Biomedical subjects

Reiko Furuta

Publications and source records attributed to Reiko Furuta.

6 recordsLinked to original sources

PubMed2006

Histological features of human papilloma virus 16 and its association with the development and progression of anal squamous cell carcinoma.

PURPOSE: To investigate the development of anal squamous cell carcinoma (SCC) and the expression patterns of human papillomavirus (HPV). METHODS: We performed typing of HPV-DNA using a polymerase chain reaction (PCR), and amplified the Duchenne muscular dystrophy (DMD) genes simultaneously, to investigate the tumor DNA state. The expression patterns of HPV in the cancer cell nuclei was investigated by in situ hybridization (ISH) using HPV probes. RESULTS: Amplification of DMD genes was confirmed in 8 of 20 patients with anal SCC, suggesting that tumor DNA was preserved in these patients. In seven of these eight patients, only HPV16 was detected by both PCR and ISH, suggesting HPV16-induced carcinogenesis. In two patients with carcinoma in situ (CIS), the cancer cells showed only a diffuse pattern (DP), and in two patients with invasive cancer, the cancer cell showed only an oligo-dot pattern (OP). In one patient with lesions ranging from CIS to invasive cancer, the histologic features varied in each area, from DP to OP. This change originated in the deep part of the microinvasive area. CONCLUSIONS: These findings show that HPV16 infection is closely involved in the development of anal SCC and suggest that the change in the genome occurs at the stage of microinvasive cancer.

Anus Neoplasms↗

PubMed2004

Putative gene loci associated with carcinogenesis and metastasis of endocervical adenocarcinomas of uterus determined by conventional and array-based CGH.

OBJECTIVES: This study aimed to estimate the gene loci associated with carcinogenesis of endocervical adenocarcinoma of uterus (EA) and metastasis. Study design Sixteen patients with EA were studied; 6 had nodal metastasis. DNA was extracted from EAs, and subjected to both conventional comparative genomic hybridization (CGH) and array-based CGH. Copy number abnormalities were compared between cases with and without nodal metastasis. RESULTS: In all EAs, high frequencies of copy number losses were detected in genes LRP1B (on 2q21.2), DAB2 (5p13), and DCC (18q21.3), as well as regions 3p, 16q, and 22q, and copy number amplifications in genes NRAS (1p13.2), TOP2A (17q21-q22), NCOA3(AIB1) (20q12), and ARSA (22q tel). Nodal metastasis was associated with high frequencies of copy number loss in genes PGRMC2 and LAMA3 and amplification in CDK6 and NCOA3(AIB1). CONCLUSION: This is the first report of gene copy number alterations spanning the whole genome in EA. These altered genes are speculated to be associated with EAs as a tumor suppressor and/or oncogene.

Acetyltransferases↗

PubMed2004

Conventional and array-based comparative genomic hybridization analyses of novel cell lines harboring HPV18 from glassy cell carcinoma of the uterine cervix.

We established 2 novel human cell lines (GCCOT-1, GCCRK) from glassy cell carcinoma. Both cell lines showed dual tendencies of glandular and squamous differentiation, and thus possess the characteristics resembling reserve cells, the putative origin of most carcinomas arising from the uterine cervix. HPV type 18 DNA including E6-E7, which is commonly found in cell types other than squamous cell carcinoma of uterine cervix, was detected in both cell lines. We analyzed gene copy number alterations of the 2 cell lines using conventional comparative genomic hybridization (CGH) coupled with array-based CGH. Among the putative oncogenes demonstrating copy number gain in both cell lines, FGR(SRC2) at 1p36.2-1 and LAMC2 at 1q25-31 have not been reported to show amplification in previous analyses of conventional cervical cell lines. These oncogenes are thus speculated to be directly associated with oncogenesis of glassy cell carcinoma. On the other hand, among the putative suppressor genes demonstrating copy number loss in both cell lines, the 9q region, ATM at 11q22.3, and CYLD at 16q12-13 have not been reported to show loss in conventional cervical cancer cell lines. These sites are speculated to be important as tumor suppressors directly associated with oncogenesis of glassy cell carcinoma. This study suggests for the first time that together with the presence of HPV type 18, alterations at the above sites are closely associated with oncogenesis of glassy cell carcinoma, a special type of carcinoma in the uterine cervix.

Adult↗

PubMed2003

Ectopic chromosome around centrosome in metaphase cells as a marker of high-risk human papillomavirus-associated cervical intraepithelial neoplasias.

This report describes the appearance of ectopic chromosome around centrosome (ECAC) in metaphase cell nuclei of high-risk HPV-associated cervical neoplasms. ECAC are clearly visible on HE-stained sections as a tiny (approx. 0.7 micro), round, dark structure or an aggregate of filamentous chromosome, often symmetrical at bilateral centrosomes. They appear in CINs from an early stage (CIN I), with the highest incidence in HPV16-associated CIN II-III (75%), and are less common in HPV-related invasive carcinomas (21%) and in lesions associated with high-risk HPV types other than 16. Rates for ECAC-positive nuclei in metaphase preparations (ECAC rate) for each lesion ranged 3.6-30%, the average being 14.5%. ECAC appeared very rarely in CINs associated with intermediate-risk HPVs and was never encountered in HPV6/11-induced condylomas or HPV-unrelated neoplasms in other organs. ECAC may be morphologic evidence of HPV-induced chromosomal instability working as a background mechanism in cervical carcinogenesis and also a useful marker for the histopathologic differentiation of high-risk CINs.

Aneuploidy↗

PubMed2003

Early invasive cervical adenocarcinoma: its potential for nodal metastasis or recurrence.

OBJECTIVE: To investigate the potential for nodal spread or recurrence in patients with early invasive cervical adenocarcinoma. The possible application of the International Federation of Gynecology and Obstetrics (FIGO) classification (1994) to this variant was also examined. DESIGN: Retrospective observational study. SETTING: Gynaecological oncology division of Cancer Institute Hospital, Japan. POPULATION: 302 patients with FIGO Stage 0-IIB cervical adenocarcinoma treated surgically at the Cancer Institute Hospital. METHODS: Clinicopathological analysis was performed on 47 patients with early invasive cervical adenocarcinoma in whom the depth of stromal invasion was 5 mm or less. All patients underwent radical hysterectomy and pelvic lymphadenectomy. RESULTS: In 30 patients with a depth of tumour invasion of 3 mm or less, no lymph node metastasis was found, while two patients developed recurrence; one had a depth of invasion of 3 mm and a horizontal tumour spread of 3 mm, and the other had horizontal spread of more than 7 mm. In 17 patients with a depth of invasion from 3 to 5 mm, there was also no lymph node metastasis, but two patients developed recurrence; one had horizontal tumour spread of 7 mm or less, and the other had horizontal spread of more than 7 mm. CONCLUSIONS: Early invasive cervical adenocarcinoma with a depth of invasion of 3 mm or less and a horizontal spread of 7 mm or less has little potential for nodal metastasis or recurrence. It seems possible that the FIGO definition (1994) of early cervical cancer may be applicable in its present form to early cervical adenocarcinoma.

Adenocarcinoma↗

PubMed2002

Loss of heterozygosity and the smoking index increase with decrease in differentiation of lung adenocarcinomas: etiologic implications.

To better understand causative relations of smoking to lung adenocarcinomas, the frequency of loss of heterozygosity (LOH) of all autosomal chromosomes was compared among the three grades of histological differentiation with 119 pulmonary adenocarcinomas (AC) and 41 squamous cell carcinomas (SCC), using Southern blotting. The fractional allelic loss (FAL) values, defined as (number of chromosome arms with LOH)/(number of informative arms), and smoking index (a product of number of cigarettes per day and duration in years) for all ACs were 0.19 and 520 whereas those for SCCs were 0.34 and 1,160, respectively. Those for well- (n=33), moderately (n=63) and poorly (n=23) differentiated ACs were 0.100, 0.197, 0.295 and 310, 480, 1,010, respectively. These results showed that less differentiated ACs are more similar to SCC in terms of LOH frequency and smoking.

Adenocarcinoma↗