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Biomedical subjects

T Tong

Publications and source records attributed to T Tong.

At least 37 records · Page 2Linked to original sources
PubMed1999

Use of a parotid fascia flap to prevent postoperative fistula.

OBJECTIVE: The purpose of this study was to investigate the usefulness of a fascia flap technique designed to improve the post-operative results of regional excision in cases of benign tumor in the superficial lobe of the parotid gland and to reduce formation of postoperative fistula. STUDY DESIGN: During surgery in each of 32 patients with benign tumor in the superficial lobe of the parotid gland, a fascia flap was raised from beneath the ear lobe, placed in its original position, and firmly sutured after regional resection of the tumor. The results were compared with those in a control group of 30 patients, whose operations were the same as those of the experimental group except for the fact that the fascia overlying the tumor was excised with the tumor in the controls. RESULTS: The wounds of the 32 patients repaired with the fascia flap healed well without any complication. Among the 30 patients in the control group, fistula occurred in 4 patients (13.3%). The difference was significant when the 2 groups were compared (chi2 test: P = .049 , P < .05). CONCLUSIONS: Use of a parotid fascia flap in partial parotidectomy for benign tumors in the superficial lobe holds promise for the prevention of postoperative fistula formation.

Adenolymphoma↗
PubMed1999

[Alterations of cell apoptosis and proliferation during transformation of a human bronchial epithelial cell line].

OBJECTIVE: To investigate the alterations of cell apoptosis and proliferation and its mechanism during transformation of a human bronchial epithelial cell line Y. METHODS: Terminal deoxyribonucleotidyl transferase in situ labelling, BrdU incorporation, Western blotting and fluorescence in situ hybridization were used in the study. RESULTS: During serial passages of the immortalized human bronchial epithelial cell line Y, some phenotypic alterations, such as higher colony forming efficiency in soft agar, resistance to serum-induced differentiation and low dependence on EGF were observed. The increase in cell proliferation and decrease in cisplatinum-induced apoptosis and the enhanced protein expression of Bcl-2, MDM2, PCNA and Cyclin D1 were found in the late passages of the cell line. The chromosomes of Y cells were diploid at the early passages, but became aneuploid in the late passages. CONCLUSION: In addition to the increase in cell proliferation, inhibition of apoptosis might also contribute to the cytogenetic abnormality and the transformation of human bronchial epithelial cells.

Apoptosis↗
PubMed1998

Establishment and characterization of a SV40T-transformed human bronchial epithelial cell line.

The majority of human lung cancers originate from the carcinogenesis of bronchial epithelial cells. To study the malignant progression of human bronchial epithelial cells, we established a SV40T-transformed human bronchial epithelial cell line, and observed some biological and genetic changes of the cell line at different passages. In a 2-year culture, this cell line was approaching malignancy without obvious senescence. Cells in a later passage proliferated faster and required less growth factors than those of an early passage. After continued passaging, these cells were resistant to the terminal squamous differentiation effects of serum, and many of the cells grew anchorage independently. However, no tumor formed after cells were injected into nude mice. Some genetic alterations were found accompanying those morphological changes, such as 3p- and activation of c-myc, c-erbB-2 and bcl2, suggesting that those genetic alterations may contribute to the carcinogenesis of human bronchial epithelial cells at an early stage. This cell line should be particularly useful for studying the progression of human lung cancers.

Animals↗
PubMed1998

GLUT1 glucose transporter: a highly sensitive marker of malignancy in body cavity effusions.

Malignant cells exhibit increased rates of glycolysis and glucose uptake, and several types of cancer have been reported to overexpress the GLUT1 glucose transporter. The diagnosis of malignancy in body cavity effusions remains a dilemma in certain cases, despite recent progress in diagnostic immunocytochemistry. We used immunostaining to detect the facilitative glucose transporter, GLUT1, in cytologic preparations of body cavity effusions and washes. With the use of standard avidin-biotin immunostaining for GLUT1, we examined cell blocks of body cavity effusions or washings from 31 carcinomas, 1 lymphoma, and 25 benign effusions or washes. GLUT1 staining occurred in the malignant cell population in 29 (93.5%) of 31 carcinomatous effusions or washes. The characteristic staining pattern consisted of dense, linear staining of the plasma membrane, with accentuation at cell-cell borders, with or without cytoplasmic staining. Erythrocytes showed positive GLUT1 membrane staining, consistent with previous reports. Of 25 benign effusions, 20 were nonstaining (excepting erythrocytes), and 5 contained rare single mesothelial cells, with equivocal to very weak membrane staining. Staining of these cells was readily distinguishable from the characteristic strong staining of malignant cells, and these cells were easily distinguished from tumor cells by their benign morphologic characteristics. At least three of these latter five specimens were from patients with cirrhosis. In all of the other cases, mesothelial cells, histiocytes, and other inflammatory cells did not stain. These findings suggest that GLUT1 immunostaining could be useful in diagnostic cytopathology. The findings also suggest that enhanced glycolysis, which requires increased glucose transport, might be a survival adaptation for tumor cells in effusions, a significant number of which are hypoxic.

Biomarkers, Tumor↗
PubMed1997

[Study on antitumor drug-induced apoptosis in human cancer cells by terminal deoxynucleotidyl transferase assay].

OBJECTIVE: Considerable evidence has showed that apoptosis is involved in both cancer development and inhibition. A new assay (terminal deoxynucleotidyl transferase assay, TdT assay) was recently reported to have advantages in the detection of apoptosis. In this study, this assay was used to investigate antitumor drug-induced apoptosis in human cancer cells. METHODS: TdT assay, DNA gel electrophoresis, electron and light microscopy were used to observe apoptosis. RESULTS: Our results showed that cisplatin-induced apoptosis in both HL-60 and SV40T-transformed human bronchial epithelial cells was detected with a good dose and time response. The occurrence of the apoptosis was preceded by the decrease of bcl-2 mRNA expression. With TdT assay, apoptotic cells were observed in the ovarian tumor of patients treated with carboplatin. CONCLUSION: TdT assay may be applicable to moniter apoptosis in human cancers induced by chemotherapy, and to evaluate tumor cell response during treatment.

Antineoplastic Agents↗
PubMed1997

Molecular cytogenetic alterations in the early stage at human bronchial epithelial cell carcinogenesis.

Lung carcinogenesis is a multi-step process involving activation of oncogenes and inactivation of tumor suppress genes. Many molecular and cytogenetic alterations occur in the early stages of carcinogenesis. We have developed an effective culture system for human bronchial epithelial cells and lung cancer cells. Four immortalized human bronchial epithelial cell lines were established by transfecting the epithelial cells with plasmid DNA containing the early region of SV40. Some molecular and cytogenetic alterations, such as 3p-, 2q-, 9p-, c-myc translocation t(8;14) (q23; q32), were found in one immortalized bronchial epithelial cell line M when approaching malignant transformation. An increase in cell proliferation and decrease of apoptosis were noted in the late passages of the immortalized cell line M. Some molecular cytogenetic alterations were also observed in human primary non-small cell lung cancers. Molecular cytogenetic alterations during the early stage of carcinogenesis of human bronchial epithelial cells may be useful as biomarkers for both diagnosis and intermediate endpoint of chemoprevention of lung cancer.

Animals↗
PubMed1997

Induction of c-fos/c-myc expression by epidermal growth factor decreases with alteration of their gene binding proteins in senescent fibroblasts.

OBJECTIVE: To observe the changes of proto-oncogene c-fos/c-myc expression and its relation to specific transcription factors in human senescent fibroblast after epidermal growth factor (EGF) addition. METHODS: The c-fos/c-myc expression were analysed by Northern blot. Transcription factors were analysed by Southwestern blot. RESULTS: (1) The expression of c-fos/c-myc was less susceptible to induction by EGF as the cells aged. (2) EGF increased the binding of protein P91 to c-fos with regulatory sequence and P80 to c-myc with regulatory sequence, but the increased levels of both proteins were significantly reduced in senescent cells. CONCLUSIONS: Inability of c-fos/c-myc gene induction by EGF in senescent cells might be correlated with some DNA-binding proteins.

Cellular Senescence↗
PubMed1996

Dot-immunogold filtration assay as a screening test for syphilis.

A dot-immunogold filtration assay (DIGFA) for the rapid detection of reaginic antibody in the serum of syphilitic patients was developed. The assay was simple, rapid, and reproducible. The test completion time was 2 min, and the assay required no equipment. The positive dot was very obvious, and the results could easily be determined with the naked eye. A total of 350 serum samples were examined by DIGFA, the rapid plasma reagin test, and the fluorescent treponemal antibody-absorption test. The levels of agreement between DIGFA and the rapid reagin test and between DIGFA and the fluorescent treponemal antibody-absorption test were 100 and 98%, respectively. The results of clinical application indicated that DIGFA could be used as a routine screening test for syphilis.

Antibodies, Bacterial↗
PubMed1996

Familial cardiomyopathy with cataracts and lactic acidosis: a defect in complex I (NADH-dehydrogenase) of the mitochondria respiratory chain.

Four patients in one generation of a multiply consanguineous pedigree died with cardiomyopathy, cataracts, and lactic acidemia. Postmortem heart and skeletal muscle tissues from one patient were analyzed. A low (12% control) activity of NADH-CoQ reductase (complex I) in heart and normal activity in skeletal muscle mitochondria was found. Cultured skin fibroblasts obtained from two individuals in the pedigree showed elevated lactate to pyruvate ratios in the range of 2 to 3.5 times normal and decreased complex I + III activity (42 and 54% of control activities) in isolated mitochondria. Western blot analysis and enzymatic assay showed normal levels of CuZn-superoxide dismutase, but grossly elevated levels of the mitochondrial Mn-superoxide dismutase. Southern blot analysis in heart muscle cells from the patient tested revealed multiple mitochondrial DNA deletions which indicate free oxygen radical damage. We hypothesize that a nuclear-encoded defect in the respiratory chain is responsible for excessive free oxygen radical production in these infants which contributes to the prenatal onset of cardiomyopathy and cataracts.

Acidosis, Lactic↗
PubMed1995

The proliferative response and anti-oncogene expression in old 2BS cells after growth factor stimulation.

The limited replicative lifespan of diploid human cells in vitro (cellular senescence) serves as a cellular model of aging. We examined the proliferative response of 2BS cells of different population doubling levels to fibroblast growth factor (FGF). DNA synthesis was measured by thymidine incorporation. As the cells aged, there was a significant decrease in the stimulation of DNA synthesis by FGF addition (P < 0.01). The effective concentration of FGF and the latent period prior to DNA synthesis did not change. Expression of Rb and p53 mRNA after growth factor stimulation was also examined. Young and old cells had similar Rb mRNA levels, whereas the p53 mRNA level was significantly reduced in old cells. After both cells were treated by FGF or epidermal growth factor (EGF), Rb expression increased 210-275% in young cells and 50-60% in old ones. However, no significant change was found in p53 gene transcriptions after FGF addition. The results further suggest that cell aging is associated with a progressive loss of the ability of cells to respond to growth factors.

Cell Division↗
PubMed1994

Cell aging of human diploid fibroblasts is associated with changes in responsiveness to epidermal growth factor and changes in HER-2 expression.

The limited replicative life span of diploid human cells in vitro (cellular senescence) serves as a cellular model of aging. We examined the proliferative response of 2BS cells of different population doubling levels to epidermal growth factor (EGF). DNA synthesis was measured by thymidine incorporation. As the cells aged, there was a significant decrease both in the baseline level of DNA synthesis and in the stimulation of DNA synthesis by EGF addition. The effective concentration of EGF and the latent period prior to DNA synthesis did not change. EGF receptor mRNA expression also remained unchanged as the cells aged, in the absence or presence of EGF, suggesting that the defect in old cells lies downstream in the EGF signaling pathway. As the cells reached 100% of their life span, however, there was a 70% decrease in EGF receptor mRNA. Expression of the EGF receptor homologue HER-2 was also examined. The HER-2 mRNA level was significantly reduced in old cells. Moreover, HER-2 expression was stimulated by EGF addition in young cells but not in old cells. The results suggest that cell aging is associated with a progressive loss in the ability of cells to respond to growth factors.

Cell Division↗
PubMed1994

TGF-beta 1 gene expression in cultured human keratinocytes does not decrease with biologic age.

The biologic activity of cultured epithelial grafts is believed to diminish with increasing cellular age. Therefore, keratinocytes from young donors are used preferentially in the production of cultured allografts for wound treatment. However, the impact of biologic age on cytokine gene expression by human keratinocytes has not been previously investigated. In this study, transforming growth factor-beta 1 (TGF-beta 1) gene expression in human keratinocytes derived from normal foreskins of males ranging in age from 7 months to 82 years was analyzed. Keratinocytes were harvested from fresh specimens and cultivated in vitro on 3T3 fibroblast feeder layers through second passage. The cells were analyzed both qualitatively and semiquantitatively for TGF-beta 1 gene expression using three separate techniques: in situ hybridization, Northern hybridization, and competitive polymerase chain reaction. By in situ hybridization, the signal representing TGF-beta 1 transcript was detected in cells in all layers of the stratified cultures, and immunohistochemical staining for TGF-beta 1 protein was equally intense in all layers. Northern blots of total RNA extracted from the cultivated cells showed no decrease in band density with increasing biologic age. Likewise, no decrease in TGF-beta 1 mRNA levels with biologic age was observed using a semiquantitative polymerase chain reaction assay. These results indicate that the potential for TGF-beta 1 gene expression in cultured foreskin keratinocytes does not decline with increasing cellular age. The findings imply that the clinical performance of cultured grafts, at least as it relates to the elaboration of this growth factor, may not be significantly altered by the biologic age of the keratinocyte donor.

Adult↗
PubMed1993

The lifetime risk of developing breast cancer.

BACKGROUND: The lifetime risk of developing breast cancer in U.S. women, often quoted as one in nine, is a commonly cited cancer statistic. However, many estimates have used cancer rates derived from total rather than the cancer-free population and have not properly accounted for multiple cancers in the same individual. PURPOSE: Our purpose was to provide a revised method for calculating estimates of the lifetime risk of developing breast cancer and to aid in interpretation of the estimates. METHODS: A multiple decrement life table was derived by applying age-specific incidence and mortality rates from cross-sectional data to a hypothetical cohort of women. Incidence, mortality, and population data from 1975-1988 were used, representing the geographic areas of the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program. The incidence rates reflected only the first breast primary cancer; mortality rates reflected causes other than breast cancer. The population denominator used in calculating incidence rates was adjusted to reflect only those women without previously diagnosed breast cancers in the hypothetical cohort. RESULTS: Our calculations showed an overall lifetime risk for developing invasive breast cancer of approximately one in eight with use of 1987-1988 SEER data, although up to age 85, it was still the commonly quoted one in nine. CONCLUSION: Our estimate was calculated assuming constant age-specific rates derived from 1987-1988 SEER data. Because incidence and mortality rates change over time, conditional risk estimates over the short term (10 or 20 years) may be more reliable. A large portion of the rise in the lifetime risk of breast cancer estimated using 1975-1977 data (one in 10.6) to an estimate using 1987-1988 data (one in eight) may be attributed to 1) early detection of prevalent cases due to increased use of mammographic screening and 2) lower mortality due to causes other than breast cancer. A common misperception is that the lifetime risk estimate assumes that all women live to a particular age (e.g., 85 or 95). In fact, the calculation assumes that women can die from causes other than breast cancer at any possible age. Cutting off the lifetime risk calculation at age 85 assumes that no women develop breast cancer after that age. While the lifetime risk of developing breast cancer rose over the period 1976-1977 to 1987-1988, the lifetime risk of dying of breast cancer increased from one in 30 to one in 28, reflecting generally flat mortality trends.

Adolescent↗