association between the consumption of several foods and nutrients and the risk of colorectal cancer in epidemiological and experimental studies.