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F S Liu

Publications and source records attributed to F S Liu.

At least 19 recordsLinked to original sources

Factors that affect recurrence after anterior colporrhaphy procedure reinforced with four-corner anchored polypropylene mesh.

The purpose of this study was to evaluate the effectiveness of the anterior colporrhaphy procedure reinforced with four-corner anchored polypropylene mesh in patients with severe (stage III or IV) anterior vaginal prolapse. Thirty-eight consecutive women were enlisted for this prospective study. The procedure consisted of an extensive vaginal dissection to join the vesicovaginal and retropubic space and an anchoring of a polypropylene mesh patch between the two Arcus Tendineus Fasciae Pelvis in a tension-free manner. The mean age of the study group was 63 (33-80) years. The success rate was 87% (33/38) at a mean follow-up interval of 21 (12-29) months. A total of eight (100%) patients were also cured of concomitant stress incontinence (five overt and three occult type) with an additional tension-free vaginal tape (TVT) operation. During follow-up, there were five de-novo stress incontinence cases (16.7%) and four vaginal erosions of mesh (10.5%). Four clinical variables--diabetes mellitus, recurrent anterior vaginal prolapse, chronic cough and vaginal erosions of mesh--were found to have a significant correlation with an unsatisfactory surgical result with large values of hazard ratios found by survival analysis. We concluded that the anterior colporrhaphy procedure reinforced with four-corner anchored polypropylene mesh was effective for most, but failed in some patients who had specific risk factors within short convalescence periods. Concomitant stress incontinence can be successfully treated by a TVT operation in combination with the anterior colporrhaphy procedure reinforced with four-corner anchored polypropylene mesh. However, the anterior colporrhaphy procedure may itself have adverse effects on urethral sphincter function.

Adult↗

Analysis of two sling procedures using polypropylene mesh for treatment of stress urinary incontinence.

OBJECTIVES: To evaluate and compare the surgical outcome between the innovative tension-free vaginal tape (TVT) and conventional pubovaginal sling (PVS) procedures using polypropylene mesh. METHODS: Eighty consecutive women with urodynamic stress urinary incontinence (SUI), who chose to undergo either a TVT (n=23) or a PVS (n=57) procedure using polypropylene mesh based on financial consideration, were recruited for this study. The surgical results were analyzed and compared subjectively and objectively. RESULTS: The mean follow-up interval was 23 months for the TVT and 20 months for the PVS procedure (P=0.062). Postoperatively, SUI (91.3% vs. 93.0%), concomitant urge symptoms (85.0% vs. 85.3%) and the negative impact of incontinence and urogenital distress on patients' quality of life (79.8% vs. 77.8%) (77.4% vs. 68.8%) had improved markedly. After a multivariable logistic regression analysis, the treatment outcome of SUI was found to be independent of the main effects of patient age, parity, concurrent gynecological surgeries, intrinsic sphincter deficiency, previous failed incontinence surgeries, and concomitant urge symptoms. However, it was significantly related to treatment procedures (TVT vs. PVS) and their interaction with patient body mass index (BMI). Based on the fitted logistic model, we see that TVT performs better than PVS when BMI is less than 27.27 kg/m2, and the advantage of TVT decreases as BMI increases. CONCLUSION: Both TVT and PVS procedures using polypropylene mesh are effective treatment modalities for female SUI. However, TVT was not as effective in treating overweight or obese women as PVS.

Adult↗

p53 mutation is infrequent in clear cell carcinoma of the ovary.

OBJECTIVE: p53 gene alteration has been extensively studied in epithelial ovarian cancer. However, its occurrence in clear cell carcinoma, an infrequent histologic subtype of epithelial ovarian cancer, is rarely reported. The aim of this study is to determine the status of p53 gene alteration in this distinct type of ovarian carcinoma. METHODS: Paraffin blocks of tumors from 38 patients with primary or recurrent ovarian clear cell carcinoma were studied for p53 alteration. All these tumors were subjected to immunohistochemical and molecular analysis. Two monoclonal antibodies (DO-7 and PAb 1801) were used for immunohistochemical staining. Genomic DNAs extracted from paraffin blocks of the 38 tumors were subscribed for a nested polymerase chain reaction/single-strand conformation polymorphism (PCR/SSCP) analysis. Tumors showing band shift on SSCP were further prepared for DNA sequencing to determine the site of mutation. RESULTS: Overexpression of p53 was observed in only one stage III clear cell carcinoma. However, focal positive p53 staining was noted in another five tumors. Of the six tumors showing positive immunohistochemistry, p53 alterations were noted in four tumors. Three tumors revealed a missense point mutation: two were in exon 7 (TCT(227) --> TTT and GGC(245) --> AGC) and one was in exon 5 (CGC(156) --> CAC). Another tumor revealed a 12-bp deletion in two possible ways: it might involve the last four codons at the 3' end of exon 4 (nucleotides 12,288-12,299) or it might cross over the splice junction between exon 4 and intron 4 (nucleotides 12,290-12,301). The former would result in a predicted protein product of 389 amino acids whereas the latter would cause a frameshift in the gene sequence and would result in a truncated protein. CONCLUSION: Mutations in p53 appear to be much less frequent in clear cell carcinoma than in other histologic types of epithelial ovarian cancer. We suggest that p53 alterations may not play an important role in the development of clear cell carcinoma.

Adenocarcinoma, Clear Cell↗

FHIT (fragile histidine triad) gene analysis in cervical intraepithelial neoplasia.

OBJECTIVE: Recently a candidate tumor suppressor gene, FHIT (fragile histidine triad), was identified at chromosome 3p14.2. Abnormality of this gene has been observed in a variety of human tumors. Although aberrant FHIT transcripts in a substantial percentage of cervical cancer cell lines and primary cervical tumors were also noted, some other studies revealed different results. Therefore, its association with the development of cervical cancer is still debatable. Because allelic loss in chromosome 3p is also a frequent finding in cervical intraepithelial neoplasia (CIN), we compared the transcription pattern and expression of FHIT in the preinvasive cervical lesions and normal cervical epithelia to investigate its possible role in cervical carcinogenesis. METHODS: Thirty-five consecutive CIN lesions taken from conization specimens and 33 normal cervical epithelial tissues taken from hysterectomy for benign diseases were included in this study. Total RNA was extracted from the pathology-confirmed tissue samples and first-strand cDNA was synthesized. It was amplified using a nested reverse transcription polymerase chain reaction (RT-PCR) method. The PCR products were then subjected to subcloned sequence analysis. Paraffin blocks from all of the samples were selected and prepared for immunohistochemical study with an anti-FHIT polyclonal antibody. RESULTS: All the cDNAs of CIN and normal cervical epithelial tissues showed the expected size of RT-PCR product. However, 7 of the 35 (20%) CIN lesions and 5 of the 33 (15%) normal cervical epithelia also presented aberrant transcripts in addition to the normal-sized transcript of FHIT. Deletion of the cDNA segment covering exon 4 to exon 8 was the most frequent finding in the cases that showed abnormal FHIT transcripts. FHIT protein was intermediately or strongly expressed in most of the CIN lesions and normal squamous epithelia. However, reduced or absent FHIT expression was observed heterogeneously in the 7 CIN lesions and 5 normal cervices in which aberrant FHIT transcripts were detected. CONCLUSION: Because the normal-sized FHIT transcript was present robustly in all of the CIN lesions and the abnormal FHIT transcripts occurred with similar frequency and pattern in the CIN lesions and normal cervical tissues, we suggest that abnormal FHIT transcription might not be causal in the early process of cervical carcinogenesis.

Acid Anhydride Hydrolases↗

KAI1 metastasis suppressor gene is frequently down-regulated in cervical carcinoma.

KAI1 is a metastasis suppressor gene located on human chromosome 11p11.2. It belongs to a structurally distinct family of cell surface glycoproteins. Decreased KAI1 expression has been observed in several common solid epithelial tumors, including prostatic, pancreatic, lung, hepatic, colorectal, ovarian, and esophageal cancers. A recent study also observed frequent loss of KAI1 expression in a number of squamous cell carcinomas of the cervix by immunohistochemical technique. To further confirm whether this gene is altered in this malignancy, we analyzed KAI1 expression in various stages of cervical carcinoma by a molecular method. Total cellular RNA was extracted from 84 primary invasive cervical carcinomas and 6 metastatic or recurrent lesions. cDNA was synthesized and was used for real-time quantitative polymerase chain reaction analysis. The level of KAI1 expression was obtained as the value of threshold cycle (Ct) and was quantitated with a comparative Ct method. In addition, paraffin blocks of the tumors were selected and prepared for immunohistochemical study with an anti-KAI1 polyclonal antibody, C-16. Both the real-time quantitative polymerase chain reaction method and immunohistochemical study revealed a frequent decrease in KAI1 expression in invasive cervical cancers and metastatic or recurrent lesions. However, the reduction in KAI1 was not related to progression of the disease. When tumor cell differentiation was analyzed, poorly differentiated tumors showed a greater decrease in KAI1 expression than well or moderately differentiated tumors (P < 0.001). Histologically, KAI1 loss was observed equally in both squamous cell carcinoma and adeno-/adenosquamous carcinoma. Since down-regulation of KAI1 occurs in both early and late stages of cervical cancer, we suggest that its involvement in the progression of this malignancy is an early event.

Adenocarcinoma↗

[Application of wide-bore capillary gas chromatography in the synthesis of special esters of methacrylic acid].

A simple, rapid and accurate method for separating and analysing components in the synthesis of special esters of methacrylic acid by gas chromatography is reported. An SE-54 wide-bore capillary column of 50 m x 0.53 mm i.d. x 0.6 microns was used. The esters include dimethylaminoethyl methacrylate(DMAM), n-butyl methacrylate(BMA) and ethylene glycol dimethacrylate(EGDMA). Crude materials such as methyl methacrylate(MMA) and N, N-dimethyl ethanol amine (DMEA) were also analysed. The recoveries were 99.71%-102.89%, and the RSDs of the main components were below 0.1%. The method can be used to control the production of the esters.

English Abstract↗

Frequent down-regulation and lack of mutation of the KAI1 metastasis suppressor gene in epithelial ovarian carcinoma.

OBJECTIVE: KAI1 is a recently identified metastasis suppressor gene on human chromosome 11p11.2. It belongs to a structurally distinct family of cell surface glycoproteins. Decreased KAI1 expression seems to be involved in the progression of human prostate, lung, pancreatic, and possibly breast cancer, and recently a reduced KAI1 protein expression has been demonstrated in several ovarian carcinoma cell lines. The aim of this study is to determine whether the KAI1 gene is altered in human epithelial ovarian carcinomas. In addition, its prognostic significance in this tumor is also evaluated. METHODS: To detect KAI1 expression, 102 tumor samples from benign, borderline, primary invasive, metastatic, and recurrent epithelial ovarian tumors were prepared for immunohistochemical study with C-16, an anti-KAI1 polyclonal antibody. In addition, cellular RNA from 24 primary invasive and 7 recurrent tumors was also analyzed for KAI1 expression by using a reverse transcriptase PCR (RT-PCR) technique. The PCR single-strand conformation polymorphism method and direct DNA sequencing were used to detect KAI1 mutation in the 44 primary invasive and 8 recurrent ovarian carcinomas. RESULTS: In immunohistochemical study, decrease of KAI1 protein expression was associated with the progression of ovarian tumor. However, it had no relation to the stage of primary invasive cancers because of its frequent occurrence in early stage tumors. KAI1 expression was also frequently down-regulated in primary invasive and recurrent tumors in RT-PCR analysis. Except for a missense change at codon 241 (ATC to GTC), which causes the substitution of a valine for an isoleucine in the amino acid sequence and occurs in both normal and tumor tissues, no mutation of the KAI1 gene was found in any of the 52 carcinomas. Although there was a trend for deteriorating survival from patients with KAI1-preserved tumors to those with KAI1-decreased and -negative tumors, statistically it was not significant (P = 0.079). CONCLUSION: KAI1 may play a role in the malignant progression of epithelial ovarian carcinoma through the down-regulation of expression rather than gene mutation. Since the decreased expression presented frequently in early stage tumors, it may be an early event in the progression of this tumor and its prognostic significance needs further investigation with a larger number of cases.

Adolescent↗

Predictive factors for residual disease in subsequent hysterectomy following conization for CIN III.

OBJECTIVE: The aim of this study was to determine predictive factors for post-cone residual disease in subsequent hysterectomy for CIN III. METHODS: From June 1994 to June 1999, 120 patients with CIN III who received hysterectomy within 6 months of conization regardless of marginal status were identified from 1450 conization cases. The demographic features and pathologic parameters were analyzed for the predictive rate of post-cone residual disease. RESULTS: Age >==50 years and parity >==5 were significant factors associated with residual disease. The incidence of residual disease was 56.5 and 29. 3% in patients >==50 and <50 years, respectively, and 61.8 and 36.0% in patients with parity >==5 and <5. Post-cone endocervical curettage (ECC) and multiple-quadrant disease were the only pathologic predictive factors identified. The incidence of residual disease was 64.6 and 29.2% in patients with positive ECC and negative ECC, respectively, and 48.4 and 25.9% in patient with multiple-quadrant disease and one- or two-quadrant disease. Other pathologic parameters, including endocervical margins, ectocervical margins, endocervical gland involvement, and depth of conization, were not predictive of residual disease. When ECC was combined individually with age, endocervical margins, or multiple-quadrant disease, there was no increase of positive predictive rate. CONCLUSIONS: (1) Age 50 years or more and parity >==5 were two demographic features that predicted post-cone residual disease. (2) ECC and multiple-quadrant disease were the only pathologic parameters that predicted post-cone residual disease. (3) With the appropriate application of the predictive factors, post-cone hysterectomy may be further decreased.

Adult↗

Ultrasonic diagnosis of ureteral injury after laparoscopically-assisted vaginal hysterectomy.

Ureteral injuries are uncommon but serious complications of laparoscopically-assisted vaginal hysterectomy. The ureter is particularly at risk for inadvertent injury when the cardinal-uterosacral ligament complex is coagulated and divided below the uterine vessels. We present two recent cases which describe the application of transabdominal ultrasound including color Doppler mapping in the diagnosis of ureteral injury after laparoscopically-assisted vaginal hysterectomy. Transabdominal ultrasound including color Doppler mapping has great diagnostic potential as a method for non-invasive evaluation of post-operative ureteral conditions. Ultrasonic triads (absence of a ureteric jet, ascites, and the presence or absence of hydronephrosis) are capable of differentiating diagnosis of complete, partial, or nonobstructive surgical ureteral injuries.

Adult↗

Expression and prognostic significance of proliferating cell nuclear antigen and Ki-67 in malignant ovarian germ cell tumors.

BACKGROUND: Both proliferating cell nuclear antigen (PCNA) and Ki-67 are proliferative markers known to correlate with the cell proliferative state. The aim of this study was to evaluate the usefulness of PCNA and Ki-67 immunoreactivity in the assessment of clinicopathologic features and prognosis in patients with malignant ovarian germ cell tumors. METHODS: Thirty-one patients with surgically resected malignant ovarian germ cell tumors were investigated. The clinicopathologic features and survival data of these patients were recorded. Immunohistochemical staining with monoclonal antibodies (PC 10 for PCNA, and MIB-1 for Ki-67) were performed on paraffin embedded tissue from each patient. The correlation of the immunoreactivity of these two markers with the clinicopathologic features and prognosis were studied. RESULTS: All of the tumors were positive for PCNA and Ki-67, but the intensity of expression varied widely. The immunoreactivity in each tumor was also heterogeneous. The scoring of PCNA and Ki-67 was determined by a semiquantitative method. Both advanced tumor stage (stages III and IV) and high PCNA score (scores 3 and 4) indicated a poorer prognosis for survival than did early stage (stages I and II) and a low PCNA score (scores 1 and 2) (p = 0.017 and p = 0.008, respectively). In addition, the proportion of tumor relapse and tumor-induced death was more accurately predicted by PCNA and Ki-67 scoring than by tumor staging (chi 2 = 0.3159, chi 2 = 0.7186 and chi 2 = 1.9689, respectively). CONCLUSIONS: PCNA and Ki-67 proliferative markers appear promising to differentiate patients into low- and high-risk groups. In the presence of a high PCNA or Ki-67 score, aggressive postoperative chemotherapy is warranted, even if the disease is in a very early stage.

Adolescent↗

Mutational analysis of the BRCA1 tumor suppressor gene in endometrial carcinoma.

OBJECTIVE: To investigate whether alteration of BRCA1 tumor suppressor gene occurs in sporadic endometrial carcinomas. METHODS: Genomic DNAs were prepared from 33 consecutively collected endometrial carcinoma tissues for BRCA1 mutational analysis. To screen for BRCA1 mutation, polymerase chain reaction (PCR) amplification and single strand conformation polymorphism (SSCP) technique were used with 41 overlapping PCR primer pairs for the 23 coding exons of BRCA1. Tumors that demonstrated SSCP variants were further subjected to direct DNA sequencing in the appropriate exons to identify the DNA alteration. RESULTS: In addition to detecting a previously described polymorphism in exon 11, single strand conformation polymorphism analysis of the 33 endometrial cancers identified 3 tumors with mobility shifts. Two tumors shifted in exon 3 and showed the same pattern of band shift. The other tumor shifted in exon 9. DNA sequencing revealed sequence alterations in the 3 tumors; all appeared heterozygous. In the 2 tumors shifted in exon 3, the sequence alteration caused no amino acid change and was consistent with an infrequent silent polymorphism. In the third tumor, a missense alteration at codon 191 was detected and was recognized as germline in origin. CONCLUSIONS: Because a normal allele of BRCA1 was retained in the tumor where a germline missense alteration was detected, the heterozygous DNA alteration should not be cancer predisposing in terms of the two-hit model for inactivation of the tumor suppressor gene. We conclude that mutation of BRCA1 may not be involved in the development of sporadic endometrial cancer.

DNA Mutational Analysis↗

Studies of esophageal balloon cytology in Linxian, China.

Esophageal cancer is the second leading cause of cancer death in China. Esophageal cancer has a very poor prognosis, principally because most tumors are asymptomatic until they are unresectable. Esophageal balloon cytology is an early detection method developed by Chinese scientists to identify resectable early cancers and precursor lesions. Previous studies have reported high sensitivities for detecting esophageal cancer in symptomatic patients. The current report describes several studies evaluating this diagnostic technique in asymptomatic individuals. A comparison of Chinese and U. S. cytological diagnoses of the same esophageal samples showed that the Chinese categories of precancerous neoplasia were more inclusive than the corresponding U. S. categories. Comparisons of both Chinese and U. S. cytological diagnoses with concurrent histological findings showed low (14-36%) sensitivities for the cytological detection of biopsy-proven cancers. Prospective follow-up studies of several screened cohorts showed a consistent progression of risk for developing esophageal cancer with increasing severity of initial cytological diagnosis. These preliminary studies suggest that esophageal balloon cytology is a useful technique that can benefit from additional research to improve its optimal performance.

Adult↗

Molecular genetic analysis of clear cell adenocarcinomas of the vagina and cervix associated and unassociated with diethylstilbestrol exposure in utero.

BACKGROUND: Prenatal exposure to the synthetic estrogen diethylstilbestrol (DES) is associated with the subsequent development of clear cell adenocarcinoma of the lower reproductive tract in young women, and data concerning the molecular genetic alterations involved in the etiology of this tumor type have not previously been reported. Such knowledge would be of potential value by providing insight into the molecular mechanisms of hormonal carcinogenesis in general, as well as by suggesting molecular markers for risk assessment in the estrogen-exposed population. METHODS: A total of 24 samples of clear cell adenocarcinoma of the vagina or cervix, 16 associated with exposure in utero to DES and 8 with no history of DES exposure, were obtained as archival fixed and embedded tissue specimens. DNA was purified from these tissues and used to examine a number of biologically plausible molecular genetic endpoints for tumor specific alterations. RESULTS: No evidence was found for mutations in the K-ras or H-ras protooncogenes, the Wilms' tumor (WT1) tumor suppressor gene, or the estrogen receptor gene. Sporadic overexpression of the p53 tumor suppressor gene was detected in some tumor cell nuclei by immunohistochemistry, but in the absence of detectable p53 gene mutation. Genetic instability as manifested by somatic mutation of microsatellite repeats was widespread in these tumors, with evidence of microsatellite instability in all DES-associated tumors examined, and in 50% of those tumors not associated with DES exposure. CONCLUSIONS: These data are consistent with the hypothesis that the induction of genomic instability may be an important mechanism of DES-induced carcinogenesis.

Adenocarcinoma, Clear Cell↗

Overexpression of p53 is not a feature of ovarian granulosa cell tumors.

The p53 tumor suppressor gene has been extensively studied in various human tumors including epithelial ovarian cancers. However, little is known about the expression of this gene in ovarian granulosa cell tumors, the most common histologic type of sex cord-stromal tumors. We investigated whether overexpression of the p53 gene product occurs in this specific ovarian tumor. Nineteen patients with ovarian granulosa cell tumors were recruited in this study. Immunohistochemical staining for the p53 protein with monoclonal antibody PAb 1801 was performed in the paraffin-embedded tissue of each case to screen for p53 overexpression. Among the 19 ovarian granulosa cell tumors, there was only one well-differentiated tumor found to have nuclear immunoreactivity in a small fraction of tumor cells. Polymerase chain reaction--single-stranded conformation polymorphism was used to study the tumor showing focal p53 positivity, but no mobility shift was noted from exon 4 through exon 9 of the p53 gene. On the basis of this observation, we propose that alteration of the p53 tumor suppressor gene is not a common finding in ovarian granulosa cell tumors.

Adolescent↗

High complete response rate of concomitant chemoradiotherapy for locally advanced squamous cell carcinoma of the uterine cervix.

A prospective study with a newly designed schedule of concomitant chemoradiotherapy was initiated for 42 patients with previously untreated squamous cell carcinoma of the uterine cervix. Their ages ranged from 34 to 77 years, median 57 years. There were 13 FIGO stage IIB, 1 IIIA, 27 IIIB, and 1 IVA. Radiotherapy was administered using 1.8 Gy/day, 5 days a week, to the whole pelvis (50.4 Gy/28 fractions) with local boost if indicated. Intracavitary brachytherapy of 5 Gy for five times was delivered after 1-2 weeks of rest. The first 21 patients received concomitant chemotherapy of biweekly PEB regimen (100 mg/m2 etoposide + 50 mg/m2 cisplatin + 50 mg/m2 bleomycin) for two to three cycles during external irradiation. The chemotherapy for the latter 21 patients was modified to weekly PEBF (50 mg/m2 etoposide + 20 mg/m2 cisplatin + 10 mg/m2 bleomycin + 800 mg/m2 5-FU, mixed in normal saline, 24-hr continuous iv infusion) for five to six cycles. All except 1 patient achieved complete response (97.6%) and sustain so after a median follow-up time of 30 months. There were three relapses--one with persistent pelvic disease and two with distant metastasis. Two-year overall survival and disease-free survival rates were 97.6 and 92.9%, respectively. Myelosuppression was moderate but fully recovered. Other acute toxicities were tolerated except for 1 patient who encountered grade IV radiation colitis with cecum perforation and required surgery. As to late morbidity, the incidence of radiation proctitis was high (21.4%) but of a mild degree, with 1 patient needing repeated transfusion. One patient developed chronic cystitis with an acontractile bladder. Our preliminary results show that concomitant chemoradiotherapy for advanced cervical carcinoma is both feasible and effective with acceptable toxicities. Further follow-up is mandatory to ensure whether this high complete response protocol will translate into long-term local control and survival.

Adult↗

Overexpression or mutation of the p53 tumor suppressor gene does not occur in malignant ovarian germ cell tumors.

BACKGROUND: The p53 tumor suppressor gene has been well studied in epithelial ovarian cancers. However, little is known of the expression of this gene in ovarian germ cell tumors. The authors attempted to investigate whether p53 alterations occurred in this group of tumors. METHODS: Twenty-two patients with malignant ovarian germ cell tumors were included in this study. Immunohistochemical staining for p53 was performed on paraffin embedded tissue of each case. Single-strand conformation polymorphism analysis of exons 4-9 of the p53 gene was performed on 9 of the 22 tumors where genomic DNAs were obtained from the frozen tissue samples. Three tumors that revealed focal p53 positivity by immunostaining were studied further with direct DNA sequencing. RESULTS: Overexpression of p53 was not observed in all of the 22 ovarian germ cell tumors; only 3 were found to have nuclear staining in a small fraction of the malignant cells (< 5% in 1 immature teratoma, 5-10% in 2 yolk-sac tumors). Among the nine frozen tumors subjected to single-strand conformation polymorphism analysis, none revealed p53 mutation in exons 4-9. There was no p53 mutation detected by DNA sequencing of the three tumors with focal immunoreactivity. CONCLUSIONS: Alterations of the p53 tumor suppressor gene may not be associated with the pathogenesis of ovarian germ cell tumors. Instead, genetic changes such as inactivation of other tumor suppressor genes and/or activation of some protooncogenes need to be studied to determine the genetic mechanisms of the tumor development.

Adolescent↗

Squamous esophageal histology and subsequent risk of squamous cell carcinoma of the esophagus. A prospective follow-up study from Linxian, China.

BACKGROUND: Linxian, China, has some of the highest rates of esophageal cancer in the world. Previous authors have proposed that esophagitis, atrophy, and dysplasia may be precursor lesions of esophageal cancer in such high risk populations. METHODS: To examine the relationship between squamous esophageal histology and subsequent esophageal cancer in Linxian, the authors prospectively followed 682 participants of a 1987 endoscopic survey for 3.5 years and compared their initial biopsy diagnoses with the occurrence of squamous cell carcinoma during this follow-up period. RESULTS: Squamous cell carcinoma of the esophagus was identified in 52 (7.6%) of the participants during the follow-up period. After adjusting for potential confounding factors, relative risks (95% confidence intervals) for squamous cell carcinoma incidence by initial histologic diagnoses were as follows: normal, 1.0 (reference); basal cell hyperplasia, 2.1 (0.4-9.8); mild dysplasia, 2.2 (0.7-7.5); moderate dysplasia, 15.8 (5.9-42.2); severe dysplasia, 72.6 (29.8-176.9); dysplasia not otherwise specified, 22.9 (6.7-78.0); and carcinoma in situ, 62.5 (24.1-161.9). CONCLUSION: In this study, moderate dysplasia, severe dysplasia, and carcinoma in situ were the only histologic lesions associated with a significantly increased risk of developing squamous cell carcinoma of the esophagus within 3.5 years after endoscopy. Increasing grades of dysplasia were associated with increasing risk, but severe dysplasia were associated with increasing risk, but severe dysplasia and carcinoma in situ had similar degrees of risk, findings that suggest a continuous spectrum of esophageal intraepithelial neoplasia, without morphologically distinguishable dysplasia and in situ carcinoma. A longer follow-up will be necessary to fully evaluate the less severe diagnostic categories, which may take more than 3.5 years to affect the occurrence of squamous cell carcinoma in this high risk population.

Adult↗

Allelotype of endometrial carcinoma.

An allelotype analysis of endometrial carcinoma was undertaken to identify chromosomal loci that are relevant to this tumor type. A total of 70 highly polymorphic microsatellite markers, distributed among all nonacrocentric chromosome arms, were examined for evidence of loss of heterozygosity or allelic imbalance in DNA samples from matched normal and tumor tissues. An average of 21 informative tumor cases were obtained for each marker. Allelic deletions or imbalance were observed on 31 of 41 chromosome arms with no marker showing an allelic loss ratio of greater than 33%. Those chromosome arms most frequently involved were 3p, 8p, 9p, 14q, 16q and 18q. There was a strong correlation between loss of heterozygosity on chromosome 14q and death from disease. These data indicate that the molecular genetic character of endometrial carcinoma is complex and that a relatively large number of different chromosomal loci are likely to play a role in the etiology and progression of this tumor type.

Chromosomes, Human, Pair 14↗