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Your search keyword '"H. Helen Lin"' showing total 2 results
Start Over Author "H. Helen Lin" Journal scientific reports
2 results on '"H. Helen Lin"'

1. Ductal activation of oncogenic KRAS alone induces sarcomatoid phenotype

Author

Zobeida Cruz-Monserrate, Yong Fu, Baoan Ji, Steven Vonderfecht, Craig D. Logsdon, Chien-Feng Li, Yiyin Chung, H. Helen Lin, Szu Min Lin, and David K. Ann

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Ductal cells, Submandibular Gland, Cetuximab, Biology, medicine.disease_cause, Malignancy, Article, Salivary duct carcinoma, Proto-Oncogene Proteins p21(ras), Carcinoma, medicine, Humans, Salivary Ducts, Aged, Cell Proliferation, Aged, 80 and over, Multidisciplinary, Sarcoma, Middle Aged, medicine.disease, Salivary Gland Neoplasms, 3. Good health, ErbB Receptors, Phenotype, Drug Resistance, Neoplasm, Mutation, Female, KRAS, Tamoxifen, medicine.drug, Signal Transduction
Abstract

Salivary duct carcinoma (SDC) is an uncommon, but aggressive malignant tumor with a high mortality rate. Herein, we reported the detection of somatic KRAS A146T and Q61H mutations in 2 out of 4 (50%) sarcomatoid SDC variants. Transgenic mice carrying the human oncogenic KRASG12V, which spatiotemporal activation by tamoxifen (TAM)-inducible Cre recombinase Ela-CreERT in the submandibular gland (SMG) ductal cells, was established and characterized. Visible carcinoma was detected as early as day-15 following oncogenic KRASG12V induction alone and these tumors proliferate rapidly with a median survival of 28-days accompanied with histological reminiscences to human sarcomatoid SDC variants. Moreover, these tumors were resistant to cetuximab treatment despite augmented EGFR signaling, attesting its malignancy. Our findings suggest that LGL-KRasG12V;Ela-CreERT transgenic mice could serve as a useful preclinical model for investigating underlying mechanisms and developing potential therapies.

Published
2015

2. Ductal activation of oncogenic KRAS alone induces sarcomatoid phenotype.

Author

Fu Y, Cruz-Monserrate Z, Helen Lin H, Chung Y, Ji B, Lin SM, Vonderfecht S, Logsdon CD, Li CF, and Ann DK

Subjects
Adult, Aged, Aged, 80 and over, Cell Proliferation, Cetuximab pharmacology, Drug Resistance, Neoplasm drug effects, ErbB Receptors genetics, Female, Humans, Male, Middle Aged, Mutation genetics, Phenotype, Signal Transduction drug effects, Submandibular Gland pathology, Proto-Oncogene Proteins p21(ras) genetics, Salivary Ducts pathology, Salivary Gland Neoplasms genetics, Salivary Gland Neoplasms pathology, Sarcoma genetics, Sarcoma pathology
Abstract

Salivary duct carcinoma (SDC) is an uncommon, but aggressive malignant tumor with a high mortality rate. Herein, we reported the detection of somatic KRAS A146T and Q61H mutations in 2 out of 4 (50%) sarcomatoid SDC variants. Transgenic mice carrying the human oncogenic KRAS(G12V), which spatiotemporal activation by tamoxifen (TAM)-inducible Cre recombinase Ela-CreERT in the submandibular gland (SMG) ductal cells, was established and characterized. Visible carcinoma was detected as early as day-15 following oncogenic KRAS(G12V) induction alone, and these tumors proliferate rapidly with a median survival of 28-days accompanied with histological reminiscences to human sarcomatoid SDC variants. Moreover, these tumors were resistant to cetuximab treatment despite augmented EGFR signaling, attesting its malignancy. Our findings suggest that LGL-KRas(G12V);Ela-CreERT transgenic mice could serve as a useful preclinical model for investigating underlying mechanisms and developing potential therapies.

Published
2015
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