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Lindsey Ulkus

Researcher at Harvard University

Publications -  6
Citations -  5970

Lindsey Ulkus is an academic researcher from Harvard University. The author has contributed to research in topics: Circulating tumor cell & Cancer. The author has an hindex of 6, co-authored 6 publications receiving 5590 citations.

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Isolation of rare circulating tumour cells in cancer patients by microchip technology.

TL;DR: The CTC-chip successfully identified CTCs in the peripheral blood of patients with metastatic lung, prostate, pancreatic, breast and colon cancer in 115 of 116 samples, with a range of 5–1,281CTCs per ml and approximately 50% purity.
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Detection of Mutations in EGFR in Circulating Lung-Cancer Cells

TL;DR: Molecular analysis of circulating tumor cells from the blood of patients with lung cancer offers the possibility of monitoring changes in epithelial tumor genotypes during the course of treatment, and shows that a reduction in the number of captured cells was associated with a radiographic tumor response; an increase in theNumber of cells wasassociated with tumor progression, with the emergence of additional EGFR mutations in some cases.
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Isolation and Characterization of Circulating Tumor Cells from Patients with Localized and Metastatic Prostate Cancer

TL;DR: A silicon microfluidic cell-capture technology that, when coupled to an automated imaging system, enables the detection and enumeration of prostate cancer cells fished out from the blood, taking advantage of prostate-specific antigen (PSA), a unique prostate tumor–associated marker.
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The T790M “gatekeeper” mutation in EGFR mediates resistance to low concentrations of an irreversible EGFR inhibitor

TL;DR: It is suggested that HKI-272 treatment at maximally tolerated dosing may lead to the emergence of T790M-mediated resistance, whereas treatment with a more potent irreversible inhibitor could yield a resistance mutation at EGFR C797.
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Oncogenic Activity of Epidermal Growth Factor Receptor Kinase Mutant Alleles Is Enhanced by the T790M Drug Resistance Mutation

TL;DR: Although T790M alone has only a modest effect on EGFR function, when combined with the characteristic activating mutations L858R or del746-750, it results in a dramatic enhancement of EGFR activity, which suggests that they may contribute to the adverse clinical course of TKI-resistant NSCLC.