Loss of heterozygosity for chromosomes 16q in Wilms tumors predicts outcomes:A meta-analysis

BACKGROUND The research findings suggest that the prognosis of children with Wilms tumor(WT)is affected by various factors.Some scholars have indicated that loss of heterozygosity(LOH)on chromosome 16q is associated with a poor prognosis in patients with WT.AIM To further elucidate this relationship,we conducted a meta-analysis.METHODS This meta-analysis was registered in INPLASY(INPLASY2023100060).We systematically searched databases including Embase,PubMed,Web of Science,Cochrane,and Google Scholar up to May 31,2020,for randomized trials reporting any intrapartum fetal surveillance approach.The meta-analysis was performed within a frequentist framework,and the quality and network inconsistency of trials were assessed.Odds ratios and 95%CIs were calculated to report the relationship between event-free survival and 16q LOH in patients with WT.RESULTS Eleven cohort studies were included in this meta-analysis to estimate the relationship between event-free survival and 16q LOH in patients with WT(I^(2)=25%,P<0.001).As expected,16q LOH can serve as an effective predictor of eventfree survival in patients with WT(risk ratio=1.95,95%CI:1.52–2.49,P<0.001).CONCLUSION In pediatric patients with WT,there exists a partial correlation between 16q LOH and an unfavorable treatment prognosis.Clinical detection of 16q chromosome LOH warrants increased attention to the patient’s prognosis.

Telomere erosion is independent of microsatellite instability but related to loss of heterozygosity in gastric cancer

AIM: To correlate the length of the telomere to microsatellite instability (MSI) and loss of heterozygosity (LOH) of APC, MCC and DCC genes in gastric carcinomas. METHODS: Telomeric restriction fragment (TRF) length of gastric cancer was measured with Southern blot. LOH of APC, MCC and DCC genes, microsatellite instability (MSI) and frameshift mutation of hMSH6, TGF-betaRII and BAX genes were analyzed by PCR-based methods. RESULTS: Sixty-eight cases of sporadic gastric carcinoma were studied for MSI using five microsatellite markers. MSI in at least one locus was detected in 17 (25%) of 68 tumors analyzed. Frameshift mutations of hMSH6, TGF-betaRII and BAX were detected in 2,6 and 3 of gastric carcinomas respectively showing high MSI (】 or = 2 loci, n = 8), but none was found in those showing low MSI (only one locus, n = 9) or MSS (tumor lacking MSI or stable, n = 51). Thirty-five cases, including all high MSI and low MSI, were studied for TRF. The mean TRF length was not correlated with clinicopathological parameters. No association was observed between TRF length and MSI or frameshift mutation. On the contrary, LOH at the DCC locus was related to telomere shortening (P【0.01). This tendency was also observed in APC and MCC genes, although there was no statistical significance. CONCLUSION: The development of gastric cancer can arise through two different genetic pathways. In high MSI gastric cancers, defective mismatch repair allows mutations to accumulate and generate the high MSI phenotype. In gastric cancers showing either low MSI or MSS, multiple deletions may represent the LOH pathway. Telomere erosion is independent of high MSI phenotype but related to the LOH pathway in gastric cancer.

Loss of heterozygosity on 10q23.3 and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions

AIM: To investigate the loss of heterozygosity (LOH) and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions. METHODS: Thirty cases of normal gastric mucosa, advanced and early stage gastric cancer, intestinal metaplasia, atrophic gastritis, and atypical hyperplasia were analyzed for PTEN LOH and mutations within the entire coding region of PTEN gene by PCR-SSCP denaturing PAGE gel electrophoresis, and PTEN mutation was detected by PCR-SSCP sequencing followed by silver staining. RESULTS: LOH rate found in respectively atrophic gastritis was 10% (3/30), intestinal metaplasia 10% (3/30), atypical hyperplasia 13.3% (4/30), early stage gastric cancer 20% (6/30), and advanced stage gastric cancer 33.3% (9/30), None of the precancerous lesions and early stage gastric cancer showed PTEN mutations, but 10% (3/30) of the advanced stage gastric cancers, which were all positive for LOH, showed PTEN mutation. CONCLUSION: LOH of PTEN gene appears in precancerous lesions, and PTEN mutations are restricted to advanced gastric cancer, LOH and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer.

Frequent loss of heterozygosity in two distinct regions,8p23.1 and 8p22, in hepatocellular carcinoma

AIM： To identify the precise location of putative tumor suppressor genes （TSGs） on the short arm of chromosome 8 in patients with hepatocellular carcinoma （HCC）. METHODS： We used 16 microsatellite markers informative in Japanese patients, which were selected from 61 pub- lished markers, on 81：）, to analyze the frequency of loss of heterozygosity （LOH） in each region in 33 cases （56 lesions） of HCC. RESULTS： The frequency of LOH at 8p23.2-21 with at least one marker was 63% （20/32） in the informative cases. More specifically, the frequency of LOH at 8p23.2, 8p23.1, 8p22, and 8p21 was 6%, 52%, 47%, and 13% in HCC cases. The LOH was significantly more frequent at 8p23.1 and 8p22 than the average （52% vs 220, P = 0.0008; and 47% vs 22%, P = 0.004, respectively） or others sites, such as 8p23.2 （52% vs 60, P = 0.003; 47% vs 220, P = 0.004） and 8p21 （52% vs 13%, P = 0.001; 47% vs 13%, P = 0.005） in liver cancer on the basis of cases. Notably, LOH frequency was significantly higher at D85277, DSS503, DSS1130, DSS552, DSS254 and D8S258 than at the other sites. However, no allelic loss was detected at any marker on 8p in the lesions of nontumor liver tissues. CONCLUSION： Deletion of 8p, especially the loss of 8p23.1-22, is an important event in the initiation or promotion of HCC. Our results should be useful in identi- fying critical genes that might lie at 8p23.1-22.

Frequent loss of heterozygosity at 8p22 chromosomal region in diffuse type of gastric cancer

AIM: To study the loss of heterozygosity (LOH) at 8p21-23 locus in diffuse gastric cancer.METHODS: To evaluate the involvement of this region in gastric cancer, we used eight microsatellite markers covering two Mb of mentioned region, to perform a high-resolution analysis of allele loss in 42 cases of late diffuse gastric adenocarcinoma.RESULTS: Six of these STS makers: D8S1149, D8S1645, D8S1643, D8S1508, D8S1591, and D8S1145 showed 36%, 28%, 37%, 41%, 44% and 53% LOH, respectively.CONCLUSION: A critical region of loss, close to the NAT2 locus and relatively far from FEZ1 gene currently postulated as tumor suppressor gene in this region.

Clinical significance of loss of heterozygosity for M6P/IGF2R in patients with primary hepatocellular carcinoma

AIM:To investigate the relationship between loss of heterozygosity (LOH) for mannose 6-phosphate/insulin- like growth factor 2 receptor (M6P/IGF2R) and the outcomes for primary HCC patients treated with partial hepatectomy. METHODS: The LOH for M6P/IGF2R in primary HCC patients was assessed using six different gene-specific nucleotide polymorphisms. The patients studied were enrolled to undergo partial hepatectomy. RESULTS: M6P/IGF2R was found to be polymorphic in 73.3% (22/30) of the patients, and of these patients, 50.0% (11/22) had tumors showing LOH in M6P/IGF2R. Loss of heterozygosity in M6P/IGF2R was associated with significant reductions in the two year overall survival rate (24.9% vs 65.5%; P = 0.04) and the disease-free survival rate (17.8% vs 59.3%; P = 0.03). CONCLUSION: These results show M6P/IGF2R LOH predicts poor clinical outcomes in surgically resected primary HCC patients.

Loss of heterozygosity of Kras2 gene on 12p12-13 in Chinese colon carcinoma patients

AIM： To study the loss of heterozygosity （LOH） on 12p12-13 in Chinese colon carcinoma patients.METHODS： DNA was extracted from 10 specimens of cancer tissue, 10 specimens of adjacent tissue and 10 specimens of normal tissue, respectively. LOH of Kras2 gene was analyzed by polymerase chain reaction （PCR） and denaturing polyacrylamide gel electrophoresis using 11 microsatellite markers on 12p-12-13.RESULTS： LOH of Kras gene was detected at least on one marker of 12p-12-13 in 30% （3/10） of adjacent tissue specimens. The highest frequency of LOH was identified on D12S1034 in 28.57% （2]7） of adjacent tissue specimens. LOH was detected at least on one marker of 12p12-13 in 60% （6/10） of carcinoma tissue specimens, the most frequent LOH was found on D12S1034 and D12S1591 in 42.86% （3/7） of carcinoma tissue specimens. LOH was detected in 30% （3/10） of carcinoma tissue specimens, 30% （3/10） of adjacent tissue specimens, and no signal in 1% （1/0） carcinoma tissue specimen. The occurrence of LOH did not correlate with sex, age, tumor size and lymph node metastasis.CONCLUSION： Genomic instability may occur on 12p-12-13 of Kras2 gene in the development and progression of colon carcinoma. The high LOH of Kras2 gene may directly influence the transcription and translation of wild type Kras2 gene.

Loss of heterozygosity: An independent prognostic factor of colorectal cancer

AIM: Colorectal cancers result from the accumulation of several distinct genetic alterations. This study was to investigate the frequency and prognostic value of loss of heterozygosity (LOH) and microsatellite instability (MSI) at 14 genetic loci located near or within regions containing important genes implicated in colorectal tumorigenesis. METHODS: We studied colorectal cancers with corresponding normal mucosae in 207 patients (139 males and 68 females, mean age at the time of tumor resection 66.2±12.4 years, range 22-88 years). There were 37 right-sided colonic tumors, 85 left-sided colonic tumors and 85 rectal tumors. The distribution of tumor staging was stage Ⅰ in 25, stage Ⅱ in 73, stage Ⅲ in 68, and stage Ⅳ in 41. We analyzed the LOH and MSI of HPC1, hMSH2, hMLH1, APC, MET, P53, NH23-H1, DCC, BAT25, BAT26, D17S250, MYCL1 and D8S254 with fluorescent polymerase chain reaction and denatured gel electrophoresis. High-frequency LOH was determined to be greater than three, or more than 50% of the informative marker with LOH. High-frequency MSI (MSI-H) was determined as more than four markers with instability (>30%). Correlations of LOH and MSI with clinical outcomes and pathological features were analyzed and compared. RESULTS: The occurrence of MSI-H was 7.25%, located predominantly in the right colons (7/15) and had a higher frequency of poor differentiation (6/15) and mucin production (7/15). LOH in at least one genetic locus occurred in 78.7% of the tumors and was significantly associated with disease progression. Of the 166 potentially cured patients, 45 developed tumor recurrence within 36 mo of follow-up. Clinicopathological factors affecting 3-year disease-free survival (DFS) were TNM staging, grade of differentiation, preoperative CEA level, and high LOH status. Patients with high LOH tumors had a significantly lower DFS (50%) compared with patients with low LOH tumors (84%). Of the patients developing subsequent tumor recurrence, the number and percentage of LOH were 2.97 and 46.8% respectively, similar to the stage IV disease patients. TNM staging had the most significant impact on DFS, followed by high LOH status. CONCLUSION: Clinical manifestations of LOH and MSI are different in colorectal cancer patients. High-frequency LOH is associated with high metastatic potential of colorectal cancers.

Loss of heterozygosity analyzed by single nucleotide polymorphism array in cancer

Neoplastic progression is generally characterized by the accumulation of multiple genetic alterations including loss of tumor suppression gene function. Loss of heterozygosity （LOH） has been used to identify genomic regions that harbor tumor suppressor genes and to characterize different tumor types, pathological stages and progression. LOH pattern has been detected by allelotyping using restriction fragment length polymorphism, and later by simple sequence length polymorphisms （SSLPs or microsatellite） for 10 years. This paper reviews the detection of LOH by recently developed single nucleotide polymorphism （SNP） arrays （all analyzed by Affymetrix array）; furthermore, its advantage and disadvantage were analyzed in several kinds of cancer.

Refined mapping of loss of heterozygosity on 1q31.1-32.1 in sporadic colorectal carcinoma

AIM: To explore precise deleted regions and screen the candidate tumor suppressor genes related to sporadic colorectal carcinoma. METHODS: Six markers on 1q31.1-32.1 were chosen. These polymorphic microsatellite markers in 83 colorectal cancer patients tumor and normal DNA were analyzed via PCR. PCR products were electrophoresed on an ABI 377 DNA sequencer. Genescan 3.1 and Genotype 2.1 software were used for Loss of heterozygosity (LOH) scanning and analysis. Comparison between LOH frequency and clinicopathological factors was performed by χ2 test. RESULTS: 1q31.1-32.1 exhibited higher LOH frequency in colorectal carcinoma. The average LOH frequency of 1q31.1-32.1 was 23.0%, with the highest frequency of 36.7% (18/49) at D1S2622, and the lowest of 16.4% (11/67) at D1S412, respectively. A minimal region of frequent deletion was located within a 2 cM genomic segment at D1S413-D1S2622 (1q31.3-32.1). There was no significant association between LOH of each marker on 1q31.1-32.1 and the clinicopathological data (patient sex, age, tumor size, growth pattern or Dukes stage), which indicated that on 1q31.1-32.1, LOH was a common phenomenon in all kinds of sporadic colorectal carcinoma. CONCLUSION: Through our refined deletion mapping,the critical and precise deleted region was located within 2 cM chromosomal segment encompassing 2 loci (D1S413, D1S2622). No significant association was found between LOH and clinicopathologic features in 1q31.1-32.1.

Loss of heterozygosity for loci on chromosome arms 1p and 10q in oligoden-droglial tumors: relationship to outcome and chemosensitivity

Oligodendroglial tumors frequently have deletions ofchromosomal loci on lp and l9q.Loas of heterozygosity(LOH)of chromosome 10 may be a negative prognostic factor.We reviewed 23 patients with oligodendroglial tumors,toevaluate the frequency of lp and 10q LOH and correlate with clinical outcome.Three loci(DlS402,DlSl 172,MCT118)on lp and 2 loci(Dl0S520 and D10S521)on 10q were analyzed for LOH using PCR techniques.

LOSS OF HETEROZYGOSITY OF ER GENE IN BREAST CANCER AND ITS CLINICAL SIGNIFICANCE

Objective: Clinically, the reason of resistance for breast cancer to endocrine therapy has not been well known. The current study attempted to examine loss of heterozygosity (LOH) on the estrogen receptor (ER) gene in breast cancer and its relationship to clinicopathologic findings. Methods: DNAs of tumor tissues and blood lymphocytes were collected from 40 cases of primary breast cancer patients and LOH were detected using the microsatellite repeat assay and combined with other ER immunohistochemical assays. Results: ER-positive staining was observed in 65% of breast cancer. Heterogeneity of ER expression was found. Seven of the patients (17.5%) showed LOH. In three of the seven cases, there was total loss, and there was a marked reduction in the intensity of signal in the other four cases. LOH was associated with histologic grade, occurring more frequently in ER-negative and lymph node metastasis group, but not with tumor size and patient ages. Conclusion: This result implied that LOH of the ER gene may have an important role in the progression of breast cancer. It was postulated that the lack of ER function induced by LOH may contributed to endocrine therapy resistance of breast cancer since the tumor clone would escape from the ER regulation, obtain growth predisposition and finally lost response to therapy.

LOSS OF HETEROZYGOSITY AT 17p13 IN GASTRIC CANCER AND COLORECTAL CANCER

Southern hybridization was done on DNA samples of22 gastric tumors and corresponding normal tissues, 14colorectal tumors and corresponding normal tissues by probe phs53B mapping at 17P13.1 and probe PYNZ22mapping at 17pl3.3 which were purchased from the American Type Culture Collection. RFLP heterozygosity was observed in 12 normal tissues of gastric cancers and 10 normal tissues of colorectal cancers. Among these informative tumors, 6(50%) cases of gastric cancers and 6(60%) cases of colorectal cancers showed the loss of beterozygosity at 17p13. Our results demonstrated that the inactivation of wild type p53 might be involved in the carcinogenesis of gastric cancers and colorectal cancers.Furthermore, the mode of inactivation of p53 was in accord with the 'two hits' hypothesis by Anudson. The signincance was discussed regarding the presence of LOH detected by probe PYNZ22 mapping at 17pl3.3.

LOSS OF HETEROZYGOSITY FOR MARKERS ON 22 CHROMOSOME IN SPORADIC SCHWANNOMA

Objective To analyze the loss of heterozygosity (LOH) for markers on chromosew 22 (CHR 22 ) and its significance with their clinical behaviors. Methods The frequency of CHR22 LOH in 36 schwannomas was observed by denatured polyacrylamide gels and silver staining, and the proliferative index of schwannoma wes calculated by Ki-67 and PCNA immunohistochemistry. Results 15 schwannomas (41. 6% ) shawed allele lass. The proliferative index of schwannomas with LOH were significantly higher than those without LOH (P< 0. 05). In acoustic neuromas, patients with LOH were younger at the age of diagnosis, larger size of tumor, shorter history and higher growth rate than those without LOH, but with no significance. Conclusion CHR22 IDH was the frequent event in the tumorigenesis of sporadic schwannoma. There were some links beteen CHR22 LOH and clinical behavior.

The Loss of Heterozygosity of FHIT Gene in Sporadic Breast Cancer

function.FHIT is a potential tumor suppressor gene.Although the precise FHIT molecular mechanism of action is not well understood,evidences suggest that Fhit protein reduced levels are involved in mammary carcinogenesis.The aim of this study was to investigate if FHIT LOH could influence on sporadic breast cancer(BC)biological behavior,through its association with prognostic factors for sporadic BC.Tumor tissue and peripheral blood samples were analyzed using the microsatellite marker D3S1300.The findings were associated with clinicopathological parameters including overall survival.LOH was detected in 31.1%(52/167)of the informative BC’cases.Considering clinical and pathological characteristics we have found no significant association with FHIT LOH status.The mean follow-up time was 80 months.After the Cox regression analysis two parameters remained associated with BC’s risk of death:TNM stage III and IV-HR=3.74(95%CI,1.16-12.1)P=0.027 and disease relapse HR=3.14(CI 95%1.26-7.80)P=0.014.This study shows that FHIT LOH by itself is not a prognostic factor for sporadic BC.Further researches are required to elucidate the functional role of FHIT LOH concerning to BC.

High frequency loss of heterozygosity on the long arms of chromosomes 13 and 14 in nasopharyngeal carcinoma in Southern China

OBJECTIVE: To investigate the loss of heterozygosity (LOH) on chromosomal arms 13q and 14q in nasopharyngeal carcinoma (NPC) using 21 microsatellite polymorphic markers and to study whether there is a correlation between LOH and clinicopathologic parameters and/or Epstein-Barr virus (EBV) infection in NPC. METHODS: Sixty cases of NPC were studied using polymerase chain reaction based microsatellite analysis with genescan and genotyping techniques. RESULTS: LOH was detected on 13q in 78% of NPC tumors, high frequency LOH loci (more than 30%) clustered to 13q12.3-q14.3 and 13q32. On chromosome 14q, LOH was detected in 80% of NPC tumors; high frequency LOH loci clustered to 14q11-q13, 14q21-q24 and 14q32. High frequency LOH at 13q31-q32 correlated with a lower level of EBV infection; LOH on chromosome 14q was closely associated with poor differentiation of NPC tumor cells. CONCLUSION: Our results suggest that in NPC, LOH on chromosome 13q and 14q are common genetic events, and putative tumor suppressor genes (TSG) residing in these regions may be involved in tumorigenesis.

High frequency loss of heterozygosity on the long arms of chromosomes 13 and 14 in nasopharyngeal carcinoma in Southern China

To investigate the loss of heterozygosity (LOH) on chromosomal arms 13q and 14q in nasopharyngeal carcinoma (NPC) using 21 microsatellite polymorphic markers an d to study whether there is a correlation between LOH and clinicopathologic para meters and/or Epstein Barr virus (EBV) infection in NPC Methods Sixty cases of NPC were studied using polymerase chain reaction based microsa tellite analysis with genescan and genotyping techniques Results LOH was detected on 13q in 78% of NPC tumors, high frequency LOH loci (more than 30%) clustered to 13q12 3 q14 3 and 13q32 On chromosome 14q, LOH was detec ted in 80% of NPC tumors; high frequency LOH loci clustered to 14q11 q13, 14q21 q24 and 14q32 High frequency LOH at 13q31 q32 correlated with a lower l evel of EBV infection; LOH on chromosome 14q was closely associated with poor di fferentiation of NPC tumor cells Conclusion Our results suggest that in NPC, LOH on chromosome 13q and 14q are common geneti c events, and putative tumor suppressor genes (TSG) residing in these regions ma y be involved in tumorigenesis

Genetic aberration in primary hepatocellular carcinoma:correlation between p53 gene mutation and loss-of-heterozygosity on chromosome 16q21-q23 and 9p21-p23

To elucidate the molecular pathology underlying the development of hepatocellular carcinoma (HCC), we used 41 highly polymorphic microsatellite markers to examine 55 HCC and corresponding non-tumor liver tissues on chromosome 9, 16 and 17. Loss-of-heterozygosity (LOH) is observed with high frequency on chromosomal region 17p13 (36/55, 65%), 9p21-p23 (28/55, 51%), 16q21-q23 (27/55, 49%) in tumors. Meanwhile, microsatellite instability is rarely found in these microsatellite loci. Direct sequencing was performed to detect the tentative mutation of tumor suppressor genes in these regions: p53, MTS1/p16, and CDH1/E-cadherin. Within exon 5-9 of p53 gene, 14 out of 55 HCC specimens (24%) have somatic mutations, and nucleotide deletion of this gene is reported in HCC for the first time. Mutation in MTS1/pl6 is found only in one tumor case. We do not find mutations in CDH1/E-cadherin. Furthermore, a statistically significant correlation is present between p53 gene mutation and loss of chromosome region 16q21q23 and 9p21-p23, which indicates that synergism between p53 inactivation and deletion of 16q21-q23 and 9p21-p23 may play a role in the pathogenesis of HCC. Genetic aberration in hepatocellular

Two unrelated patients with rare Crigler-Najjar syndrome type I:two novel mutations and a patient with loss of heterozygosity of UGT1A1 gene

Cdgler-Najjar syndrome type Ⅰ （CN-I） is the most severe type of hereditary unconjugated hyperbilirubinemia. It is caused by homozygous or compound heterozygous mutations of the UDP-glycuronosyltransferase gene （UGT1A1） on chromosome 2q37. Two patients clinically diagnosed with CN-I were examined in this paper. We sequenced five exons and their flanking sequences, specifically the promoter region of UGT1A 1, of the two patients and their parents. Quantitative real-time polymerase chain reaction （qRT-PCR） was used to determine the UGT1A1 gene copy number of one patient. In patient A, two mutations, c.239_245delCTGTGCC （p.Pro80HisfsX6; had not been reported previously） and c.1156G〉T （p.Va1386Phe）, were identified. In patient B, we found that this patient had lost heterozygosity of the UGTIA1 gene by inheriting a deletion of one allele, and had a novel mutation c.1253delT （p.Met418ArgfsX5） in the other allele. In summary, we detected three UGTIA 1 mutations in two CN-I patients： c.239_ 245delCTGTGCC （p.Pro80HisfsX6）, c.1253delT （p.MeH18ArgfsX5）, and c.1156G〉T （p.Va1386Phe）. The former two mutations are pathogenic; however, the pathogenic mechanism of c.1156G〉T （p.Va1386Phe） is unknown.

Loss of heterozygosity on chromosome 22 in sporadic schwannoma and its relation to the proliferation of tumor cells

Background Schwannoma is the tumor arising mainly from the cranial and spinal nerves. Bilateral vestibular schwannoma is the hallmark of neurofibromatosis type 2 （NF2）. The NF2 gene has been cloned with comprehensive analysis of its mutations in schwannoma. However, most studies focused on vestibular schwannoma. There are differences in proliferation of tumor cell and uhrastructure between vestibular and spinal schwannomas. It is unknown whether genetic alterations in vestibular schwannoma are different from those in non-vestibular schwannoma. We analyzed the loss of heterozygosity （LOH） on chromosome 22 in patients with sporadic schwannoma including vestibular and spinal schwannomas and correlated this genetic alteration with tumor proliferation. Methods In 54 unrelated patients without clinical NF1 or NF2, 36 patients had sporadic vestibular schwannoma, and 18 dorsal spinal root schwannoma. Four highly polymorphic linkage to NF2 gene microsatellite DNA markers （D22S264, D22S268, D22S280, CRYB2） were used to analyze LOH. The proliferative index was evaluated by Ki-67 and proliferative cell nuclear antigen （PCNA） immunostaining. Student＇s t test was used to analyze the difference of the proliferative index between schwannoma with LOH and that without LOH. The difference of the frequency of LOH in vestibular and spinal schwannomas was investigated by the chi-square test. Results Twenty-three schwannomas （42. 6% , 23/54） showed allele loss. The frequency of LOH in vestibular schwannoma was significantly higher than that in spinal schwannoma （ X^2 = 5.14, P 〈 0.05 ）. The proliferative index of schwannoma with LOH was significantly higher than that without LOH （tki-67 = 2. 97, P= 0. 0045 ; tPCNA =2.93, P =0. 0051）. Conclusions LOH on chromosome 22 is a frequent there is a correlation between LOH on chromosome 22 event in the tumorigenesis of sporadic schwannoma. And, and proliferative activity in schwannoma. The frequency of LOH in vestibular schwannoma is significantly different from that in spinal schwannoma.