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Biomedical subjects

N Voravud

Publications and source records attributed to N Voravud.

At least 37 records · Page 2Linked to original sources
PubMed1998

13-cis-retinoic acid and interferon-alpha 2a therapy in locally advanced squamous cell carcinoma of the cervix: p53 alteration, proliferating cell nuclear antigen expression and angiogenesis response.

OBJECTIVE: To evaluate prognostic importance of p53, PCNA and vascularization alteration in patients with locally advanced cervical squamous cell carcinoma (SCC) after combination therapy with 13-cis-retinoic acid (13cRA) and interferon-alpha 2a (IFN-alpha 2a). METHODS: 13cRA and IFN-alpha 2a were administered to patients with locally advanced cervical SCC. Formalin fixed, paraffin embedded tissues sections obtained at pre- and post-therapy, respectively, were stained immunohistochemically with anti-p53, anti-PCNA and anti CD31. RESULTS: p53 alteration was demonstrated in 5/10 patients and 3/10 patients pre- and post-therapy, respectively. There was no correlation between p53 alteration and prognosis. After therapy, two patients with complete response had lower PCNA expression whereas the non-responders demonstrated the opposite result. The vascularization showed a correlation with PCNA and prognosis. In the response group, patients had lower microvessel count while the metastatic group exhibited higher count. CONCLUSIONS: The present study suggests that p53 alteration is neither related to the prognosis of cervical SCC nor is it influenced by the combination therapy while PCNA expression and vascularization might be constitute potential markers for tumorigenesis, prognosis and responsiveness to this novel regimen.

Adult↗
PubMed1998

MPXI and early neutrophilia: new potential therapeutic biomarkers for recombinant human granulocyte colony-stimulating factor.

We evaluated the effect of recombinant human granulocyte colony-stimulating factor (rhG-CSF) given after myelosuppressive chemotherapy in 15 cancer patients. No severe neutropenia (absolute neutrophil count, ANC < 0.5 x 10(3)/microL) was noticed in 10 rhG-CSF primary prophylactic patients, but was noticed in two of five rhG-CSF secondary prophylactic patients. Neutrophilia characterized by shift to the left occurred within 24 hours after starting rhG-CSF prophylaxis. Thereafter, conversion to normal level occurred within 24 hours. The peak of neutrophilia occurred earlier in the primary group than in the secondary prophylactic group. The detection of myeloperoxidase (MPO) using flow cytochemistry blood autoanalyzer (TechniconR H * 1) was evaluated as mean peroxidase index (MPXI). Leukocyte alkaline phosphatase (LAP) using the method of Kaplow (Am J Clin Pathol 39:439-449, 1963) was recorded as LAP score. There was a statistically significant elevation of MPXI in the primary group over the secondary prophylactic patients. The LAP activity was in normal range. There was a slightly decreased red blood cell (RBC) count, hemoglobin (Hb), and platelet count. In conclusion, rhG-CSF induced neutrophilia with efficient enzymatic activity. These findings demonstrate the value of rhG-CSF in patients receiving chemotherapy. MPXI and early neutrophilia may serve as a potential biomarker of therapeutic efficacy of rhG-CSF.

Adult↗
PubMed1998

Epstein-Barr viral DNA in serum of patients with nasopharyngeal carcinoma.

This study evaluated Epstein-Barr virus (EBV) DNA in sera of 42 patients with nasopharyngeal carcinoma (NPC) and 82 healthy individuals who had been infected previously with EBV. Thirteen of 42 NPC samples were positive for EBV DNA in their sera, whereas all 82 normal controls were negative. In addition, EBV typing between primary tumors and sera showed identical results, suggesting that serum EBV DNA represented tumor DNA. To evaluate the importance of the serum NPC DNA, clinical data and tumor phenotypes including age, sex, WHO type, EBV type, stage, tumor invasion, metastasis, and apoptosis were correlated with serum EBV DNA, and only apoptosis was found statistically significant. In conclusion, EBV DNA was detectable in the serum of some patients with NPC, represented tumor DNA, and might have clinical implications in the future.

Adult↗
PubMed1998

Reference ranges of reticulocytes in adults.

According to the International Committee for Standardization in Haematology (ICSH), we determined the reference values for reticulocytes using an automated blood cell analyzer Technicon H*3 RTC in 200 healthy adult blood donors, aged between 17 and 60 years, 100 of whom were male and 100 female. The parameters included reticulocyte count, and its corpuscular indices; mean reticulocyte corpuscular volume (MCVr), mean reticulocyte corpuscular hemoglobin concentration (CHCMr), mean reticulocyte hemoglobin content (CHr), reticulocyte distribution width (RDWr), reticulocyte hemoglobin distribution width (HDWr) and reticulocyte corpuscular hemoglobin concentration distribution width (CHDWr). The reference ranges were established by setting the reference limits at two standard deviations from the arithmetic reference mean.

Adolescent↗
PubMed1997

Genomic alterations in nasopharyngeal carcinoma: loss of heterozygosity and Epstein-Barr virus infection.

Nasopharyngeal carcinoma is a subset of head and neck squamous cell cancers with unique endemic distribution and aetiological co-factors. Epstein-Barr virus has been revealed to be an important aetiological factor for most nasopharyngeal carcinomas. Nevertheless, additional genetic alterations may be involved in their development and progression. The aim of this study was to determine the likely chromosomal locations of tumour-suppressor genes related to Epstein-Barr virus-associated nasopharyngeal carcinoma. Fifty-six microsatellite polymorphic markers located on every autosomal arm were used to estimate the incidence of loss of heterozygosity in 27 Epstein-Barr virus-associated nasopharyngeal carcinomas. High frequencies of allelic loss were observed on chromosome 3p (75.0%) and 9p (87.0%). Chromosome 9q, 11q, 13q and 14q displayed loss in over 50%, while chromosome 3q, 6p, 16q, 19q and 22q exhibited loss in 35-50%. Furthermore, several other chromosomal arms demonstrated allelic loss in 20-35%. Additionally, 1 of the 27 cases showed microsatellite instability at multiple loci. These findings provide evidence of multiple genetic alterations during cancer development and clues for further studies of tumour-suppressor genes in Epstein-Barr virus-associated nasopharyngeal carcinoma.

Carcinoma↗
PubMed1997

Squamous cell carcinoma of head and neck.

Head and neck cancers are a major heath problem and common malignancies in Thailand. Up to 80 per cent of cases are caused by smoking and alcohol consumption. Epithelial mucosa of the aerodigestive tract exposed to carcinogens results in cellular mutations at different areas by a process called field cancerization and causes multistep carcinogenesis. Over 90 per cent of cases are squamous cell carcinoma. Prognostic factors depend on the patients, diseases and treatment. Currently, several molecular pathogenesis have been discovered such as abnormalities of c-myc, c-ras, c-erbB-1, bcl, int-2, hst1 oncogenes, p53 and p16 tumor suppressor genes. Common chromosomal abnormalities are 3p, 9p, 11q, 13q, 17p. Diagnosis requires symptoms and signs, radioimaging, and pathology. Stage I and II can be treated by surgery or radiotherapy. However, stage II requires and combination of surgery and radiotherapy, and studies of chemotherapy and local treatment to increase therapeutic efficacy by several approaches such as combination chemotherapy, new drugs, and biologic therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Ruptured primary hepatocellular carcinoma at Chulalongkorn University Hospital: a retrospective study of 32 cases.

Rupture of Primary hepatocellular carcinoma (HCC) is relatively common in high incidence areas including Thailand. There have been attempts to establish a standard treatment to manage this phenomenon. We retrospectively reviewed the records of patients with HCC from January 1989 to June 1997, and ten per cent (32/306) had tumor rupture during the course of the disease. Overall median survival of the patients with tumor rupture was 2.7 months [95% confidence interval (CI), 0-5.9 months] that was not significantly different from that of the patients without rupture (median 6.6 months; 95% CI, 4.0-9.1 months) (P = 0.4605). Among the ruptured group, the patients treated with surgical intervention survived longer than those receiving supportive care alone (median = 15.5 months; 95% CI, 8.7-22.2 months and median = 0.4 months; 95% CI, 0.2-0.5 months, P = 0.0027). The resectional and non-resectional surgical subgroups also had better survival than the supportive group (P = 0.0300 and P = 0.0209, respectively). In conclusion, surgical intervention, if applicable, should be performed in managing ruptured HCC.

Adolescent↗
PubMed1996

Telomerase activity in oral leukoplakia and head and neck squamous cell carcinoma.

The expression of telomerase, a ribonucleoprotein complex, is necessary to overcome cellular senescence, and it is associated with immortal cells and cancer. However, its role in precancerous lesions such as oral leukoplakias is less known. The purpose of this study is to investigate the presence of telomerase activity in oral leukoplakia and the relationship between the enzyme and multistep tumorigenesis. Telomerase activity was detectable in 14 of 16 human head and neck squamous cell carcinomas and 10 of 26 oral leukoplakia tissues. We also showed that the expression of telomerase in the premalignant lesions was associated with phenotypic progression, the degree of dysplasia. These results indicate that telomerase is activated frequently during the late stage of oral premalignancy and may play a crucial role in head and neck squamous cell carcinogenesis.

Adult↗
PubMed1996

Value of radioimmunoscintigraphy with technetium-99m labelled anti-CEA monoclonal antibody (BW431/26) in the detection of colorectal cancer.

This study was undertaken as part of a Coordinated Research Programme initiated by the International Atomic Energy Agency to evaluate the usefulness of radioimmunoscintigraphy (RIS) in the management of patients with colorectal cancer. Technetium-99m labelled BW431/26, a monoclonal antibody against carcinoembryonic antigen (CEA), was used. The study included 73 patients (31 females and 42 males). Sixty-eight patients were suspected of having recurrent colorectal adenocarcinoma while another five were suspected to have primary colorectal cancer. Images were acquired at 10 min and 4 and 24 h following the injection of radioantibody. The efficacy of RIS in tumour detection was evaluated by the findings at surgery, histological investigation and/or other diagnostic modalities and clinical follow-up. Four of five patients with suspected primary colorectal cancer gave true-positive results (three at primary sites, one at the site of a metastatic lesion) while one was false-positive. The overall accuracy of RIS in the diagnosis of recurrent colorectal cancer was 87%. Its sensitivity in the detection of locoregional or abdominal recurrence and liver metastases was 97% and 89% respectively. RIS was more accurate than computed tomography (CT) scan in the detection of pelvic recurrence and liver metastases while CT scan was far superior to RIS in detecting lung metastases. RIS proved most useful in patents who had rising CEA levels on clinical follow-up but in whom other work-up, including CT scan, was negative. The advantages of RIS include the ability to detect tumour recurrence prior to other investigations and to identify tumour recurrence in areas such as the pelvis, where CT and magnetic resonance imaging have their greatest weaknesses in diagnosing recurrent disease. The imaging accuracy is significantly increased when combined CT and antibody imaging is performed.

Adenocarcinoma↗
PubMed1996

Chemoprevention of head and neck cancer.

Tobacco-related upper aerodigestive tract cancer is a worldwide health problem. Clinical advances in surgery, radiation, and chemotherapy have shown only marginal improvement on the survival rate of these malignancies in the past two decades. The concept of multistage carcinogenesis and field cancerization, the high incidence of SPTs, and the promising results of chemopreventive agents especially 13 cRA to effectively reverse oral premalignancy and prevent SPTs indicate a new avenue to improve the outcome of these newplastic diseases. The study of second primary tumor prevention is too early to show any survival benefit in the treatment arm and toxicity of high dose 13 cRA is significant. The current prospective large scale phase III SPT prevention trial of low-dose 3 cRA may establish a new standard approach for the control of head and neck neoplasms. Identification of potentially useful panels of biomarkers as intermediate endpoints will undoubtedly reduce time and cost currently required to conduct chemoprevention trials.

Anticarcinogenic Agents↗
PubMed1996

In situ hybridization: a new tool in molecular medicine.

In situ hybridization (ISH) is a molecular technique that been used over three decades to detect specific nucleic acid sequences of gene expression at the cellular level. It is a morphologic method of localizing specific DNA or RNA sequences in the individual cell. The technique can be applied to cells frozen or fixed tissues or whole organisms and cytologic preparations; various types of probes can be utilized and the reaction can be visualized by autoradiography using isotopic markers or by colorimetric methods using fluorochromes or enzymes. It has been used primarily for localization of DNA sequences and applied recently to the localization of viral DNA sequences which provides insight into the pathology of viral infection and is enabling the diagnosis of viral infection. Analysis of gene expression by in situ hybridization messenger RNA (mRNA) is a crucial step towards understanding gene function and biology at molecular level. Nowadays, ISH is applied in three major categories: 1) infectious disease 2.) cytogenetics and 3.) gene expression. This technique has undoubtedly become a powerful new tool for molecular diagnostic techniques and is increasingly important in several areas of molecular medicine.

Genetics, Medical↗
PubMed1996

Molecular biology of head and neck tumorigenesis: the role of p53 expression and genetic instability.

Head and neck cancers progress as multistep tumorigenesis through accumulation of genetic instability. The p53 tumor-suppressor gene encodes a cell-cycle checkpoint protein that functions in the G1 phase of the cell cycle. When DNA damage is incurred, p53 transactivates a number of downstream genes whose products, with diverse biologic activities, contribute to the cellular response to DNA damage. One major p53-mediated function in response to DNA damage is to induce the G1 cell-cycle arrest, or delay, which probably allows time for the cell to repair DNA damage prior to S-phase entry. In cell lacking of p53 function, a condition of genetic instability results from checkpoint loss (Fig. 4.). These events occur early from ANL to SCC and increase gradually through multistep tumorigenesis. Due to the potential role of p53 expression and genetic instability, both might be useful biomarkers in assessing the risk of head and neck tumorigenesis.

Animals↗
PubMed1996

Genetic instability and the development of recurrence of primary tumor and second primary tumor during head and neck tumorigenesis.

To determine whether the degree of genetic instability is associated with the development of recurrence of primary tumor (RPT) and second primary tumor (SPT), we examined 46 cases of head and neck squamous cell carcinomas (HNSCC) by nonisotopic in situ hybridization using chromosome specific DNA probes for chromosome 9 and 17. Forty-six cases were classified into three groups; group I, 15 cases without developing RPT and SPT; group II, 21 cases with RPT, and group III, 10 cases with SPT. We demonstrated the statistical significant increment of genetic instability in terms of normalized chromosome index (NCI) and polysomy index (PI) of chromosome 9 and 17 from normal adjacent to malignant lesions (ANL), to hyperplasia (HYP), to dysplasia (DYP), to squamous cell carcinomas (SCC). Our results demonstrated the trend of increased chromosome indices as the tissue progressed from ANL to SCC in group II over group I. However, when we compared the genetic instability between group I and the specimens from the patients who developed RPT within 6 months (group III), we found the significant increment of PI of both chromosome 9 (0.84 +/- 0.54 vs 1.25 +/- 0.46, p = 0.10) and 17 (1.02 +/- 0.62 vs 1.89 +/- 0.87, p = 0.06) on ANL in the later group. Our results also demonstrated the higher trend of genetic instability on ANL in group III over group I as shown by the statistical significance of NCI of both chromosome 9 (0.98 +/- 0.12 vs 1.06 +/- 0.02, p = 0.05) and 17 (1.02 +/- 0.09 vs 1.10 +/- 0.05, p = 0.05). These results suggested that the degree of genetic instability might be used as a potential molecular marker for the risk assessment of early RPT and SPT development during head and neck tumorigenesis.

Adult↗
PubMed1996

Genetic instabilities of chromosome 9, 17 and accumulation of p53 overexpression during multistage tumorigesis in head and neck cancer.

Malignant transformation and tumor progression are currently thought to be the result of the accumulation of genetic alterations in critical genes, the proto-oncogenes and the tumor suppressor genes. Among the tumor suppressor genes, the p53 tumor suppressor gene mutations are the most prevalent. In order to determine genetic instability and p53 expression, we analyzed the genetic changes of chromosome 9 and 17 by non-isotopic in situ hybridization in formalin-fixed, paraffin embedded tissues and calculated for normalized chromosome index (NCI) and polysomy index (PI), and the expression of p53 by using immunohistochemistry (IHC). The means of chromosome 9 and 17 NCI were found to increase gradually as the tissues progressed from normal to squamous cell carcinoma; 1.02 and 1.03, respectively, in normal adjacent tissue (ANL), 1.19 and 1.20 in hyperplasia (HYP), 1.28 and 1.31 in mild dysplasia (MD), 1.38 and 1.43 in moderate dysplasia (ModD), 1.39 and 1.66 in severe dysplasia/carcinoma in situ (SD/CIS), and 1.65 and 1.83 in squamous cell carcinoma (SCC). Moreover, the PI 9 and 17 means also increased as the tissues passed from histologically normal epithelium to HYP to dysplasia (DYP) to cancer. In ANL, PI 9 and 17 means were 0.90 and 1.53 percent, compared to 3.78 and 3.38 percent in HYP, 3.73 and 5.12 percent in MD, 5.66 and 8.47 percent in ModD, 13.56 and 20.99 percent in SD/CIS, and 17.74 and 22.50 percent in SCC. Interestingly, p53 expression also increased continuously, not only in amount but also in the incidence of its expression, as the tissues progressed from normal to cancer, 2.29 percent in ANL, 4.65 percent in HYP, 9.09 per cent in MD, 9.58 per cent in ModD, 29 percent in SD/CIS, and 38.67 per cent in SCC in the amount; and 3 of 33 (9%) in ANL, 6 of 37 (16%) in HYP, 5 of 21 (24%) in MD, 3 of 12 (25%) in ModD, 8 of 18 (44%) in SD/CIS, and 24 of 49 (49%) in SCC in the incidence. Our studies demonstrated that genetic instability and p35 expression occurred very early from ANL to SCC and increased gradually through HYP, DYP, to SCC in head and neck cancer. The genetic instability and the loss of normal p53 function play the potential role in multistep tumorigenesis in head and neck cancer and might be the useful biomarkers in assessing the risk of tumor development.

Carcinoma, Squamous Cell↗
PubMed1996

Leukocyte alkaline phosphatase activity and peripheral changes of granulocyte following administration of granulocyte colony-stimulating factor.

The rhG-CSF had specificity of stimulation proliferation and differentiation of the neutrophil lineage in which there was an increase of younger stages, the earliest was myelocyte, of granulocyte in circulation. The effect of it was demonstrated within 24 hours of administration and reduced immediately after withdrawal. LAP activity in this condition was normal. The pattern of hematologic change in this condition may mimic CML and leukemoid reaction. It differed clearly from CML, since LAP activity in CML was lower than normal, but LAP activity could not define it from leukemoid reaction. The detection of young cells in peripheral blood through automated measurement of nuclear density by TechniconH*1 was observed for the high sensitivity (100%) and low specificity (54.8%). Furthermore, the study of cell kinetic in bone marrow should be evaluated to complete the cell kinetic effect of rhG-CSF and give a better evaluation for the H*1 blast flag.

Aged↗
PubMed1995

CA 50: a tumor marker for gastrointestinal malignancies.

Efforts to find the ideal tumor marker, together with the advanced knowledge of the carbohydrate expression by cancer and the development of monoclonal antibody technology have facilitated the generation of many new tests used in clinical oncology. CA 50, a novel cancer-associated carbohydrate marker, is detected by the C 50 antibody that has been obtained by immunization of mice with a human colorectal adenocarcinoma cell line. This antibody that defines CA 50 reacts with both the afucosyl form of sialylated Lewis(a) carbohydrate moiety and sialylated Lewis(a) moiety which is also the antigenic epitope in the CA 19-9 assay. CA 50 is not organ-specific and its elevated levels in serum can be observed in a variety of malignancies, especially gastrointestinal cancers. In contrast to CA 19-9, high CA 50 levels can also be seen in malignant tumors outside the digestive tract. The expectation, that CA 50 might be positive in the Lewis negative patients who cannot synthesize CA 19-9, is supported by the histoimmunologic study. However, in serum determination close correlation between CA 50 and CA 19-9 has been observed even in patients who have Lewis negative phenotype. In clinical application, CA 50 is marginally beneficial for the diagnosis, but very useful for the follow-up of patients with pancreatic cancers. It gives results rather similar to CA 19-9. Moderately high serum levels of CA 50 can also be seen in benign hepatobiliary diseases, especially in jaundice cases. Therefore, this should be considered in order to obtain the most advantage of the marker. For other gastrointestinal cancers, CA 50 in combination with other previously defined markers may give additional information for the evaluation of some patients with colorectal, biliary, or gastric cancers. At present, there are many new emerging tumor markers used in clinical oncology. Increasing our knowledge about these markers, their capabilities and limitations will enable us to use them effectively in the evaluation of cancer patients.

Antigens, Tumor-Associated, Carbohydrate↗