Steve A. Alas

Steve A. Alas

Director of SEES, LSAMP, SPIRES & Discovery Camp Programs, Professor of Biological Sciences, College of Science


Research Lab


Cellular Inflammation and Prosthetics

As the need for better prosthetic replacements increases so must our understanding of possible replacement materials. Currently materials such as stainless steel, titanium and other metal alloys are implanted into patients as prosthetic devices. There have been serious clinical issues surrounding prosthetic implants, such as prosthetic loosening. Loosening is caused by the generation of debris particles at the site of implantation, released from the surface of the prosthetic. A typical joint replacement will produce millions of particles and will elicit a unique immune response from various cell types, including macrophages, adult stromal stem cells and fibroblasts.

Macrophages engulf the particles in an attempt to destroy them, and secrete pro-inflammatory cytokines. Adult stromal stem cells comprise the bone marrow microenvironment, to which metal prosthetics are directly exposed and secrete pro-inflammatory cytokines. Fibroblasts lay down extracellular matrix and build connective tissue on implants. Their cytokines also heighten local inflammation. The inflammatory reaction results in the activation of osteoclasts, which erode bone around the implant, causing loosening and necessitating prosthetic replacement. As the inflammatory response heightens so does the amount of bone resorbtion.

The goal of this research is to examine the immune response against novel metal alloys by examining cytokine secretion of human macrophages, bone marrow stromal cells and fibroblasts in the presence of the biometals and testing the activation of human osteoclasts and bone resorbtion in response to the various alloys.

 Human prostheticInflammation


DNA Damage and Tumorigenesis

My laboratory studies the DNA damage response and DNA repair mechanisms in various human tumor cell models. A major focus of this work is the signaling of programmed cell death and cell cycle control by DNA damage. Related to this is another major area we examine which is how tumor cells become resistant to chemotherapeutic drugs.

Genetic mutations within cells can cause them to lose control over their growth, function and response to physiological signals. These cells may progressively become increasingly unstable and develop into malignant cells. As these cancerous cells continue to divide and form a mass comprised of tumor cells, they continue to accumulate additional mutations and genetic alterations throughout their DNA. Through the process of natural selection, within the tumor cell population, these genetic mutations can lead to chemotherapy-resistant cells and a tumor cell population characteristic of aggressive growth.


These genetic alterations occur when DNA surveillance and repair mechanisms fail. Our work focuses on the mismatch repair pathway, DNA damage response pathway and the cell cycle checkpoint response. The genes involved in these cellular pathways regulate DNA repair, cellular growth, intracellular signaling, and programmed cell death. The most prominent consequence of humans having defective or inefficient mismatch repair systems is the onset of colon cancer, the second leading cause of cancer deaths among Americans. Morever, people who develop hereditary non-polyposis colorectal carcinoma (HNPCC) are also more susceptible to develop additional cancers, such as cancer of the ovary, stomach, urinary tract, pancreas, small bowel, skin and brain.

DNAColon cancer