Biomedical subjects

Shou-Tung Chen

Publications and source records attributed to Shou-Tung Chen.

At least 19 recordsLinked to original sources

PubMed2007

Breast cancer risk associated with genotypic polymorphism of the mitotic checkpoint genes: a multigenic study on cancer susceptibility.

Aneuploidy occurs early during tumorigenesis and may contribute to tumor formation. Tumor cells become aneuploid as a result of aberrant mitotic divisions, suggesting a tumorigenic contribution of the mechanisms in maintaining chromosomal number stability. We therefore speculated that the genes TTK, MAD2L1, BUB1, BUB1B and PTTG1 (Securin), jointly implicated in the regulation of mitotic checkpoint, might be associated with breast tumorigenesis. To test this hypothesis, this case-control study of 698 primary breast cancer patients and 1492 healthy controls examined single-nucleotide polymorphisms (SNPs) in these mitotic checkpoint genes to define their tumorigenic contribution. Because estrogen is known to promote breast cancer development via its mitogenic effect leading to malignant proliferation of breast epithelium and the mitotic checkpoint genes are involved in regulating mitosis, we were also interested in knowing whether any association between genotypes and breast cancer risk was modified by reproductive risk factors. Support for these hypotheses came from the observations that (i) two SNPs in TTK and PTTG1 were associated with breast cancer risk; (ii) haplotype and haplotype combination analyses in TTK, BUB1B and PTTG1 revealed a strong association with breast cancer risk; (iii) a trend to an increased risk of breast cancer was found in women harboring a greater number of putative high-risk genotypes/haplotypes of mitotic checkpoint genes and (iv) a significant interaction between high-risk genotypes/haplotypes and reproductive risk factors in determining breast cancer risk was defined. This study provides new support for the mutator role of mitotic checkpoint genes in breast cancer development, suggesting that breast cancer could be driven by genomic instability associated with variant mitotic checkpoint genes, the tumorigenic contribution of which could be enhanced as a result of increased mitosis due to estrogen exposure.

Adult↗

PubMed2006

Breast cancer risk associated with genotypic polymorphism of the genes involved in the estrogen-receptor-signaling pathway: a multigenic study on cancer susceptibility.

The reproductive hormone, estrogen, contributes to the development of breast cancer by binding to the estrogen receptor (ER) in the nucleus, triggering cell growth and tumor promotion. In addition to its role in regulating target genes and signaling pathways involved in cell cycle progression, the ER-signaling pathway may regulate the expression of chromatin-remodeling gene, Metastasis-associated 3 (MTA3), or interact with chromatin-remodeling protein, Metastasis-associated 1 (MTA1). The invasion-suppressor gene, E-Cadherin (E-Cad), has recently been identified as a downstream target gene regulated by the ER-MTA3 pathway via the transcriptional repressor, Snail, and the ER-MTA3-Snail-E-Cad pathway has therefore been evoked to explain the clinical observation that ER expression in breast cancer is generally associated with a better clinical outcome. Since E-Cad may play an initiating role during breast tumorigenesis, we hypothesized that this ER-signaling pathway may also determine susceptibility to breast cancer, and examined this in a multigenic case-control study of 468 incident breast cancer patients and 470 healthy controls by genotyping the single nucleotide polymorphisms (SNPs) in five genes (ER, MTA3, Snail, E-Cad, and MTA1) in the ER-signaling pathways. Support for this hypothesis came from the observations that (a) with the exception of Snail, which interacted differently with reproductive risk factors in relation to breast cancer risk, there was a joint effect of the SNPs of these genes and estrogen-related risk factors (age at first full-term pregnancy and obesity, measured by the body mass index) on breast cancer risk (p < 0.05); (b) a trend toward increased risk of developing breast cancer was seen in women harboring a greater number of putative high-risk genotypes of these genes in ER-signaling pathways; (c) this association between risk and the number of putative high-risk genotypes was stronger and more significant in women thought to have experienced higher estrogen level, i.e., obese women; and (d) the risk effect conferred by obesity was only significant in women with a higher number of putative high-risk genotypes of the ER-signaling genes. These epidemiological findings highlight the role of newly identified novel ER-related pathways in breast cancer development and provide a more comprehensive picture of the tumorigenic effect of estrogen in breast cancer development.

Breast Neoplasms↗

PubMed2006

Evolution of breast cancer screening in countries with intermediate and increasing incidence of breast cancer.

BACKGROUND: Few studies have been published regarding the practice of breast cancer screening in Asian countries. AIMS: The present study illustrates how the health policy for breast cancer screening has evolved in Taiwan from selective mammographic screening within a high-risk group, firstly to a programme of physical examination by public health nurses, and finally to a two-stage breast cancer screening programme, with a risk assessment followed by mammography for those at moderate to high risk. DATA SOURCES: Breast cancer screening has evolved from 1995 to 2004 in Taiwan in three stages: (1) selective screening for breast cancer with mammography, ultrasound and physical examination only in first-degree relatives of breast cancer cases (1995-1998); (2) a programme of mass screening (1999-2001) with physical examination by public health nurses; and (3) two-stage breast cancer screening with a risk factor questionnaire and mammography for those deemed at moderate-to-high risk (2002-2004). The questionnaire was based on significant risk factors in a previous epidemiological study, in conjunction with the physical examination programme, a risk score was constructed from the logistic regression coefficients from the previous study, and women with a score above the median in the previous epidemiological study were assigned to mammography. RESULTS: Two-stage mammography screening had the most favourable results compared with the two previous screening regimes. It had a positive predictive value of recall after mammography of 14%, compared with 8% for selective screening and 2% for physical examination. Of screen-detected cancers in the two-stage programme, 71% were either ductal carcinoma in situ or stage T1, compared with 61% for selective screening and 60% for physical examination. The area under the receiver operating characteristic curve was 71% for the two-stage programme. CONCLUSIONS: For a low- to medium-risk country such as Taiwan, two-stage screening has acceptable parameters of recall and cancer detection, and compares well with other screening strategies.

Aged↗

PubMed2005

Breast cancer risk associated with genotypic polymorphism of the mitosis-regulating gene Aurora-A/STK15/BTAK.

Aneuploidy, an abnormal number of chromosomes, is relatively common and occurs early in breast cancer development. This observation supports a breast tumorigenic contribution of mechanisms responsible for maintaining chromosome number stability in which centrosomes play an essential role. We therefore speculated that the Aurora-A/STK15/BTAK gene, implicated in the regulation of centrosome duplication, may be associated with breast tumorigenesis. To test this hypothesis, we conducted a case-control study of 709 primary breast cancer patients and 1,972 healthy controls, examining single-nucleotide polymorphisms (SNPs), including a suggested functional Phe31Ile SNP, in Aurora-A. We were also interested in knowing whether any association between Aurora-A and breast cancer was modified by reproductive risk factors reflecting susceptibility to estrogen exposure. Our hypothesis is that, since estrogen is known to promote breast cancer development via its mitogenic effect leading to malignant proliferation on breast epithelium and since Aurora-A is involved in regulating mitosis, the discovery of a joint effect between the Aurora-A genotype and reproductive risk factors on cancer risk might yield valuable clues to the association of breast tumorigenesis with estrogen. Support for this hypothesis came from the following observations. (i) Two SNPs in Aurora-A were significantly associated with breast cancer risk (p < 0.05). (ii) Haplotype analyses, based on different combinations of multiple SNPs in Aurora-A, revealed a strong association with breast cancer risk; interestingly, the genotypic distribution of the suggested functional Phe31Ile SNP was not significantly different between breast cancer patients and controls, but the specific haplotype containing the putative at-risk Ile allele was more common in patients. (iii) This association between risk and putative high-risk genotypes was stronger and more significant in women thought to be more susceptible to estrogen, i.e., those with a longer interval between menarche and first full-term pregnancy. (iv) The protective effect conferred by a history of full-term pregnancy was significant only in women with a putative low-risk genotype of Aurora-A. Our study provides new findings supporting the mutator role of Aurora-A in breast cancer development, suggesting that breast cancer could be driven by genomic instability associated with variant Aurora-A, the tumorigenic contribution of which could be enhanced as a result of increased mitosis due to estrogen exposure.

Aurora Kinase A↗

PubMed2005

Deregulated expression of the PER1, PER2 and PER3 genes in breast cancers.

Disruption of circadian rhythm may be a risk factor in the development of breast cancer, but molecular changes in circadian rhythm controlled genes in breast cancer cells are still unexplored. We used immunohistochemical staining, methylation specific PCR and direct sequencing methods to analyze molecular changes in three most important genes, namely PER1, PER2 and PER3, in circadian rhythm in 55 cases of breast cancer of Taiwanese women. Our results reveal disturbances in the expression of the three period (PER) genes in most (>95%) of the breast cancerous cells in comparison with the nearby non-cancerous cells. The PER gene deregulation is not caused by genetic mutations but most probably by methylation of the PER1 or PER2 promoter. Methylation of the PER gene promoters has a strong correlation with c-erbB2 expression (P = 0.017). Since the circadian clock controls expression of cell-cycle related genes, we suggest that disturbances in PER gene expression may result in disruption of the control of the normal circadian clock, thus benefiting the survival of cancer cells and promoting carcinogenesis. Differential expression of circadian genes in non-cancerous and cancerous cells may provide a molecular basis for chronotherapy of breast cancer.

Adult↗

PubMed2005

Breast cancer risk associated with genotype polymorphism of the catechol estrogen-metabolizing genes: a multigenic study on cancer susceptibility.

Estrogen has been suggested to trigger breast cancer development via an initiating mechanism involving its metabolite, catechol estrogen (CE). To examine this hypothesis, we carried out a multigenic case-control study of 469 incident breast cancer patients and 740 healthy controls to define the role of important genes involved in the different metabolic steps that protect against the potentially harmful effects of CE metabolism. We studied the 3 genes involved in CE detoxification by conjugation reactions involving methylation (catechol-O-methyltransferase, COMT), sulfation (sulfotransferase 1A1, SULT1A1), or glucuronidation (UDP-glucuronosyltransferase 1A1, UGT1A1), one (manganese superoxide dismutase, MnSOD) involved in protection against reactive oxidative species-mediated oxidation during the conversion of CE-semiquinone (CE-SQ) to CE-quinone (CE-Q), and 2 of the glutathione S-transferase superfamily, GSTM1 and GSTT1, involved in CE-Q metabolism. Support for this hypothesis came from the observations that (i) there was a trend toward an increased risk of breast cancer in women harboring a greater number of putative high-risk genotypes of these genes (p < 0.05); (ii) this association was stronger and more significant in those women who were more susceptible to estrogen [no history of pregnancy or older (> or =26 years) at first full-term pregnancy (FFTP)]; and (iii) the risks associated with having one or more high-risk genotypes were not the same in women having experienced different menarche-to-FFTP intervals, being more significant in women having been exposed to estrogen for a longer period (> or =12 years) before FFTP. Furthermore, because CE-Q can attack DNA, leading to the formation of double-strand breaks (DSB), we examined whether the relationship between cancer risk and the genotypic polymorphism of CE-metabolizing genes was modified by the genotypes of DSB repair genes, and found that a joint effect of CE-metabolizing genes and one of the two DSB repair pathways, the homologous recombination pathway, was significantly associated with breast cancer development. Based on comprehensive CE metabolizing gene profiles, our study provides support to the hypotheses that breast cancer can be initiated by estrogen exposure and that increased estrogen exposure confers a higher risk of breast cancer by causing DSB to DNA.

Adult↗

PubMed2005

3-D ultrasound texture classification using run difference matrix.

Ultrasonography is one of the most useful diagnostic tools for human soft tissue and it is in routine use in nearly all hospitals and many physicians' offices and clinics. However, the diagnosis mostly depends upon the personal experiences of the physicians. Moreover, the surface features and internal architecture of a tumor are not easy to be demonstrated simultaneously using the conventional two-dimensional (2-D) ultrasound. Recently, three-dimensional (3-D) ultrasound has been developed and allows the physician to view the 3-D anatomy. 3-D breast US can provide transverse, longitudinal planes as well as in addition simultaneously the coronal plane. This additional information has been proved to be helpful for clinical applications. In this paper, a new approach of texture classification of 3-D ultrasound breast diagnosis using run difference matrix with neural networks is developed. The test 3-D US image database includes 54 malignant and 161 benign tumors. In the experiments, the area index A(z) under the ROC curve of the proposal 3-D RDM method can achieve 0.9680. The accuracy, sensitivity, specificity, positive predictive value and negative predictive value of the proposed 3-D RDM method is 91.9%(148/161), 88.9%(48/54), 93.5%(100/107), 87.3%(48/55), and 94.3%(100/105), respectively.

Area Under Curve↗

PubMed2004

Breast cancer risk and the DNA double-strand break end-joining capacity of nonhomologous end-joining genes are affected by BRCA1.

A tumorigenic role of the nonhomologous end-joining (NHEJ) pathway for the repair of DNA double-strand breaks (DSBs) has been suggested by the finding of a significant association between increased breast cancer risk and a cooperative effect of single nucleotide polymorphisms (SNPs) in NHEJ genes. However, the lack of an association between hereditary breast cancer and defective NHEJ genes prevents conclusions from being drawn about a link between NHEJ and breast cancer development. Recently, BRCA1-deficient mouse embryonic fibroblasts were found to have significantly reduced NHEJ activity, suggesting an accessory role of BRCA1 in NHEJ. The present study was performed to confirm this observation in human breast cancer cell lines and to examine whether the interaction between BRCA1 and NHEJ was of tumorigenic significance. Support for this hypothesis came from the findings that (a) a case-control study (469 breast cancer patients and 740 healthy controls) showed that the breast cancer risk associated with high-risk genotypes of NHEJ genes was significantly modified by the BRCA1 genotype. A significant increase in the cancer risk associated either with harboring one additional putative high-risk NHEJ genotype or with the joint effect of having reproductive risk factors (reflected by an interval of > or =12 years between menarche and first full-term pregnancy) and a higher number of high-risk genotypes of the NHEJ genes was only seen in women with at least one variant BRCA1 allele (i.e., the Glu/Gly or Gly/Gly forms of BRCA1 Glu(1038)Gly); and (b) a phenotype-based study measuring in vitro and in vivo NHEJ capacity showed that the precise end-joining capacity was different in breast cancer cell lines with different BRCA1 statuses being higher in BRCA1-expressing MCF-7 cells than in HCC1937 cells (defective BRCA1 expression). Furthermore, this end-joining capacity was decreased in MCF-7 cells in which BRCA1 expression was blocked using small interfering RNA and increased in HCC1937 transfected with full-length BRCA1. Because BRCA1 is a well-documented breast cancer susceptibility gene, this association between NHEJ and BRCA1 not only suggests a role of BRCA1 in NHEJ but also provides essential support for the tumorigenic contribution of NHEJ in breast cancer development.

BRCA1 Protein↗

PubMed2004

Promoter CpG methylation of tumor suppressor genes in colorectal cancer and its relationship to clinical features.

Aberrant promoter methylation of CpG islands of tumor suppressor genes inhibits expression of the genes and may lead to tumorigenesis. We investigated the aberrant methylation profile of potential tumor suppressor genes of p15, p16, SOCS-1, and Wnt signaling pathway in colorectal cancers and correlated the data with clinical findings. Cancerous and nearby non-cancerous tissues of 185 sporadic colorectal cancer samples were studied. Methylation specific PCR was performed to explore the mechanism of inactivation in p15, p16, SOCS-1, E-cadherin, APC, GSK-3beta, and Axin1 genes. Aberrant promoter methylation in p15, p16, SOCS-1, E-cadherin, APC, GSK-3beta, and Axin1 genes were 5.9, 7.0, 3.8, 5.9, 12.4, 2.2, and 0% for cancerous tissues, respectively, whereas the frequencies were 3.8, 0, 0, 7.0, 2.7, 0.5, and 0% for nearby non-cancerous tissues, respectively. The frequency of aberrant promoter methylation of cancerous tissues was significant higher than non-cancerous tissues in p16, SOCS-1, and APC genes (p<0.05) and methylation status of these genes had no clear relationship with clinical parameters. Of the 66 patients who showed at least one aberrant promoter methylation in the tumor-suppressor genes, 5 (7.6%) patients demonstrated multiple methylation phenotype (methylation > or =3) and associated with increased lymph node metastasis (p=0.036). Our findings suggest that inactivation of some tumor suppressor genes through aberrant promoter methylation of CpG islands may play a role in the development of colorectal cancer and methylation inactivation of these genes except p16 and SOCS1 may occur at the precancerous stage. Multiple methylation pathways may be involved in the tumorigenesis of colorectal cancer and associated with aggressiveness of clinical disease.

Base Sequence↗

PubMed2004

Complex decongestive physiotherapy for patients with chronic cancer-associated lymphedema.

BACKGROUND AND PURPOSE: Lymphedema of the limbs after cancer therapy is the most common cause of lymphedema in developed countries. There is no cure for chronic cancer-associated lymphedema. Multidisciplinary complex decongestive physiotherapy (CDP) is commonly used as a primary treatment. This prospective study assessed the efficacy of intensive CDP treatment in chronic cancer-associated lymphedema. METHODS: Thirty women who had unilateral upper or lower limb chronic lymphedema after breast or pelvic cancer therapy were enrolled in the study. All patients received CDP once per day, in consecutive full treatment sessions, which took place between 4 and 21 times. Assessment of the results of therapy included measuring the circumference, calculated volume, and edema ratio (excess volume/unaffected side volume) of the limb volume. The main outcome measure was the percentage reduction in excess limb volume. RESULTS: The pretreatment edema ratio demonstrated a high correlation with the patient's age (r = 0.508, p = 0.004) and the duration of the lymphedema (r = 0.634, p < 0.000). After the intensive CDP, the limb circumference, calculated volume, and edema ratio were significantly reduced compared with their pretreatment values (p < 0.000). The mean percentage reduction of excess volume was 67.8 +/- 33.2% in all patients. CONCLUSIONS: Intensive CDP was effectively able to reduce the limb volume of patients with chronic cancer-associated lymphedema. Further follow-up study is needed to confirm the effectiveness of CDP in the maintenance phase, and its long-term effectiveness in Taiwanese.

Adult↗

PubMed2004

Mutational, epigenetic and expressional analyses of caveolin-1 gene in breast cancers.

Caveolin-1, an integral membrane protein of caveolae found in many cell types, has been suggested as a candidate tumor suppressor. However, the mechanism underlying caveolin-1 decreased expression is not fully understood. The purpose of this study is to investigate the role of aberrant promoter methylation in the regulation of caveolin-1 gene in breast cancer correlated with clinical findings. We used methylation specific PCR, direct sequencing and immunohistochemistry stain methods to explore the role of caveolin-1 gene in the development of breast cancer. We demonstrated that 14 of 55 cases (25.5%) and 4 of 55 cases (7.3%) had methylated CpG-island on caveolin-1 promoter in cancerous and non-cancerous cells, respectively. The frequency of aberrant promoter methylation of breast cancer tissues was significant higher than non-cancerous tissues (p<0.05). There were four types of methylation pattern of caveolin-1 gene in the breast cancer tissues. No mutation but one polymorphism GAC right curved arrow GAT at codon 82 was found in the whole exonic sequences of caveolin-1 gene. The methylation status of caveolin-1 gene had no clear relationship with age, cell grade, stage of tumor, and status of estrogen receptor, p53 and c-erbB2 in the breast cancer tissues. However, in breast tissue with aberrant promoter methylation of caveolin-1 gene, the presence of progesterone receptor showed borderline statistic difference compared to unmethylated promoter (p=0.11). Immunohistochemistry demonstrated that expression of caveolin-1 gene correlated with aberrant promoter methylation status in sporadic breast cancer tissues. Our findings suggest that aberrant promoter methylation of caveolin-1 gene is associated with inactivation of expression. This process occurs in the precancerous stage and may play an important role in the development of breast cancer.

Base Sequence↗

PubMed2003

Mutational screening of breast cancer susceptibility gene 1 from early onset, bi-lateral, and familial breast cancer patients in Taiwan.

The BRCA1 gene has been shown to be strongly associated with the occurrence of familial breast cancer. The spectrum of BRCA1 gene mutations in breast cancer patients in various populations has been investigated. In this study, patients in Central Taiwan with breast cancer were screened for BRCA1 mutations by sequencing PCR products spanning the coding region and partial intronic regions of the BRCA1 gene. Twelve polymorphisms in four exons and three introns were found. One mutation was found in one patient with familial breast cancer. Two patients showed LOH at the locus of BRCA1. Also found in the Taiwanese population were two common haplotypes and one rare haplotype of BRCA1. These results suggest that the mutation of BRCA1 contributes little to the occurrence of breast cancer in the Taiwanese population.

Adult↗

PubMed2002

Sulfotransferase 1A2*2 is a risk factor for early-onset breast cancer.

The estrogen-signaling pathway plays an important role in the pathophysiology of breast cancer, and the sulfotransferase 1A (SULT1A) family has been found to be both downstream targets of tamoxifen and a risk factor of breast cancer. We have used PCR-RFLP and direct sequencing methods to determine SULT1A2 polymorphisms in 230 Taiwanese breast cancer patients. The results showed that the frequencies of SULT1A2*1 and SULT1A2*2 occurring were 94.8% and 5.2%, respectively. No SULT1A2*3 allele was found in these patients. In comparison with the frequency of healthy controls (96.0% and 4.0% for SULT1A2*1 and SULT1A2*2, respectively), the allelic frequencies of SULT1A2 polymorphisms in these patients were not statistically significant (p=0.398). However, the SULT1A2*2 allele seems to influence the age of onset among early-onset breast cancer patients (p=0.021, OR=2.74, 95%CI=1.13-6.65).

Adolescent↗

PubMedDate not supplied

Classification of breast ultrasound images using fractal feature.

Fractal analyses have been applied successfully for the image compression, texture analysis, and texture image segmentation. The fractal dimension could be used to quantify the texture information. In this study, the differences of gray value of neighboring pixels are used to estimate the fractal dimension of an ultrasound image of breast lesion by using the fractal Brownian motion. Furthermore, a computer-aided diagnosis (CAD) system based on the fractal analysis is proposed to classify the breast lesions into two classes: benign and malignant. To improve the classification performances, the ultrasound images are preprocessed by using morphology operations and histogram equalization. Finally, the k-means classification method is used to classify benign tumors from malignant ones. The US breast image databases include only histologically confirmed cases: 110 malignant and 140 benign tumors, which were recorded. All the digital images were obtained prior to biopsy using by an ATL HDI 3000 system. The receiver operator characteristic (ROC) area index AZ is 0.9218, which represents the diagnostic performance.

Adolescent↗

PubMedDate not supplied

Transparenchymal retraction maneuver: a simple technique in laparoscopic hepatectomy.

The performance of laparoscopic hepatectomy still presents technical problems. One of the main difficulties is the impossibility of directly grasping the liver during resection. To overcome this problem, we have begun using transparenchymal suture traction in laparoscopic hepatectomy. From January 2000 through August 2001, eight laparoscopic hepatectomies were performed using suture traction during parenchymal resection. The advantages of this technique include no leakage of pneumoperitoneum, no increased trocar hole, ability to repeat application to the liver from various directions, and better exposure of the transected line.

Hepatectomy↗

PubMedDate not supplied

Extrahepatic division of the right hepatic vein in right hepatectomy for blunt liver trauma.

During a 5-year period, 10 patients with right-side blunt liver injury received an anatomic liver resection, using the technique of extrahepatic right hepatic vein division before hepatectomy. Five patients required a right posterior sectionectomy and 5 patients needed a right hemihepatectomy. The mean operation time was 146 minutes and median perioperative blood transfusion was 21.5 units (range, 4-94 units, packed red blood cell (PRBC) or whole blood). There was one hospital mortality; the patient died from multiple organs failure on postoperative day 5. Postoperative complications occurred in 4 of 9 surviving patients. Liver-related morbidity occurred in 2 patients who required reoperation for evacuation of subphrenic hematoma. The median hospital stay was 17 days (range, 6-84 days). Application of extrahepatic division of the right hepatic vein during a right hepatectomy for blunt liver trauma has several advantages: compression of a traumatic liver during mobilization; shortening of the ischemia duration; complete mobilization of the liver before parenchymal resection; and prevention of oozing with easier approximation of the raw surface.

Adolescent↗

PubMedDate not supplied

An easier technique for minimally invasive video-assisted thyroidectomy.

Because of the efforts of many pioneer surgeons, the minimally invasive video-assisted thyroidectomy (MIVAT) has been recognized as a safe procedure, offering advantages such as better cosmetic outcome and less analgesic need. The MIVAT technique was described in 51 selected patients in 2001. The technique was not therefore widely used because of the excess operating time compared with traditional thyroidectomy, and most importantly, this method needed a steep learning period. This study reports a modified MIVAT procedure, which can make this operation easier and shorten the time of learning. We compared the outcomes of the originally described methods with our modified method. The selection criteria for performing MIVAT were as follows: thyroid nodules in one lobe and less than 50 mm on their largest diameter, benign lesion proved by fine-needle biopsy, patient without history of thyroiditis, and no previous neck surgery or irradiation. All patients received lobectomy. Sixty patients were eligible for MIVAT during a period of 27 months. The patients were divided into two groups. Group A consisted of the 17 patients who underwent MIVAT using the original technique that was described previously. Group B consisted of the 43 patients who underwent MIVAT using a self-designed Army retractor with a mosaic ring. The mean operation time of Group A was 120 minutes and that of Group B was 59.2 minutes. The size of the incisions was no difference in either group. There were no postoperative complications except in one patient with transient recurrent laryngeal nerve palsy in Group A. There was one conversion to open thyroidectomy in Group A and none in Group B. The cosmetic results were no different between the two groups. In conclusion, the use of a modified Army retractor with a mosaic ring made the MIVAT procedure easier and offered similar advantages.

Adolescent↗

PubMedDate not supplied

A 10-year experience of unsuspected gallbladder cancer after laparoscopic cholecystectomy.

Unsuspected gallbladder cancer after laparoscopic cholecystectomy (LC) is a cancer that was previously manipulated by laparoscopic technique. The reported incidence was 0.3-1% and became an emerging problem as the popularity of LC increased. Lack of reliable data could address the outcome of reresection or nonreresection patients and the standard management. This study reviewed a single center experience in managing unsuspected gallbladder cancer patients after LC between July 1, 1992 and July 1, 2000 who had at least 2 years of follow-up. There were 11 patients (0.6%) postoperatively diagnosed with gallbladder cancer after 1825 LCs. Group A included three patients (28%) with nontransmural invasion, group B included four patients (36%) who had transmural invasion without secondary surgical intervention, and group C included four patients (36%) with reresection. The perioperation parameters and strategies were collected and compared. A review of the literature was performed simultaneously, and we concluded that unsuspected gallbladder cancer with nontransmural invasion needs no further treatment; however, aggressive reresection is beneficial to transmural invasion cancer, and prevention of bile spillage during LC should be the goal of every surgeon.

Adult↗