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Your search keyword '"Chin, Koei"' showing total 12 results
Start Over Author "Chin, Koei" Journal cancer research
12 results on '"Chin, Koei"'

1. Abstract C087: Window-of-opportunity trial of metastatic pancreatic cancer reveals mechanisms of response to targeting RAS signaling

Author

Tsuda, Motoyuki, primary, Daniel, Colin J., additional, Pelz, Carl, additional, Sivagnanam, Sam, additional, Keith, Dove, additional, Corless, Christopher L., additional, Chin, Koei, additional, Coussens, Lisa M., additional, Brody, Jonathan R., additional, Lopez, Charles D., additional, Mills, Gordon B., additional, and Sears, Rosalie C., additional

Published
2024
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5. Abstract PO-059: The genomic landscape of the in situ to invasive ductal breast carcinoma transition shaped by the immune system

Author

Trinh, Anne, primary, Gil Del Alcazar, Carlos R., additional, Shukla, Sachet A., additional, Chin, Koei, additional, Chen, Young Hwan, additional, Thibault, Guillaume, additional, Eng, Jennifer, additional, Jovanovic, Bojana, additional, Aldaz, C. Marcelo, additional, Park, So Yeon, additional, Jong, Joon, additional, Wu, Catherine, additional, Gray, Joe, additional, and Polyak, Kornelia, additional

Published
2020
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6. Abstract 3296: SMMART: Serial measurements of molecular and architectural responses to therapy

Author

Johnson, Brett, primary, Keck, Jamie, additional, Morris, Max, additional, Siex, Kiara, additional, Kolodzie, Annette, additional, Parmar, Swapnil, additional, Riesterer, Jessica, additional, Chin, Koei, additional, Gibbs, Summer, additional, Heiser, Laura, additional, Spellman, Paul, additional, Ellrott, Kyle, additional, Babur, Ozgun, additional, Demir, Emek, additional, Margolin, Adam, additional, Goecks, Jeremy, additional, Coussens, Lisa, additional, Bergan, Raymond, additional, and Gray, Joe, additional

Published
2018
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7. A Human Breast Cell Model of Preinvasive to Invasive Transition

Author

Rizki, Aylin, primary, Weaver, Valerie M., additional, Lee, Sun-Young, additional, Rozenberg, Gabriela I., additional, Chin, Koei, additional, Myers, Connie A., additional, Bascom, Jamie L., additional, Mott, Joni D., additional, Semeiks, Jeremy R., additional, Grate, Leslie R., additional, Mian, I. Saira, additional, Borowsky, Alexander D., additional, Jensen, Roy A., additional, Idowu, Michael O., additional, Chen, Fanqing, additional, Chen, David J., additional, Petersen, Ole W., additional, Gray, Joe W., additional, and Bissell, Mina J., additional

Published
2008
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9. Frequent Silencing ofLow Density Lipoprotein Receptor-Related Protein 1B (LRP1B ) Expression by Genetic and Epigenetic Mechanisms in Esophageal Squamous Cell Carcinoma

Author

Sonoda, Itaru, primary, Imoto, Issei, additional, Inoue, Jun, additional, Shibata, Tatsuhiro, additional, Shimada, Yutaka, additional, Chin, Koei, additional, Imamura, Masayuki, additional, Amagasa, Teruo, additional, Gray, Joe W., additional, Hirohashi, Setsuo, additional, and Inazawa, Johji, additional

Published
2004
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10. An Integrated View of Copy Number and Allelic Alterations in the Cancer Genome Using Single Nucleotide Polymorphism Arrays

Author

Zhao, Xiaojun, primary, Li, Cheng, additional, Paez, J. Guillermo, additional, Chin, Koei, additional, Jänne, Pasi A., additional, Chen, Tzu-Hsiu, additional, Girard, Luc, additional, Minna, John, additional, Christiani, David, additional, Leo, Chris, additional, Gray, Joe W., additional, Sellers, William R., additional, and Meyerson, Matthew, additional

Published
2004
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11. Frequent silencing of low density lipoprotein receptor-related protein 1B (LRP1B) expression by genetic and epigenetic mechanisms in esophageal squamous cell carcinoma.

Author

Sonoda I, Imoto I, Inoue J, Shibata T, Shimada Y, Chin K, Imamura M, Amagasa T, Gray JW, Hirohashi S, and Inazawa J

Subjects
Acetylation, Antimetabolites, Antineoplastic pharmacology, Azacitidine pharmacology, Carcinoma, Squamous Cell metabolism, Carcinoma, Squamous Cell pathology, Cell Division genetics, Cell Line, Tumor, CpG Islands genetics, DNA Methylation drug effects, Decitabine, Esophageal Neoplasms metabolism, Esophageal Neoplasms pathology, Gene Deletion, Gene Expression Regulation, Neoplastic drug effects, Histones metabolism, Humans, Nucleic Acid Hybridization, RNA, Messenger biosynthesis, RNA, Messenger genetics, Receptors, LDL biosynthesis, Reverse Transcriptase Polymerase Chain Reaction, Azacitidine analogs & derivatives, Carcinoma, Squamous Cell genetics, Esophageal Neoplasms genetics, Gene Silencing, Receptors, LDL genetics
Abstract

Low-density lipoprotein receptor-related protein 1B (LRP1B) is frequently deleted in tumors of various types, but its status and expression in esophageal squamous cell carcinomas (ESCs) have never been reported. In the course of a program to screen ESC cell lines for copy-number aberrations using array-based comparative genomic hybridization, we identified a homozygous deletion of LRP1B. Genomic PCR experiments revealed homozygous deletions of LRP1B in additional ESC cell lines (total, 6 of 43; 14.0%) and in primary esophageal tumors (30 of 70; 42.9%). Moreover, expression of LRP1B mRNA was frequently silenced in ESC lines without homozygous deletions (14 of 37; 37.8%). Using bisulfite-PCR analysis and sequencing, we found that LRP1B-nonexpressing cells without homozygous deletions were highly methylated at a CpG island of LRP1B, a sequence possessing promoter activity. Treatment with 5-aza-2'-deoxycytidine restored expression of LRP1B in those ESC lines. Histone acetylation status correlated directly with expression of LRP1B and inversely with the methylation status of the CpG island. Methylation of LRP1B was also detected in primary esophageal tumors. Restoration of LRP1B expression in ESC cells reduced colony formation. These results suggest that loss of LRP1B function in esophageal carcinogenesis most often occurs either by homozygous deletion or by transcriptional silencing through hypermethylation of its CpG island.

Published
2004
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12. Genomic copy number analysis of non-small cell lung cancer using array comparative genomic hybridization: implications of the phosphatidylinositol 3-kinase pathway.

Author

Massion PP, Kuo WL, Stokoe D, Olshen AB, Treseler PA, Chin K, Chen C, Polikoff D, Jain AN, Pinkel D, Albertson DG, Jablons DM, and Gray JW

Subjects
Adenocarcinoma enzymology, Adenocarcinoma genetics, Carcinoma, Non-Small-Cell Lung enzymology, Carcinoma, Squamous Cell enzymology, Carcinoma, Squamous Cell genetics, Female, Gene Dosage, Humans, Lung Neoplasms enzymology, Male, Nucleic Acid Hybridization, Oligonucleotide Array Sequence Analysis, Phosphatidylinositol 3-Kinases physiology, Signal Transduction genetics, Carcinoma, Non-Small-Cell Lung genetics, Lung Neoplasms genetics, Phosphatidylinositol 3-Kinases genetics
Abstract

Genomic abnormalities at 348 loci encoding genes that may contribute to lung cancer transformation and progression were assessed using array comparative genomic hybridization in 21 squamous carcinomas (SqCas) and 16 adenocarcinomas (AdCas). Hierarchical clustering showed a clear pattern of gains and losses for the SqCas, whereas the pattern for AdCas was less distinct. Cross-validated classification using a K-nearest-neighbor assigned, on average, 32 of 37 samples to their proper histological subtype. The most noticeable differences between SqCas and AdCas were gain of chromosome 3q22-q26 and loss of chromosome 3p. These occurred almost exclusively in SqCas. The region of recurrent increase is approximately 30 Mb in extent, ranging from EVI1 to TFRC. PIK3CA, the alpha catalytic subunit of phosphatidylinositol 3-kinase (PI3K), is in this region. The PIK3CA copy number increase was validated using fluorescence in situ hybridization to lung cancer tissue microarrays. Activity of the downstream PI3K effector protein kinase B (PKB) was higher in SqCas than in AdCas and was correlated with PIK3CA copy number (r = 0.75), suggesting that these copy number increases contribute to activation of PI3K signaling in SqCas of the lung.

Published
2002

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