Ayman Khatib


Ayman Khatib





My name is Ayman Khatib. I am currently majoring in biomedical sciences at the University of Central Florida pursuing a medical school tract. I was born in the US but raised in Syria for most of my childhood. Living in a third world country abundant with medical malpractice and insufficient resources contrasted with the astounding patient care in the United States, I decided to dedicate my life towards this field. I would like to be able to spread the knowledge that I learn across my career to third world countries such as Syria in hopes that they can grow and contribute to the growing research field. There are the beliefs that countries such as the US government must contribute resources to other countries to allow for their growth and settlement. However, with the education provided in the US, I believe that people themselves should try to spread their knowledge to their native countries. Only then will true growth and development will occur. Individual impact is not to be underestimated. One of the lectures by Jordan Peterson talked about how in our lifetime we will meet a thousand people who will know another a thousand people. Hence, we are able to influence millions of people no matter how minute our actions seem to be. I wish to spread my knowledge and experiences after I have served this country in multitudes to incredible people that lack the opportunities I was blessed with.

Faculty Mentor

Dr.Ratna Chakrabarti

Undergraduate Major

Biomedical Sciences

Future Plans

Medical School and residency in Surgery


Frabin, a RhoGEF, Promotes Pancreatic Cancer Progression

Pancreatic cancer (PCa) is the third leading cause of cancer-related deaths in the United States with a five-year survival rate of only 8%. Activation of Cdc42 in RhoGTPase pathways is shown to be involved in PCa progression and metastasis. Frabin (FGD4) is a Guanine Nucleotide Exchange Factor that activates Cdc42 and has an actin-binding domain which might contribute to tumor metastasis. PCa analysis of clinical samples from The Cancer Genome Atlas database (TCGA) showed FGD4 to be upregulated in pancreatic tumors compared to normal tissues. Survival analysis showed an inverse relationship between patient longevity and FGD4 expression. Here we show that ectopic expression of FGD4 in the less aggressive PANC-1 cell increased cell proliferation and cell cycle progression. Quantitative RT-PCR analysis was used to confirm the overexpression of FGD4 in PANC-1 cells. MTS assays showed a 35% increase in cell proliferation upon overexpression of FGD4. Cell cycle analysis revealed an increased percentage of cells in the S phase in the FGD4 expressing cells compared to control cells. These initial results suggest an oncogenic involvement of FGD4 in PCa. Further studies using overexpression and knockdown approaches will explore the role of FGD4 on cell migration and drug sensitivity in PCa cell lines. We expect that the results of this study will help to determine the function of FGD4 in PCa development and to identify a molecular marker and a therapeutic target for aggressive PCa.

Ayman Khatib