A5071696225- Lung Cancer Research Studies
- RNA modifications and cancer
- Lung Cancer Treatments and Mutations
- Cancer-related Molecular Pathways
- Peptidase Inhibition and Analysis
- Cancer Genomics and Diagnostics
- Lung Cancer Diagnosis and Treatment
- Genetic factors in colorectal cancer
- GDF15 and Related Biomarkers
- Glycosylation and Glycoproteins Research
- Telomeres, Telomerase, and Senescence
- Cancer Research and Treatments
- Neuroblastoma Research and Treatments
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Acute Myeloid Leukemia Research
- DNA Repair Mechanisms
- Epigenetics and DNA Methylation
- Cancer-related gene regulation
- Cancer, Hypoxia, and Metabolism
- Neuroendocrine Tumor Research Advances
- Chromatin Remodeling and Cancer
- Protein Degradation and Inhibitors
- Mechanisms of cancer metastasis
- Cancer Immunotherapy and Biomarkers
- Chronic Lymphocytic Leukemia Research
University of Tokyo Hospital
2012-2025
Tokyo Medical University Hospital
2021-2024
Iwate Medical University
2013-2021
Institute of Predictive and Personalized Medicine of Cancer
2014-2017
Kyushu Institute of Technology
2016
National Cancer Centre Japan
1997-2015
The University of Tokyo
1983-2014
National Cancer Research Institute
1998-2013
Genesis Research Institute
2012-2013
The Cancer Institute Hospital
2011
By a molecular genetic approach using polymorphic DNA markers that detect allelic deletion of specific chromosomal regions, we analyzed for possible loss heterozygosity in five different histological types lung cancers obtained from 47 patients. In small-cell carcinomas, the incidence deletions at three loci was extremely high; detected on chromosomes 3p 7 patients (100%), 13q 10 11 (91%), and 17p 5 (100%). The these carcinomas were observed even tumors without any clinical evidence...
Alterations of c-myc, c-rasHa, or c-myb oncogenes were found in more than one-third human solid tumors. Amplification c-myc occurred advanced, widespread tumors aggressive primary Apparent allelic deletions c-rasHa and can be correlated with progression metastasis carcinomas sarcomas.
Abstract Nutlin-3, an MDM2 inhibitor, activates p53, resulting in several types of cancer cells undergoing apoptosis. Although p53 is mutated or deleted ∼50% all cancers, still functionally active the other 50%. Consequently, nutlin-3 and similar drugs could be candidates for neoadjuvant therapy cancers with a functional p53. Cellular senescence also phenotype induced by activation plays critical role protecting against tumor development. In this report, we found that nutlin-3a can induce...
IntroductionThe information regarding therapeutically relevant genomic alterations in small cell lung cancer (SCLC) is not well developed. We analyzed the SCLC genome using an integrative approach to stratify targetable alterations.MethodsWe performed whole exon sequencing (n = 51) and copy number analysis =47) on surgically resected tumors matched normal tissue samples from treatment-naive Japanese patients.ResultsThe demographics of 51 patients included this study were as follows: median...
To obtain a landscape of gross genetic alterations in small cell lung cancer (SCLC), genome‐wide copy number analysis and whole‐transcriptome sequencing were performed 58 42 SCLCs, respectively. Focal amplification known oncogene loci, MYCL1 (1p34.2), MYCN (2p24.3), MYC (8q24.21), was frequently mutually exclusively detected. co‐amplified with other regions on either the same or different chromosome several cases. In addition, 9p24.1 region identified as being amplified SCLCs without family...
Abstract Purpose: We aimed to maximize the performance of detecting genetic alterations in lung cancer using high-throughput sequencing for patient-derived xenografts (PDXs). Experimental Design: undertook an integrated RNA and whole-exome 14 PDXs. focused on functional analysis β2-microglobulin (B2M), a component HLA class-I complex. Results: identified genes involved various functions, such as B2M immunosurveillance. extended mutational about 230 cancers. Five percent cancers carried...
The p33ING1 protein is a regulator of cell cycle, senescence, and apoptosis. Three alternatively spliced transcripts encode p47ING1a, p33ING1b, p24ING1c. We cloned an additional ING family member, p33ING2/ING1L. Unlike p33ING2 induced by the DNA-damaging agents etoposide neocarzinostatin. p33ING1b negatively regulate growth survival in p53-dependent manner through induction G(1)-phase cell-cycle arrest strongly enhances transcriptional-transactivation activity p53. Furthermore, expression...
DNAs from fifty-three primary breast cancers were hybridized with 16 different proto-oncogene or oncogene probes. Abnormalities of one more five proto-oncogenes found in fifty-eight percent tumors at the time mastectomy. Amplification c-myc and c-erbB-2, allelic deletions c-ras-Ha c-myb most common abnormalities. The presence altered correlated clinical stage cancers. Fifteen 43 evaluable stages I to III recurred, four IV progressed within 24 months surgery. All but that recurred had...
To identify genetic alterations associated with acquisition of metastatic ability in colorectal carcinoma, 31 liver metastases and 40 primary tumors carcinoma from 55 patients were analyzed for loss chromosomal heterozygosity using 46 polymorphic DNA markers covering 15 chromosomes. Loss (LOH) and/or rearrangement at the TP53 DCC loci detected all (10 10 19 DCC), observed 59% 17) 75% (18 24) respectively tumors. Furthermore, incidence LOH on chromosomes 13q 14q was higher than that other...
OGG1 protein has an ability to suppress mutagenesis induced by 8-hydroxyguanine (8OHG), oxidatively damaged promutagenic base. Here, the mutation suppressive was compared between two common polymorphic proteins, OGG1-Ser326 and OGG1-Cys326, using a supF forward assay employing 8OHG-containing plasmid. Polymorphic proteins were exogenously expressed adenoviral transduction in H1299 human lung cancer cells, which endogenous undetectable western blot analysis. Mutations 8OHG more efficiently...