Meet Our Student

Jessica Monique Silva

Jessica is a Mexican American Texan born and raised in San Antonio (Go Spurs Go). Jessica Silva was the first in her family to graduate from college and continue her graduate studies in Biochemistry and Molecular Biology. Jessica graduated from St. Mary's University in 2005 and worked her way through college in a medical oncology research lab studying breast cancer at the University of Texas Health Science Center in San Antonio. While she was conducting research her mom was diagnosed with cervical cancer and this motivated Jessica to continue her studies in cancer research and do all she can to continue the fight for a cure. During the summer of 2004, Jessica participated in the Summer Undergraduate Research Fellowship (SURF) and is currently in the Cancer Biology subtrack in Mayo Clinic Graduate School. Jessica is currently the Cancer Biology Representative for the Graduate Student Association, participates in the Mayo Clinic Initiative for Maximizing Student Diversity (IMSD) and is also the student representative for the "Mayo Clinic Education and Diversity Blog, Three Shields, Many Perspectives" committee.

Jessica is now conducting technologically advanced research in Dr. David I. Smith's lab studying non-coding transcripts which are stress responsive. It is now known that the human genome contains approximately 22,000 genes; however the protein coding portion of the genome only corresponds to less than 2% of the entire genome. Utilizing advanced technologies such as whole-genome tiling arrays have allowed her to identify a new novel class of long non-coding transcripts (NCTs) associated with stress induction by the carcinogen found in cigarette smoke NNK. The characterization of this new class of transcripts has revealed that they are located within introns of important regulatory genes that normally function in cell stress, signaling, growth, development, and migration. The majority of the NuTs are also located in genes which are associated in the development of including the human gene MET, the ephrin receptor EphA2, Kruppel-like factor 5 (KLRF5), junction plakoglobin (JUP), claudin 1 (CLDN1), and epithelial protein 1 (EMP1). These NCTs are longer than 400 bp, are abundantly expressed, and induced under stress, we refer to these as long, NNK upregulated non-coding transcripts (NuTs). The association between stress and cancer development has led us to focus on the transcripts that are induced by NNK. Our central hypothesis is that the long NuTs play an important regulatory role in controlling gene expression and are potential targets associated with the process of carcinogenesis. We have begun to characterize these NuTs and have analyzed their expression levels in both normal and cancer derived cell lines. Several NuTs have altered levels of expression in the cancer-derived cell lines precisely. We are currently testing whether these NuTs control gene expression by both over-expressing and abrogating their expression. Preliminary results suggest that decreased expression of these NuTs does affect cellular growth. We are currently attempting to determine which coding genes and molecular pathways are affected by changes in the expression of these NuTs. Our work suggests that the NuTs are an important new group of regulatory transcripts which could play a very important role both in the normal cell and during carcinogenesis.