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Comprehensive genomic profiles of small cell lung cancer
TLDR
This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.
Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer
TLDR
This study implicates histone modification as a major feature of SCLC, reveals potentially therapeutically tractable genomic alterations and provides a generalizable framework for the identification of biologically relevant genes in the context of high mutational background.
Quantitative high-throughput analysis of DNA methylation patterns by base-specific cleavage and mass spectrometry.
TLDR
A previously uncharacterized method for high-throughput DNA methylation analysis that utilizes MALDI-TOF mass spectrometry (MS) analysis of base-specifically cleaved amplification products is presented and it is demonstrated that the quantitative methylation results allow accurate classification of samples according to their histopathology.
A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25
TLDR
The results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
Lung cancer susceptibility locus at 5p15.33
TLDR
The susceptibility region contains two genes, TERT and CLPTM1L, suggesting that one or both may have a role in lung cancer etiology, and two uncorrelated disease markers at 5p15.33 are detected.
The LLP risk model: an individual risk prediction model for lung cancer
TLDR
If independent validation studies confirm these results, the LLP risk models’ application as the first stage in an early detection strategy is a logical evolution in patient care.
Frequent mutations in chromatin-remodeling genes in pulmonary carcinoids
TLDR
Pulmonary carcinoids are not early progenitor lesions of the highly aggressive lung neuroendocrine tumors but arise through independent cellular mechanisms, suggesting that inactivation of chromatin remodeling genes is sufficient to drive transformation in pulmonary carcinoids.
Second primary tumors in patients with head and neck squamous cell carcinoma
TLDR
This work has shown that second primary neoplasms are a particular feature of head and neck cancer and the concept that a patient could develop cancer twice was first put forward by Billroth.
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