How to Diagnose the cancer, a story of wart man

Precision Cancer Diagnostics and Treatments: The Lukas Wart man Story

Specialists had long acknowledged that there is no cure and that individuals who have the same ailment can react differently to each other. Precise oncology care improves the accuracy of cancers and other illness diagnostics. It evaluates the distinct genetic makeup of tumors so that the safest and most efficient therapies for each individual. Personalized therapy for cancers entails studying DNA from tumors of individuals to identify the mutation or other gene mutations responsible for their cancer. Then, doctors might be able to decide on a treatment for cancer for a particular patient that best matches or addresses the problem changes in the tumor Genome. During his final year of medical school in 2002, Lukas Wart man began to experience symptoms of fatigue, fever, and bone pain. After months of tests, he was diagnosed with adult acute lymphoblastic leukemia (ALL). After two years of chemo therapies, his cancer was in remission for three years. When the ALL recurred, his doctors treated him with intensive chemotherapy and a bone marrow transplant, which put him back into remission for another three years. After his second relapse, all attempts at treatment failed, and he rapidly deteriorated. At the time of his second relapse, Wart man was working as a physician-scientist at Washington University, researching the genetics of leukemia. His colleagues, including Timothy Led, associate director of the Washington University Genome Institute, decided to rush into a last-minute effort to save him. Using the university's sequencing facilities and supercomputers, the research team sequenced the entire genome of his normal and his cancer cells. They also analyzed his RNA types and expression levels using RNA seq technologies. As they had expected, Wart man's cancer cells contained many gene mutations. Unfortunately, no known drugs would attack the products of these mutated genes. The RNA sequence analysis, however, revealed unexpected results. It showed that the FMS-related tyrosine kinase 3 (FLT3) gene, although having a normal DNA sequence, was over expressed in his cancer cells—perhaps due to mutations in the gene's regulatory regions. The FLT3 gene encodes a protein kinase involved in normal hematopoietic cell growth and differentiation, and its over expression would potentially contribute to Wart man's cancer. Equally informative and fortunate was that the suiting was known to inhibit the FLT3 kinase and had been approved for use in treating some kidney and gastrointestinal cancers. Wartman decided to try suiting. Unfortunately, the drug cost $330 per day, and Wart man's insurance company refused to pay for it. In addition, the drug company Pfizer refused to supply the drug to him under its compassionate use program. Despite these setbacks, he collected enough money to buy a week's worth of sunitinib. Within days of starting treatment, his blood counts were approaching normal. Within two weeks, his bone marrow was free of cancer cells. Now, Pfizer reversed its decision and supplied Wartman with the drug. In addition, he underwent a second bone marrow transplant to help ensure that the cancer would not return. Although Wart man's long-term prognosis is still uncertain, his successful experience with experience cancer treatment has given him hope. It has spurred research into regulating the FLT3 gene in other cancers.