Welcome to the Feldser Laboratory

Our laboratory is part of the Department of Cancer Biology in the Perelman School of Medicine at the University of Pennsylvania. We are active members of the Penn Abramson Cancer Center, Penn Epigenetics Institute, and Penn Center for Pulmonary Biology. Our work is dedicated to deconstructing the multistep process of tumorigenesis with the ultimate goal of developing potent strategies to eliminate cancer.
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Histological view of a primary lung adenocarcinoma in the mouse. Advanced histological features include 1) multinucleate giant cells, 2) hyper chromatic nuclei, 3) prominent nucleoli, and 4) aberrant mitoses. The indicated mitotic figure in this image is being pulled in four directions and shows lagging chromosomes. This is a typical example of a moderately high grade tumor in our KrasG12D; p53LSL/LSL model.
RbTR alleles inactivate Rb gene function and report Rb gene expression. Fluorescence imaging reveals GFP expression levels reflect RbTR allele dosage.
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Adenocarcinomas have high MAPK activity and express nucleolar ARF. Immuno-fluorescence detection of activated pERK (red) and ARF (green).
Feldser et al. 2010.
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Longitudinal bioluminescent imaging of a single mouse over time. Tumor cell abundance can be measured in vivo via luciferase based imaging platforms. We are utilizing this technology to study tumor regression due to defined genetic manipulations.
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Amplification of MAPK signaling drives tumor progression, but also induces tumor formation in CC10+ cells that are recalcitrant to KrasG12D-mediated transformation. Subsequent to initiation, CC10+ cells transdifferentiate toward an alveolar type II (SPC+) phenotype. Immunostaining of lung sections from KrasLSL-G12D/+;p53flox/flox; Rosa26LSL-YFP/+ mice infected with CC10-restricted Adeno-Cre. Braf inhibition (PLX4720) expands SPC+ adenomas (upper left of image) and induces transformation of CC10+ proximal airway cells (middle and inset). DAPI (white), YFP (yellow), CC10, (cyan), and SPC (red). Cicchini et al. 2017
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Shown above is a tumor lacking H3K36me3 due to Setd2 mutation in the area on the left but retaining H3K36me3 in a smaller tumor fraction on the right. Note differences in cell morphology: H3K36me3 positive tumor cells are uniform, with minimal nuclear and cellular pleomorphism, whereas H3K36me3 negative tumor cells display nuclear and cellular pleomorphism with increased nuclear to cytoplasmic ratio. Walter et al. 2017
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