Biomedical subjects

R Yatani

Publications and source records attributed to R Yatani.

At least 55 records · Page 3Linked to original sources

PubMed1996

Primary non-Hodgkin malignant lymphoma of the male breast.

A case of primary non-Hodgkin lymphoma of the male breast is reported. The patient was a 76-year-old Japanese with a history of bilateral gynecomastia. After the patient had received sex hormone treatment for the gynecomastia, rapid growth of a tumor in the right breast was noted, with regression of a contralateral breast lesion. Clinically, inflammatory breast cancer was suspected, and right mastectomy with ipsilateral axillary lymph node dissection was performed after intraarterial infusion chemotherapy using a cis-platinum derivative. The histology of the surgical specimen was non-Hodgkin malignant lymphoma of the diffuse large cell type, with focal tumor necrosis. Immunohistochemically, the tumor cells showed a B-cell nature. The patient is currently well without disease 39 months after surgery.

Aged↗

PubMed1996

Combined analysis of expression of c-erbB-2, Ki-67 antigen, and tenascin provides a better prognostic indicator of carcinoma of the papilla of Vater.

Expression of the molecular biological factors (MBFs) c-erbB-2, Ki-67 antigen, and tenascin (TN) was assessed immunohistochemically in specimens from patients who had undergone surgery for carcinoma of the papilla of Vater. The MBFs were then analyzed by histological factors (v, d, panc, n, Stage), which have been demonstrated to be outcome predictors, and by patient outcome. None of the MBFs showed any significant correlation with the histological factors. There were significant differences (p < 0.05) in the expression of c-erbB-2, Ki-67 antigen, and TN between patients who survived >5 years and those who survived <5 years. The patients with greater expression of c-erbB-2, Ki-67 antigen, and TN had a poor prognosis, whereas those with less expression had a good prognosis. They were therefore considered independent predictors of outcome for carcinoma of the papilla of Vater. Combined analysis of both histological factors and MBFs was also performed, with the result that the combined analysis of MBFs yielded a better prediction of outcome in carcinoma of the papilla of Vater than analysis of either one histological factor or MBF.

Adult↗

PubMed1996

[Two cases of metastatic lung cancer examined by bronchoscopic cytology].

We herein report two cases of metastatic lung cancer examined with bronchoscopic cytology. The first case involved a 43-year-old female, who had undergone low anterior resection of the rectum for rectal cancer three years earlier. Routine chest X-ray showed a nodular lesion in the left upper area. Bronchoscopic examination revealed a mass occluding the left upper bronchus. Simultaneous bronchoscopic biopsy and washing cytology were performed. The cytological specimen consisted of cell clusters with tall columnar epithelium arranged in a palisading manner. The cytological findings strongly suggested metastatic adenocarcinoma originating from the colorectal region. The patient died from respiratory failure. Autopsy confirmed metastatic deposit of adenocarcinoma in the lung. Histologically, the tumor invaded the overlying bronchial wall and was exposed in the lumen. The second case was an 80-year-old female, who had been diagnosed as gastric cancer by the endoscopic examination one year earlier. She had refused surgical treatment. Routine chest X-ray showed reticulonodular lesions disseminated throughout the bilateral lungs. Bronchial endoscopy presented edematous mucosa of the right lower bronchus. Brushing cytology as well as punch biopsy were taken. Cytological examination revealed atypical cells with increased N/C ratio and reduced cohesiveness. The lesion was diagnosed as metastatic adenocarcinoma of gastric origin from cytological findings and clinical history. The patient died from respiratory failure. Postmortem examination revealed cancer cells in the lymphatic channels of the bronchial wall. Our two cases indicate that bronchoscopic cytology is useful for estimating the origin of metastatic cancer.

Adenocarcinoma↗

PubMed1996

Expression of the KAI1 protein in benign prostatic hyperplasia and prostate cancer.

The KAI1 gene, recently identified as a metastatic suppressor gene for prostate cancer, was cloned and was revealed to be identical to the C33/IA4/ R2/4R9 gene. The expression of KAI1 protein was examined immunohistochemically in the tissues from 14 cases of benign prostatic hyperplasia and 46 cases of prostate cancer using mouse monoclonal anti-human C33 antibody. In benign prostatic hyperplasia tissues, KAI1 protein was uniformly expressed in the glandular cell membrane at cell-to-cell borders. The KAI1 protein in the tissues of untreated prostate cancer was also located at similar sites to those of benign prostatic hyperplasia, but the percentage of strongly positive cancer cells was correlated inversely to the Gleason pattern (P < 0.0001, one-way analysis of variance). There was also a statistically inverse correlation between the percentage of KAI1-positive cancer cells and the clinical stage (chi 2 = 9.6; P = 0.0081). In 4 cancer death cases relapsed from endocrine therapy, KAI1 protein was not stained in either primary or metastatic foci. These results indicate that the expression of KAI1 protein correlates to tumor characteristics in prostate cancer.

Adenocarcinoma↗

PubMed1995

Localization of a tumor suppressor gene associated with progression of human prostate cancer within a 1.2 Mb region of 8p22-p21.3.

Human prostate cancers frequently show loss of heterozygosity at loci on the short arm of chromosome 8. In order to take a step toward isolation of the putative tumor suppressor gene(s) on 8p via positional cloning, we performed high-resolution deletion mapping in 46 prostate cancers (stage B, 20 cases; stage C, 8 cases; endocrine therapy-resistant cancer death, 18 cases) using new 12 restriction fragment length polymorphism markers for this chromosomal region. Allelic losses were observed in 25 of the 44 cases (57%) that were informative with at least one locus. Detailed deletion mapping defined a 1.2 Mb commonly deleted region at 8p22-p21.3 flanked by markers cMSR-32 and C18-1051. A second region of common deletion was identified between C18-1312 and C18-494 at 8p21-8p11.22, suggesting that at least two tumor suppressor genes associated with prostate cancer are present on chromosome arm 8p. Allelic losses on 8p were observed more frequently in the cancer death cases (14/17, 82%) than in early-stage tumors (11/27, 40%; P < 0.01, Fisher's exact test). In two out of 7 patients for whom DNA was available from metastatic cancers as well as from normal tissues and primary tumors, the primary cancer foci had no detectable abnormality of 8p, but the metastatic tumors showed loss of heterozygosity. These results suggest that inactivation of tumor suppressor genes on 8p plays an important role in the progression of prostate cancer.

Adenocarcinoma↗

PubMed1995

A morphological study on the histogenesis of human colorectal hyperplastic polyps.

BACKGROUND & AIMS: Little is known about the histogenesis of human colorectal hyperplastic polyp, although this polyp is clinically very common. Therefore, the structural features of the polyp and their implications regarding histogenesis were studied. METHODS: A total of 261 foci were examined using scanning electronmicroscopic observation of the isolated crypt and surface structure, NaOH cell maceration and scanning electron microscopy, dissecting microscopy, and standard histological analysis. RESULTS: In surface view, each polyp crypt was discretely demarcated as in the normal crypt, suggesting that the crypt epithelium had not replaced the adjoining crypt. Notches at the base and various stages of branching, observed in 21.8% of the isolated crypts, were considered to reflect crypt fission. Several polyps with a single crypt mouth consisting of fissioned multiple crypts suggested polyp origin from a single crypt and growth by fission. Juxtaposition of small polyps and their fusion suggested polycentric origin. Almost all polyps showed increased stromal inflammatory cell infiltration and/or a lymphoid follicle at the base. CONCLUSIONS: Hyperplastic polyps originate by the apparent fusion of single abnormal crypts within a small region of mucosa. The polyps grow by fission of the crypt and fusion of the polycentrically originated polyps. Chronic inflammation has some relation to this process.

Adenoma↗

PubMed1995

Microsatellite instability in human prostate cancer.

Microsatellite instability (MSI) was examined at 36 loci, and found in 9 (43%) of the 21 prostatic cancers. A loss of heterozygosity had occurred in five cases (24%). MSI did not correlate with clinical stage, but might play a role in the development of a subset of prostate cancers.

Adult↗

PubMed1995

Mutational analysis of CDKN2 (CDK4I/MTS1) gene in tissues and cell lines of human prostate cancer.

To study mutation of the CDKN2 gene in prostate cancer, samples from 51 Japanese patients and four human prostate cancer cell lines were examined by single-strand conformation polymorphism analysis and direct sequencing. Only one out of 51 (2%) patients revealed a mutation, which was a 24 bp deletion from the 5'-untranslated region to codon 3, resulting in loss of the initiation site. One of the four cell lines revealed a missense mutation, a GAC-->TAC (Asp-->Tyr) at codon 84. These results indicate that mutation of the CDKN2 gene is rare in prostate cancer and thus does not contribute significantly to the pathogenesis of human prostate cancer. Prostate cancer cell lines may acquire more frequent abnormality of the CDKN2 gene than tumor tissues.

Base Sequence↗

PubMed1995

p53 mutations occur in clinical, but not latent, human prostate carcinoma.

To elucidate the role of the p53 tumor suppressor gene in prostate tumorigenesis, we probed for mutations in latent and clinical prostate cancers using single strand conformation polymorphism (SSCP) and restriction fragment length polymorphism (RFLP) analysis in combination with direct gene sequencing and immunohistochemical methodologies. Fifteen cases of subclinical and 32 cases of clinical carcinoma, the latter graded in stages A through D, were available for study. While p53 point mutations were detected in only 5 of 32 (16%) clinical cancers, no mutations were detected in latent disease. Of the carcinomas in stages B, C and D, 15% (2/13), 29% (2/7) and 9% (1/11) were positive for p53 mutations, respectively. Although no specific mutational patterns were observed, the aberrations found were predominantly single base missense substitutions. The data suggest not only an association of p53 mutation and progression of clinical prostate cancer, but also imply that some other mechanism(s) are at work in latent carcinoma.

Base Sequence↗

PubMed1995

Microsatellite instability and other molecular abnormalities in human prostate cancer.

Microsatellites are highly polymorphic, short-tandem repeat sequences dispersed throughout the genome. Instability of these repeat sequences at multiple genetic loci may result from mismatch repair errors, and occurs in hereditary nonpolyposis colorectal carcinoma and certain sporadic cancers. To examine microsatellite instability during the pathogenesis of human prostate cancer, we screened 48 prostate cancer cases (20 stage B, 10 stage C and 18 endocrine therapy-resistant cancer-death cases) for replication error at 17 microsatellite marker loci on 9 chromosomes. Microsatellite instabilities were found in 7 of 48 cases (14.6%), and all 7 cases showing the instability were poorly differentiated adenocarcinomas. Moreover, microsatellite instabilities were more frequently observed in cancer-death cases (6/18, 33%) than in stage B + C cases (1/30, 3.3%). These data suggest that microsatellite instability is an important genetic change related to the progression of a subset of human prostate cancer cases. It is suggested to be associated with extensive, concurrent molecular changes including androgen receptor gene mutations, as well as frequent loss of heterozygosity at chromosomal regions 8p, 10q, and 16q.

Adenocarcinoma↗

PubMed1995

Intratumor cellular heterogeneity and alterations in ras oncogene and p53 tumor suppressor gene in human prostate carcinoma.

To assess the potential role of ras oncogene activation and p53 tumor suppressor gene mutations in the development of human prostate carcinoma, nine cases of histologically heterogeneous prostate tumors obtained from total prostatectomies were probed for these specific events. Each tumor was divided into 5 to 10 areas according to different growth or histological patterns. Targeted DNA sequences coding for ras and p53 were amplified by the polymerase chain reaction, analyzed by single-strand conformational polymorphisms, and confirmed by direct DNA sequencing. Point mutations of the ras gene were found in three of the nine tumors. Two contained K-ras codon 13 and H-ras codon 61 mutations, found in only one and three areas of each lesion, respectively. The third tumor contained two different point mutations in K-ras codons 13 and 61 in different foci of the sample. Loss of heterozygosity at the polymorphic codon 72 in the p53 gene was detected in two of four informative cases (50%) showing fragment cleavage by restriction fragment length polymorphism analysis. Mutations in p53, missense transversions, single base insertions, and two base deletions were also detected in three tumors. The present results reveal mutated ras and p53 occasionally occurring in small foci of the tumor and that genetic mutations in p53, as opposed to those in ras, are more closely associated with invasive growth of heterogeneous prostate carcinoma.

Carcinoma↗

PubMed1994

Essential role of polyamines in restoration of DNA synthesis after UV radiation and expression of UV resistance in Cockayne syndrome cells.

Activity of ornithine decarboxylase (ODC) in Cockayne syndrome (CS) cells which were characterized by a delay of the recovery of DNA synthesis after 254 nm ultraviolet light (UV) radiation was extremely inhibited by UV, followed by a progressive decrease of putrescine. When putrescine was added in the cultures, CS cells showed a rapid recovery in DNA synthesis and also an expression of UV-resistance as seen in normal cells. Thus, ODC induction system of CS cells is highly sensitive to UV. Considering current hot spots in DNA repair, our results probably reflect a defect of preferentially rapid repair in ODC gene of CS cells.

Cell Line↗

PubMed1994

International comparison on ras gene mutations in latent prostate carcinoma.

Latent carcinomas of the prostate, discovered at autopsy in men with no prior treatment for prostatic disease, were studied for ras proto-oncogene mutations. Subjects included 21 Japanese, 15 U.S. whites, 15 U.S. blacks, 20 Hawaiian Japanese and 10 Colombians. PCR and sequence-specific oligonucleotide hybridization identified mutations in 5 Japanese, in 1 Hawaiian Japanese, in 1 U.S. black, in 1 U.S. white and in 3 Colombians. The 5 Japanese tumor samples contained 3 point mutations in codon 12 of K-ras and 2 mutations in codon 12 of N-ras respectively. One tumor in a Hawaiian Japanese man also showed a K-ras point mutation at codon 12. Two Colombians and one U.S. black man had tumors with mutations at codon 61 of H-ras, while 1 Colombian showed an N-ras mutation at this codon. The overall frequency of ras gene mutations was low, but point mutations in codon 12 were most common in latent tumors of Japanese, who experienced the lowest incidence and mortality from this tumor. Latent tumors in men from ethnic groups with high mortality and incidence rates showed fewer ras mutations than the Japanese, and these were more likely to involve codon 61. This finding is consistent with prior studies of more aggressive clinical cancers in Japanese men that indicated a higher frequency of mutations at codon 61.

Aged↗

PubMed1994

Identification of a P-glycoprotein-related protein (mini-P-glycoprotein) which is overexpressed in multidrug resistant cells.

Drug resistant variant cell lines were selected in vitro for resistance to adriamycin or vincristine, P388/ADR and P388/VCR-600, respectively, from P388 murine leukemia cells. These cells were demonstrated by immunoblot studies with P-glycoprotein specific monoclonal antibody (C219) to overexpress not only P-glycoprotein but also approximately 65 kDa protein, and the expression levels were found to correlate with the degree of resistance. Furthermore, in Northern blot analysis with an MDR1 cDNA as a probe, an overexpressed transcript with the length of about 2.4 kilobases which might encode this previously uncharacterized protein was also detected in the multidrug resistant cell line. Thus, it is suggested that this protein might be associated with multidrug resistant phenotype and be related to P-glycoprotein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1994

Mediation of the physiological response of platelets by interactions of spectrin and protein 4.1 with the cytoskeleton.

Spectrin and protein 4.1 became associated with the Triton-insoluble cytoskeletons during platelet activation. Inhibition of platelet activation by a PGI2 analogue resulted in release of the proteins from the cytoskeletons. Changes in subcellular distributions of the proteins preceded changes in the state of platelet aggregation. These results suggest that interactions of spectrin and protein 4.1 with the cytoskeletons are involved in mediating the physiological response of the platelet.

Actins↗

PubMed1994

State of adenomatous polyposis coli gene and ras oncogenes in Japanese prostate cancer.

Genetic alterations of ras oncogenes (K-, H- and N-ras) and adenomatous polyposis coli (APC) gene in tissues of prostate cancer from Japanese patients were examined using PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) analysis and direct sequencing. Tissues from 8 cases of untreated stage B prostate cancer surgically removed and from 10 cases of endocrine therapy-resistant metastatic disease obtained at autopsy were used in the present study. In four out of 18 cases (22%), ras point mutations were found, two in either codon 12 or 61 of K-ras and two in either 13 or 61 of H-ras. These point mutations were detected in one of the stage B cases (13%) and in three of the autopsy cases (30%). All these cases were poorly differentiated adenocarcinoma. In autopsy cases showing ras mutation in cancerous prostate, the same alteration was observed in metastatic tissues. No APC gene mutation was detected in any sample, although polymorphism was found in some cases. These results indicate that ras oncogene mutations are related to the progression of prostate cancer, whereas APC gene alteration is not involved in tumorigenesis and development of this cancer.

Adenocarcinoma↗

PubMed1994

p53 gene mutations in human prostate cancers in Japan: different mutation spectra between Japan and western countries.

The involvement of p53 mutations in prostate cancers in Japan was investigated. To evaluate any possible clinicopathological significance, p53 mutations in 40 samples from 36 Japanese prostate cancers of different stages (five cases of latent tumors, three of stage A cancers, 10 of stage B, five of stage C and 13 of stage D), including four lymph node metastases of stage D cases, were examined by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis and sequencing. Mutations were detected in five of 40 samples (12.5%); four were in primary cancers and the other in a lymph node metastasis from one of them. All mutation-positive cases were in stage D, and the mutation frequency in stage D cases was 31%. This result indicates that p53 mutations may play a role in the progression of a subgroup of prostate cancers in Japanese, as observed for Americans and Europeans. However, a difference was noted between Japanese and Americans in the p53 mutational spectrum (at CpG site), presumably arising from variation in the underlying etiologic factors.

Aged↗

PubMed1994

Sarcomatoid carcinoma of the urinary tract.

Sarcomatoid carcinoma is a rare variant of malignant tumor arising from the urinary tract. This tumor had been termed carcinosarcoma because of its carcinomatous and sarcomatous components. There is still some confusion in the terminology between true carcinosarcoma and sarcomatoid carcinoma; however, the latter is now regarded as primarily a malignant epithelial tumor with pseudosarcomatous transformation. Four cases of sarcomatoid carcinoma arising from the urinary tract are reported. The patients were a 77 year old female, and three males aged 62, 69 and 80 years. All but the eldest patient complained of gross hematuria. Surgical removal was performed in the younger three cases, and an autopsy was done in the remaining case. All the tumors were macroscopically polypoid. Histopathologic examination revealed fasciculated spindle-cell tumors with myxoid stroma or malignant fibrous histiocytoma-like spindle cell tumors. The epithelial nature was proven in these sarcomatous cells by immunohistochemical and/or electron-microscopic examinations. Only a small amount of squamous cell carcinoma components was also evident in the latter three cases. Although the younger three patients were alive at 44, 23 and 39 months' follow-up, respectively, constant careful monitoring is recommended.

Aged↗