PubMed Health⌕ Search

Biomedical subjects

Xavier Sastre-Garau

Publications and source records attributed to Xavier Sastre-Garau.

At least 19 recordsLinked to original sources
PubMed2006

Specific TP53 mutation pattern in radiation-induced sarcomas.

The mutagenic properties of ionizing radiation are well known, but the presence of specific mutations in human radiation-induced tumours is not established. We have studied a series of 36 secondary sarcomas arising in the irradiation field of a primary tumour following radiotherapy. The allelic status and the presence of mutations of the TP53 gene were investigated. The mutation pattern was compared with data from sporadic sarcomas recorded in the IARC TP53 somatic mutations database. A high proportion (58%) of the radiation-induced sarcomas exhibited a somatic inactivating mutation for one allele of TP53, systematically associated with a loss of the other allele. The high frequency (52%) of short deletions observed in the mutation pattern of radiation-induced sarcomas may be related to the induction of DNA breaks by ionizing radiation. The lack of hyper-reactivity of CpG dinucleotides and the presence of recurrent sites of mutation at codons 135 and 237 seem also to be specific for radiation tumorigenesis.

Adult↗
PubMed2005

UDP-N-acetyl-D-galactosamine: polypeptide N-acetylgalactosaminyltransferase-6 as a new immunohistochemical breast cancer marker.

Mucin O-glycosylation is characterized in cancer by aberrant expression of immature carbohydrate structures (Tn, T, and sialyl-Tn antigens). The UDP-N-acetyl-D-galactosamine: polypeptide N-acetylgalactosaminyltransferases (ppGalNAc-T) family enzymes regulate the initial steps of mucin O-glycosylation and could be responsible for the altered glycosylation observed in cancer. Considering that we recently found the ppGalNAc-T6 mRNA expressed in breast carcinomas, we produced a highly specific monoclonal antibody (MAb T6.3) to assess the expression profile of ppGalNAc-T6 protein product in breast tissues. The expression of ppGalNAc-T6 by breast carcinoma cells was confirmed on MCF-7 and T47D cell lines. In formalin-fixed tissues, ppGalNAc-T6 expression was observed in 60/74 (81%) breast cancers, 21/23 (91.3%) adjacent ductal carcinoma in situ (DCIS), 4/20 benign breast lesions (2/2 sclerosing adenosis and 2/13 fibroadenoma), and in 0/5 normal breast samples. We observed a statistically significant association of ppGalNAc-T6 expression with T1 tumor stage. This fact, as well as the observation that ppGalNAc-T6 was strongly expressed in sclerosing adenosis and in most DCIS, suggests that ppGalNAc-T6 expression could be an early event during human breast carcinogenesis. Considering that an abnormal O-glycosylation greatly contributes to the phenotype and biology of breast cancer cells, ppGalNAc-T6 expression could provide new insights about breast cancer glycobiology.

Adult↗
PubMed2005

Identification of a proliferation gene cluster associated with HPV E6/E7 expression level and viral DNA load in invasive cervical carcinoma.

Specific HPV DNA sequences are associated with more than 90% of invasive carcinomas of the uterine cervix. Viral E6 and E7 oncogenes are key mediators in cell transformation by disrupting TP53 and RB pathways. To investigate molecular mechanisms involved in the progression of invasive cervical carcinoma, we performed a gene expression study on cases selected according to viral and clinical parameters. Using Coupled Two-Way Clustering and Sorting Points Into Neighbourhoods methods, we identified a 'cervical cancer proliferation cluster' composed of 163 highly correlated transcripts. Most of these transcripts corresponded to E2F pathway genes controlling cell division or proliferation, whereas none was known as TP53 primary target. The average expression level of the genes of this cluster was higher in tumours with an early relapse than in tumours with a favourable course (P = 0.026). Moreover, we found that E6/E7 mRNA expression level was positively correlated with the expression level of the cluster genes and with viral DNA load. These findings suggest that HPV E6/E7 expression level plays a key role in the progression of invasive carcinoma of the uterine cervix via the deregulation of cellular genes controlling tumour cell proliferation. HPV expression level may thus provide a biological marker useful for prognosis assessment and specific therapy of the disease.

Adult↗
PubMed2005

Radiation-induced sarcomas after radiotherapy for breast carcinoma: a large-scale single-institution review.

BACKGROUND: Sarcomas are a rare complication of radiotherapy for breast carcinoma and patients have a poor prognosis. The incidence, histology, and management of patients with sarcomas were reviewed in the current study. METHODS: The authors reviewed the records of 16,705 patients with breast carcinoma. Of these, 13,472 (81%) were treated with megavoltage radiotherapy and 3233 were treated without at the Institute Curie (Paris, France) between 1981 and 1997. Median doses of 50-55 grays (Gy) in 25-27 fractions were delivered to the whole breast over a period of 5-5.5 weeks (2 Gy/day, 5 weekly fractions) followed, when indicated, by a 16-26-Gy boost to the tumor or tumor bed. Treatment of radiation-induced sarcomas (RIS) consisted mostly of radical surgery and chemotherapy. RESULTS: Overall, 35 patients developed sarcomas. Of these, 27 fulfilled the Cahan criteria. The median follow-up was 9.3 years (range, 1-22.4 years). The latency period ranged from 3 years to 20.3 years. Thirteen sarcomas were located in the breast, 5- in the chest wall, 3 in the sternum, 2 in the supraclavicle, 1 in the scapula, and 3 in the axilla. Histologic evaluation identified 13 angiosarcomas, 3 osteosarcomas, 5 undifferentiated sarcomas, 1 malignant fibrous histiocytoma, 2 leiomyosarcomas, 1 fibrosarcoma, 1 rhabdomyosarcoma, and 1 myosarcoma. The cumulative RIS incidence was 0.07% (+/- 0.02) at 5 years, 0.27% (+/- 0.05) at 10 years, and 0.48% (+/- 0.11) at 15 years. Standardized incidence ratios were 10.2 (95% confidence interval, 9.03-11.59) for irradiated patients and 1.3 (0.3-3.6) for nonirradiated patients. Of the 27 patients, 15 died of sarcoma within 1 month to 14.5 years (mean, 34.2 +/- 0.7 months). The 5-year actuarial survival rate after diagnosis of RIS was 36% (+/- 0.11). CONCLUSIONS: The current study confirmed the rarity of RIS. However, it showed that the risk increased with time. Therefore, careful, long-term follow-up of patients treated with radiotherapy is needed for early detection and efficacious treatment of these malignancies.

Adult↗
PubMed2005

Clinical and biological characteristics of cervical neoplasias with FGFR3 mutation.

BACKGROUND: We have previously reported activating mutations of the gene coding for the fibroblast growth factor receptor 3 (FGFR3) in invasive cervical carcinoma. To further analyze the role of FGFR3 in cervical tumor progression, we extended our study to screen a total of 75 invasive tumors and 80 cervical intraepithelial neoplasias (40 low-grade and 40 high-grade lesions). RESULTS: Using single strand conformation polymorphism (SSCP) followed by DNA sequencing, we found FGFR3 mutation (S249C in all cases) in 5% of invasive cervical carcinomas and no mutation in intraepithelial lesions. These results suggest that, unlike in bladder carcinoma, FGFR3 mutation does not or rarely occur in non invasive lesions. Compared to patients with wildtype FGFR3 tumor, patients with S249C FGFR3 mutated tumors were older (mean age 64 vs. 49.4 years, P = 0.02), and were more likely to be associated with a non-16/18 HPV type in their tumor. Gene expression analysis demonstrated that FGFR3 mutated tumors were associated with higher FGFR3b mRNA expression levels compared to wildtype FGFR3 tumors. Supervised analysis of Affymetrix expression data identified a significant number of genes specifically differentially expressed in tumors with respect to FGFR3 mutation status. CONCLUSION: This study suggest that tumors with FGFR3 mutation appear to have distinctive clinical and biological characteristics that may help in defining a population of patients for FGFR3 mutation screening.

Adult↗
PubMed2005

Activating mutations of the tyrosine kinase receptor FGFR3 are associated with benign skin tumors in mice and humans.

Specific germline activating point mutations in the gene encoding the tyrosine kinase receptor FGFR3 (fibroblast growth factor receptor 3) result in autosomal dominant human skeletal dysplasias. The identification in multiple myeloma and in two epithelial cancers-bladder and cervical carcinomas-of somatic FGFR3 mutations identical to the germinal activating mutations found in skeletal dysplasias, together with functional studies, have suggested an oncogenic role for this receptor. Although acanthosis nigricans, a benign skin tumor, has been found in some syndromes associated with germinal activating mutations of FGFR3, the role of activated FGFR3 in the epidermis has never been investigated. Here, we targeted an activated receptor mutant (S249C FGFR3) to the basal cells of the epidermis of transgenic mice. Mice expressing the transgene developed benign epidermal tumors with no sign of malignancy. These skin lesions had features in common with acanthosis nigricans and other benign human skin tumors, including seborrheic keratosis, one of the most common benign epidermal tumors in humans. We therefore screened a series of 62 cases of seborrheic keratosis for FGFR3 mutations. A large proportion of these tumors (39%) harbored somatic activating FGFR3 mutations, identical to those associated with skeletal dysplasia syndromes and bladder and cervical neoplasms. Our findings directly implicate FGFR3 activation as a major cause of benign epidermal tumors in humans.

Animals↗
PubMed2005

Visualizing chromosomes as transcriptome correlation maps: evidence of chromosomal domains containing co-expressed genes--a study of 130 invasive ductal breast carcinomas.

Completion of the working draft of the human genome has made it possible to analyze the expression of genes according to their position on the chromosomes. Here, we used a transcriptome data analysis approach involving for each gene the calculation of the correlation between its expression profile and those of its neighbors. We used the U133 Affymetrix transcriptome data set for a series of 130 invasive ductal breast carcinomas to construct chromosomal maps of gene expression correlation (transcriptome correlation map). This highlighted nonrandom clusters of genes along the genome with correlated expression in tumors. Some of the gene clusters identified by this method probably arose because of genetic alterations, as most of the chromosomes with the highest percentage of correlated genes (1q, 8p, 8q, 16p, 16q, 17q, and 20q) were also the most frequent sites of genomic alterations in breast cancer. Our analysis showed that several known breast tumor amplicons (at 8p11-p12, 11q13, and 17q12) are located within clusters of genes with correlated expression. Using hierarchical clustering on samples and a Treeview representation of whole chromosome arms, we observed a higher-order organization of correlated genes, sometimes involving very large chromosomal domains that could extend to a whole chromosome arm. Transcription correlation maps are a new way of visualizing transcriptome data. They will help to identify new genes involved in tumor progression and new mechanisms of gene regulation in tumors.

Breast Neoplasms↗
PubMed2005

Genomic organization of amplified MYC genes suggests distinct mechanisms of amplification in tumorigenesis.

Integration of the human papillomavirus (HPV) genome into the host genome is associated with the disruption of the HPV E2 gene and with amplification and rearrangement of the viral and flanking cellular sequences. Molecular characterization of the genomic structures of coamplified HPV sequences and oncogenes provides essential information concerning the mechanisms of amplification and their roles in carcinogenesis. Using fluorescent hybridization on stretched DNA molecules in two cervical cancer-derived cell lines, we have elucidated the genomic structures of amplified regions containing HPV/myc genes over several hundreds of kilobases. Direct visualization of hybridization signals on individual DNA molecules suggests that overreplication and breakage-fusion-bridge-type mechanisms are involved in the genomic instability associated with HPV cervical cancers. Further analysis from two other genital cancer-derived cell lines reveals a recurrent motif of amplification, probably generated by a common mechanism involving overreplication upon viral integration. Interestingly, different amplification patterns seem to be correlated with the disease outcome, thus providing new insights into HPV-related cancer development and tumor progression.

Female↗
PubMed2005

Ductal breast carcinoma develops through different patterns of chromosomal evolution.

In a previous study that used comparative genomic hybridization (CGH) to analyze 43 ductal breast carcinomas selected for hyperdiploidy, we proposed the existence of two distinct pathways of chromosomal evolution. In the present study, in which we reassessed our cytogenetic findings on 158 ductal breast carcinomas selected for having a modal number of chromosomes of fewer than 60, we confirmed the existence of two subtypes of tumors. Along with the great majority of tumors (142 of 158) that evolved through structural rearrangements with no or very few whole-chromosome gains, we found that a minor subset (16 of 158) evolved through progressive gains of whole chromosomes with no or only a few associated rearrangements. In this article, we describe the karyotypes of these 16 tumors together with data from CGH, which was performed for 10 of them. Chromosomes 5, 7, 8, and 20 were the most frequently gained. Our findings support the evidence of a new pathway of chromosomal evolution in a small subset of ductal breast carcinomas characterized by numerical chromosome aberrations.

Aged↗
PubMed2005

KIT is highly expressed in adenoid cystic carcinoma of the breast, a basal-like carcinoma associated with a favorable outcome.

Recent biological studies have classified breast carcinomas into HER2-overexpressing, estrogen receptor-positive/luminal, basal- and normal-like groups. According to this new biological classification, the objectives of our study were to assess the clinical, morphologic and immunophenotypic characteristics of adenoid cystic carcinoma of the breast in order to classify this subtype of breast carcinoma. A total of 18 cases of adenoid cystic carcinoma were identified from the Institut Curie files. Clinical information was available for 16 patients with a median follow-up of 6.5 years. Morphologically, all tumors were graded according to the system defined by Kleer and Oberman (histologic and nuclear grade). Immunophenotype was assessed with anti-ER, PR, HER-2, KIT, basal (CK5/6) and luminal cytokeratins (CK8/18) and p63 antibodies. One out of 18 tumors was nuclear grade 1 (16%), nine were nuclear grade 2 (50%) and eight were nuclear grade 3 (44%). All cases were estrogen receptor, progesterone receptor and HER-2 negative. Epithelial cells were strongly positive around glandular lumina with one or both cytokeratins, identifying the coexistence of CK5/6+ cells, CK5/6 and CK8/18+ cells, CK8/18+ cells and p63+ cells. All cases (100%) were also KIT positive. In all, 15 patients were treated by surgery. Nine of them received adjuvant radiotherapy. Follow-up was available for 16 patients. In all, 14 patients were alive. Two of them, initially treated by surgery only, presented a local recurrence. Two patients died (one of them treated by radiation therapy only died from her disease). Our study shows that adenoid cystic carcinoma of the breast is a special, estrogen receptor, progesterone receptor, HER-2 negative and highly KIT-positive, basal-like breast carcinoma, associated with an excellent prognosis. This highly specific immunophenotype could be useful to differentiate adenoid cystic carcinoma of the breast from other subtypes of breast carcinoma such as cribriform carcinoma.

Adult↗
PubMed2005

MDM2 and CDK4 immunostainings are useful adjuncts in diagnosing well-differentiated and dedifferentiated liposarcoma subtypes: a comparative analysis of 559 soft tissue neoplasms with genetic data.

Atypical lipomatous tumor/well-differentiated liposarcoma (ALT-WDLPS) and dedifferentiated liposarcoma (DDLPS) may be difficult to distinguish from benign adipose tumors and from poorly differentiated sarcomas, respectively. Genetically, they are characterized by amplification of MDM2 and CDK4 genes on chromosome 12q13-15. We examined a series of 559 soft tissue tumors (44 ALT-WDLPS, 61 DDLPS, 49 benign adipose tumors, and 405 non-ALT-WDLPS/DDLPS sarcomas) for MDM2 and CDK4 expression using immunohistochemistry. MDM2 and CDK4 immunoexpressions were compared with gene amplification status (as assessed by quantitative PCR and/or comparative genomic hybridization) in 241 neoplasms. Most ALT-WDLPS/DDLPS expressed MDM2 (97%) and CDK4 (92%) as opposed to few benign adipose tumors (MDM2, 5%; CDK4, 2%) and a limited number of non-ALT-WDLSP/DDLPS sarcomas (MDM2, 19%; CDK4, 6%). The sensitivity and specificity of MDM2 and CDK4 immunostainings in identifying ALT-WDLPS/DDLPS among other soft tissue tumors were 97% and 92%, and 83% and 95%, respectively. MDM2 and CDK4 immunostainings were particularly useful to separate ALT-WDLPS from the large group of differentiated adipose tumors, and to distinguish DDLPS from poorly differentiated sarcomas. A strong correlation was observed between MDM2 and CDK4 stainings and gene amplification status. In conclusion, MDM2 and CDK4 immunostainings, which correlate with gene amplification, are helpful adjuncts to differentiate ALT-WDLPS from benign adipose tumors and to separate DDLPS from poorly differentiated sarcomas.

Aged↗
PubMed2004

Proliferation markers predictive of the pathological response and disease outcome of patients with breast carcinomas treated by anthracycline-based preoperative chemotherapy.

The cell proliferation rate has been correlated to the response of breast carcinomas to preoperative chemotherapy (CT) and to disease outcome. However, this parameter is not yet used to select which tumours should be treated with preoperative CT. Furthermore, there is no consensus in the method used to evaluate cell proliferation. In poor prognosis breast carcinomas (PPBCs) treated by intensive preoperative CT, we compared the predictive value of S phase fraction (SPF), mitotic index (MI) and Ki67. We also evaluated the prognostic significance of the variation of the MI after CT. A series of 55 T2-T4N0N1M0 breast carcinomas were treated with 4 cycles of cyclophosphamide, 5-fluorouracil (5-FU) and doxorubicin. SPF was determined by flow cytometry on pre-therapeutic needle aspiration products. MI and Ki67 were evaluated on pre-therapeutic biopsy samples and on the tumours after CT. Fifteen patients (27%) had a pathological complete response (pCR), whereas 40 (73%) had residual disease. All three proliferative markers were found to have predictive value, but this value was higher for MI than for SPF (P = 0.04) and Ki67 (P = 0.03): the rate of pCR was 50% in cases with MI > 17/3.3 mm2, but was only 7% in cases with MI under this threshold (P = 0.0003). A significant decrease of MI (mean 10.97) was observed after CT (P = 0.001). Furthermore, we observed that even for patients with residual tumour, the variation of MI after CT was a prognostic parameter and overall survival. The sequential analysis of MI in breast cancers treated by preoperative CT thus provides a surrogate for predicting long-term outcome.

Adult↗
PubMed2004

Histological margin assessment for breast ductal carcinoma in situ: precision and implications.

Local recurrence after lumpectomy for ductal carcinoma in situ (DCIS) is a major concern and is related to residual disease in the breast. We studied the predictive value of lumpectomy margins for residual DCIS and compared our results and pathological processing techniques with those published in the literature. Margin status was determined for 89 patients with screen-detected DCIS who had lumpectomy and re-excision, for the presence and extent of residual disease. Margin width was defined as the narrowest distance between tumor and any inked margin or, where margins were positive, classified into focal involvement (<1 mm of the inked surface involved), minimal (>or=1<15 mm) and extensive (>or=15 mm). The amount of residual tumor was quantified according to the number of ducts involved with tumor: small (fewer than 10 ducts) or large (10 or more ducts) residuum. The initial margin status was a significant predictor for the presence of residual tumor in re-excision specimens (P=0.006). There was residual tumor in 44 and 45% of close non-involved (>1 and 25 mm,respectively, showing residual disease. The presence of residual tumor was not significantly related to age, mammographic appearance, nuclear grade or intraductal necrosis. The initial margin status was found to predict for the amount of residual tumor. With careful margin assessment, margin status after lumpectomy for DCIS can be used to predict for the presence and amount of residual tumor in the breast and is a guide to further management decisions. A standard for margin status reporting and pathological processing of screen-detected DCIS in situ lesions will help in the interpretation of data from different institutions.

Adult↗
PubMed2004

Regression of low-grade cervical intraepithelial neoplasia in patients with HLA-DRB1*13 genotype.

OBJECTIVE: The human leukocyte antigen (HLA)-DRB1*13 allele frequency is lower in women with cervical carcinoma than in the general population, suggesting that this allele could exert a protective effect against progression of cervical intraepithelial neoplasia (CIN) associated with human papillomaviruses (HPV). To test this hypothesis, we designed a prospective study of low-grade CIN (CIN1) and analyzed the probability of regression of these lesions according to HLA-DR and HPV status. METHODS: The study sample was composed of 86 women with CIN1 who agreed to regular colposcopic follow-up and no immediate treatment. Biopsy specimens were taken under colposcopy for histology and for the determination of HPV and HLA status. Cases were classified into 3 groups: CIN1 regression, persistence for at least 12 months, or progression to CIN2 or 3. RESULTS: The rate of spontaneous regression (95% confidence interval) at 24 months was 51.6% (39-61.6%) overall compared with 34.7% (13.4-50.8%) in HPV16/18 positive cases and 59.9% (43.7-71.4%) in HPV16/18-negative cases (P =.051). The rate of regression was 71.8% (40.8-86.5%) in patients with HLA-DRB1*13 and 45.9% (31.5-57.2%) in patients with other genotypes (P =.03). Regression reached 90.5% (38.9-98.5%) at 18 months in DRB1*13 patients with HPV16/18-negative-associated CIN (15.1% of the cases). In multivariable analysis, HLA-DRB1*13 allele and HPV16/18-negative status were independently associated with an increased probability for regression (adjusted hazard ratio 2.1 [1.0-4.1] and 2.5 [1.2-5.4], respectively). CONCLUSION: A subset of approximately 15% of CIN1 highly likely to show spontaneous regression can be defined using 2 biologic parameters that characterize the viral causative agent and the host. LEVEL OF EVIDENCE: II-2

Adolescent↗
PubMed2004

Overexpression/amplification of HER-2/neu is uncommon in invasive carcinoma of the uterine cervix.

The aim of this study was to investigate HER-2/neu (c-erbB2) overexpression/amplification in carcinoma of the uterine cervix using immunohistochemistry and fluorescent in situ hybridization (FISH) to assess whether anti-p185c-erbB2 therapy might have potential benefits in patients with advanced invasive cervical carcinoma. The authors used a protocol for p185c-erbB2 immunohistochemistry (clone CB11) that has been previously calibrated using FISH as the gold standard, showing a 98% accuracy rate in a large series of breast carcinomas. Immunolabeling for p185c-erbB2 was present in 24 of 82 (29%) of the tumors, but only 2 tumors (2%) with a labeling of more than 60% of the cells were considered positive for overexpression. FISH analysis did not find HER-2/neu gene amplification in these cases, although five other tumors showed weak and/or focal immunolabeling. There was no correlation between the presence of immunolabeling and age, histologic type, or clinical stage. Overexpression/amplification of HER-2/neu is uncommon in invasive cervical carcinoma, suggesting that there is little indication for using anti-p185c-erbB2 therapy in the treatment of these patients.

Adenocarcinoma↗
PubMed2003

Macroscopic quality control improves the reliability of blue dye-only sentinel lymph node biopsy in breast cancer.

BACKGROUND: One of the problems of sentinel lymph node (SLN) biopsy is the risk of false negatives. At the Institut Curie, to reduce the false-negative rate, we have developed a histological quality control of the SLN performed by blue dye alone, which consists of verification of the SLN blue stain by the pathologist. METHODS: A total of 324 patients underwent an SLN biopsy procedure with patent blue dye only followed by an immediate axillary dissection. Initially, SLNs were checked to ensure that they were blue by macroscopic examination. Finally, a search for immunohistochemistry micrometastasis was performed. RESULTS: In 277 (85.5%) of 324 patients, an SLN was identified by the surgeon. After standard examination, the false-negative rate was 11.1% (10 of 90). After macroscopic checking of the 197 negative SLNs, 167 of the 197 were confirmed blue, and there were 5 false negatives, which brought the false-negative rate down to 5.6% (5 of 90). Sixty SLNs out of the 167 confirmed blue SLNs were then proved to be immunohistochemically micrometastatic, and there were 3 false negatives, giving a final false-negative rate of 2.2% (2 of 90; P =.002). CONCLUSIONS: In this series, the procedure of pathologic analysis of the SLN has resulted in a significant reduction of the false-negative rate.

Adult↗
PubMed2003

Efficiency of the hybrid capture 2 HPV DNA test in cervical cancer screening. A study by the French Society of Clinical Cytology.

The aim of this study was to determine the efficiency of the Hybrid Capture 2 (HC2; Digene, Gaithersburg, MD) human papillomavirus (HPV) assay for the detection of cervical neoplasia. Of the 1,785 patients recruited, 462 (25.88%) were referred for colposcopy owing to previously detected cytologic abnormalities, and 1,323 (74.12%) were voluntary candidates for screening. For all patients, a Papanicolaou smear and a monolayer smear (ThinPrep, Cytyc, Boxborough, MA) were done. HPV DNA was detected on the residual liquid-based material. False-positive results were observed in 111 cases and comprised 34 cross-reactions (1.90%) and 77 false-positive cases (4.31%) owing to a contiguous strong chemiluminescence signal. Interestingly, all these samples had a relative light units value of 1 to 3 and were contiguous to a sample with a very high HPV DNA load. The final results showed that high-risk and low-risk HPV DNA were detected in 480 samples (26.89%) and 135 samples (7.56%), respectively. Although HC2 can be considered a reliable and sensitive test for HPV DNA detection, we do not advocate its use for large-scale screening for cervical neoplasia.

Adult↗