[Advances in the treatment of acute leukemia with homologous bone marrow transplantation (author's transl)].
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Acute Disease↗
Biomedical subjects
D Tian
Publications and source records attributed to D Tian.
Detection of p53 protein accumulation in sputum and lung adenocarcinoma associated with indoor exposure to unvented coal smoke in China.
Lung cancer in Xuan Wei (XW), China has been linked to exposure to unvented coal smoke and adenocarcinoma, especially bronchioloalveolar carcinoma, is most common. p53 mutations occur commonly in lung cancers and usually generate detectable levels of p53 protein accumulation. Sputum is noninvasive to collect and ideal for screening p53 abnormalities. p53 protein accumulation was detected by immunohistochemistry in lung tumors and sputa from XW lung cancer patients to determine (1) the role of p53 in lung pathogenesis, and (2) feasibility of detecting p53 protein accumulation in sputum, p53 protein accumulation was detected in 73% (22/30) of lung adenocarcinomas from XW females exposed to coal emissions and significantly higher than the control cases (33%, p < 0.05). In sputum, we detected p53 overexpression in tumor cells in 54% (13/24) of XW cases and also in dysplastic cells (50% or 4/8). These findings suggest that p53 abnormalities is important in XW lung cancer etiology.
Adenocarcinoma↗
A sensitive immunofluorescence assay for detection of p53 protein accumulation in sputum.
p53 mutations are common genetic alterations in lung cancers and usually result in p53 protein accumulation in tumor cells. Sputum is noninvasive to collect and ideal for screening p53 abnormalities. This study was to determine the feasibility of detecting p53 protein accumulation in sputum cells using an immunofluorescence assay. Sputum samples were collected from 58 Chinese subjects, including 16 lung cancer cases from Xuan Wei (XW) County exposed to coal smoke, 25 mostly tobacco smoke-related cases from Zhengzhou City, and 17 XW controls. The p53 protein accumulation in tumor cells and some atypical cells was detected in 56% (9/16) of the coal smoke-exposed XW cases, 44% (11/25) of the Zhengzhou cases and none (0/17) in controls. The p53+ tumor cells were confirmed morphologically by Papanicolaou staining after the p53 immunofluorescence assay. This is the first report of successfully using an immunofluorescence assay to detect p53 protein accumulation in sputum.
Adenocarcinoma↗
DNA damage in buccal epithelial cells from individuals chronically exposed to arsenic via drinking water in Inner Mongolia, China.
The purpose of this pilot study was to assess DNA damage in buccal cells from individuals chronically exposed to arsenic via drinking water in Ba Men, Inner Mongolia. Buccal cells were collected from 19 Ba Men residents exposed to arsenic at 527.5 +/- 23.7 micrograms/L (mean +/- SEM) and 13 controls exposed to arsenic at 4.4 +/- 1.0 micrograms/L. DNA fragmentation by the DNA ladder and TUNEL assay were used to detect DNA damage in buccal cells. In the DNA ladder assay, 89% (17/19) of the arsenic-exposed group showed < 100 bp DNA fragments, in contrast to 15% (2/13) of the controls (p < 0.0001). For the TUNEL assay, the mean frequencies of positive cells were higher in the exposed group (15.1%) than in the controls (2.0%) (p < 0.0001). This study showed that high arsenic exposure via drinking water resulted in DNA damage and DNA fragmentation in buccal cells thus may be an appropriate biomarker for assessing chronic effects of arsenic in humans. A study investigating DNA fragmentation from the individuals with low levels of arsenic exposure in this population is in progress.
Adolescent↗
Regulation of LDH-A gene expression by transcriptional and posttranscriptional signal transduction mechanisms.
The lactate dehydrogenase-A (LDH-A) gene, whose product plays a pivotal role in normal anaerobic glycolysis and is frequently increased in human cancers, is highly regulated at the transcriptional and posttranscriptional levels. Our laboratory has carried out extensive studies concerning the regulation of LDH-A subunit expression. We have elucidated complex regulatory mechanisms by identifying multiple cis-acting promoter elements including functional sites for Sp1 and c-Myc interactions as well as sites that interact with the protein kinase A and protein kinase C substrates, CREB and AP1, respectively. Furthermore, we have reported the existence of a CRE-dependent silencer element in the LDH-A promoter. LDH-A expression is additionally regulated through the protein kinase A and C signal pathways at the posttranscriptional level, specifically mRNA stability.
Humans↗