This week's artwork was donated by Sharon, a pediatric cancer patient who received treatment at The Children's Hospital of Philadelphia . Polysomy 13 with concomitant deletion of 13q13-14 involving the retinoblastoma gene and the D13S25 locus in a case of acute myeloid leukemia. Pre-clinical studies with tumor suppressor genes. Polysomy 13 was a result of clonal evolution. In this case, the coexistence of polysomy and a partial deletion within the same chromosome point toward a possible formation of a fusion product with oncogenic potential and its consecutive amplification as a critical alteration in this case.
Lung cancer is the largest cancer killer of men and women in the world.
In addition to the progress made from antismoking primary prevention measures, new tools to help treat patients with lung cancer are emerging from the rapid advances in knowledge of the molecular pathogenesis of lung cancer. These tools include molecular and cellular biology and are starting to provide an insight into how the tumor cells, by altering oncogenes and tumor suppressor genes, achieves growth advantage, uncontrolled proliferation and metastatic behavior via disruption of key cell-cycle regulators and signal transduction cascades. These tools are being translated into clinical strategies to complement surgery, radiotherapy, and chemotherapy and also to assist in primary and secondary prevention efforts. From the current knowledge of the molecular pathogenesis of lung cancer we know that respiratory epithelial cells require many genetic alterations to become invasive and metastatic cancer. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.