Dorothea Becker

Professor of Pathology at the University of Pittsburgh School of Medicine

Dorothea Becker, PhD, is a molecular biologist whose primary scientific interest is the identification and analysis of genes that govern the progression of melanoma, which is the most aggressive and deadliest type of skin cancer.

Dr. Becker received her training at the University of Tübingen and the FU Berlin and after completing her PhD, she moved to the United States where she pursued her postdoctoral studies at the Rockefeller University and Harvard Medical School. Rising through the academic ranks, Dr. Becker was appointed Full Professor at the University of Pittsburgh where she remained until June 2014, when she returned to Germany and her hometown, Göttingen.

In 1989, Dr. Becker published a groundbreaking study, which provided the first and strong evidence that autocrine FGF signaling drives human tumorigenesis. Specifically, her pioneering study showed that advanced but not early-stage melanomas produce high levels of bFGF and that bFGF, but no other growth factor, is essential for the cells' proliferation. In subsequent studies, Dr. Becker and members of her laboratory demonstrated that the autocrine bFGF-FGFR1 loop is required for the development and progression of melanoma, and that melanomas regress irreversibly following inhibition of this pertinent growth factor/receptor signaling loop.

Dr. Becker was also one of the first investigators to show that Ubc9, the single SUMO E2 ubiquitin-conjugating enzyme/ligase, plays a crucial role in cancer. Specifically, her studies demonstrated that Ubc9 is activated and expressed at high levels in advanced melanomas, and that inhibiting expression of Ubc9 sensitizes melanoma cells to chemotherapeutic agents to which this disease is otherwise completely refractory. In further pursuit of her long-standing scientific objective to identify key regulators driving melanoma progression and governing the advanced stages of melanoma, Dr. Becker and members of her laboratory found that the pertinent DNA helicase, DDX11, is upregulated to high levels in advanced melanomas, and that blocking expression of DDX11 leads to rapid and massive melanoma cell death due to severe defects in sister chromatid cohesion and telomere shortening.

Another important research project that recently has become a major focus of Dr. Becker's scientific endeavors, seeks to determine the molecular connection(s) between melanoma and the neurodegenerative diseases Alzheimer's and Parkinson. As part of a collaborative study, Dr. Becker and Drs. Thomas Jovin and Donna Arndt-Jovin at the Max-Planck-Institut für Biophysikalische Chemie found that the beta-amyloid precursor protein (APP) is activated with progression from early to advanced melanoma, and that inhibiting the high-level expression of APP drives advanced melanomas into terminal differentiation. Given recent reports in the scientific literature, which document that patients with Parkinson's disease have a significantly elevated risk and rate of melanoma but no other type of cancer, Drs. Becker, Jovin, and Arndt-Jovin recently initiated a project that will test the hypothesis that the genes alpha-synuclein, PARK2, PINK1, LRRK2, and DJ-1, which are key players in Parkinson's disease, are activated and up-regulated to high levels with progression to advanced melanoma, and that they shield melanoma cells from external damage that would drive them into irreversible differentiation and render them susceptible to apoptosis or necroptosis.


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