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Motomu Manabe

Publications and source records attributed to Motomu Manabe.

14 recordsLinked to original sources
PubMed2006

Trichoblastic infundibular cyst.

We report 4 cases of an infundibular cyst that histopathologically showed small papillary projections of follicular germinative cells emanating from the basal layer of the cyst wall. Some of these projections branched and formed a reticulated pattern. This cystic lesion is histopathologically distinctive. We propose to designate it as a trichoblastic infundibular cyst because its lining resembles that of an infundibular cyst, yet it has cells that resemble those of the follicular germ in its wall.

Adult↗
PubMed2006

Collagen-poly glycolic acid hybrid matrix with basic fibroblast growth factor accelerated angiogenesis and granulation tissue formation in diabetic mice.

Because poor skin wound healing associated with diabetes is thought to be partly a result from impaired angiogenesis, treatments that improve angiogenesis could have important clinical applications. We herein report the effects of novel developed material, collagen-poly glycolic acid fiber hybrid matrix, being used together with basic fibroblast growth factor to promote wound healing of full-thickness skin defects on the back of type 2 diabetic Lepr(db) mice. Our data indicates that this therapeutic approach markedly promotes angiogenesis and granulation tissue formation in comparison with other conditions 14 days after wounding.

Animals↗
PubMed2005

Possible spontaneous regression of a metastatic lesion of keratoacanthoma-like squamous cell carcinoma in a regional lymph node.

We report herein a case of keratoacanthoma-like squamous cell carcinoma in an 82-year-old male that showed regional lymph node metastasis followed by self-regression of the metastatic lesion. This case is consistent with the previously reported observation that tumors compatible with the clinical features of keratoacanthoma may have malignant biological potential, however, it also demonstrates that even metastatic lesions may exhibit self-regression similar to that observed for primary lesions. Despite the view that keratoacanthoma-like squamous cell carcinoma may represent a variant of squamous cell carcinoma, occasionally it undergoes a unique clinical course.

Aged, 80 and over↗
PubMed2004

Reduced expression and aberrant localization of p120catenin in human squamous cell carcinoma of the skin.

BACKGROUND: p120catenin (p120ctn), a member of the Armadillo protein family, is ubiquitously expressed and binds to classical cadherins together with other catenins to participate in the adherens junction. p120ctn has numerous isoforms generated through extensive splicing and alternative usage of translation initiation codons. Although the involvement of p120ctn in cell growth control has been postulated, little has so far been known about its expression patterns in the skin and epidermal tumors. OBJECTIVE: To identify the isoforms expressed in benign and malignant keratinocytes and to analyze the expression patterns of p120ctn in epidermal tumor specimens. METHODS: HaCaT, DJM-1, BSCC-93, HSC-1, HSC-5 and A431 cells along with normal skin tissue were subjected to RT-PCR to identify the expressed isoforms. For immunofluorescence study, surgical specimens including 29 squamous cell carcinomas (SSCs), 4 basal cell carcinomas (BCCs) and 4 seborrheic keratoses as well as 3 normal skin samples were stained with specific antibodies to detect p120ctn and E-cadherin. RESULTS: RT-PCR revealed that the isoform 3A was predominantly expressed with faint expression of the isoform 4 and that there was no difference in expressed isoforms between the examined cell lines. Immunofluorescent staining indicated that the expression of p120ctn was significantly reduced in all of the examined squamous cell carcinomas and that p120ctn was frequently localized in cytoplasm. In benign tumors and normal samples, p120ctn was properly expressed in cell-cell boundaries. Furthermore, there were several SCCs where E-cadherin continued to be expressed with no expression of p120ctn. CONCLUSION: Reduced expression and aberrant localization of p120ctn are among the most common events during the development and/or progression of SCCs.

Carcinoma, Squamous Cell↗
PubMed2004

Immunohistochemical differentiation of extra-ocular sebaceous carcinoma from other skin cancers.

We performed an immunohistochemical study using routinely processed formalin-fixed and paraffin-embedded tissue specimens from 26 cases of extra-ocular sebaceous carcinoma (EOSC) and eight easily available antibodies. They were polyclonal anti-carcinoembryonic antigen (CEA) antibody, monoclonal anti-CEA antibody, anti-breast carcinoma associated antigen-225 antibody (CU18), anti-CA15.3 antibody (CA15.3), anti-CD15 antibody (CD15), anti-breast carcinoma associated antigen antibody (B6.2), anti-gross cystic disease fluid antigen-15 antibody (GCDFP15) and anti-Thomsen-Friedenreich antigen antibody (TFA). Squamous cell carcinoma, porocarcinoma, syringomatous carcinoma, malignant clear cell hidradenoma, apocrine adenocarcinoma, and extramammary Paget's disease with underlying adenocarcinoma were used as controls. EOSC was positive for CU18 and CA15.3 in most cases, and for CD15 in a few cases. Squamous cell carcinoma of the skin was positive for CA15.3 in only one case. Porocarcinoma, syringomatous carcinoma and malignant clear cell hidradenoma were positive for CEA, CU18, CA15.3, and B6.2 in most cases. Apocrine adenocarcinoma and extramammary Paget's disease with underlying adenocarcinoma were positive for CEA, CU18, CD15, GCDFP15, CA15.3, and B6.2 in most cases. TFA was positive not only in EOSC but also in other skin cancers. Immunohistochemical examinations using these seven of eight antibodies except for TFA and routinely processed formalin-fixed and paraffin-embedded tissue specimens are beneficial in differentiating EOSC from other skin cancers.

Adenocarcinoma, Sebaceous↗
PubMed2003

An autocrine/paracrine loop linking keratin 14 aggregates to tumor necrosis factor alpha-mediated cytotoxicity in a keratinocyte model of epidermolysis bullosa simplex.

Epidermolysis bullosa simplex (EBS) is a blistering cutaneous disease featuring protein aggregates. Here we investigate the molecular mechanisms linking protein aggregates to cell death in a cellular model of EBS in which HaCaT keratinocytes are transfected with plasmids expressing various mutant forms of keratin 14 (K14). In HaCaT cells, mutant K14 was found to form ubiquitinated protein aggregates that suppressed 20 S proteasome function instead of being degraded by 20 S proteasome. Keratinocytes with mutant K14-induced phosphorylation of the stress-activated kinase c-Jun, as well as up-regulation of unfolding protein Bip, indicates induction of endoplasmic reticulum stress. HaCaT cells were susceptible to apoptosis by activation of caspases-3, and -8, but not caspase-9 or -12. Tumor necrosis factor-alpha (TNFalpha) in the culture medium was increased in keratinocytes with mutant K14 compared with wild K14, and the addition of neutralizing anti-TNFalpha antibody to the culture medium rescued keratinocytes from cell death. Thus, TNFalpha release and the subsequent activation of the TNFalpha receptor by an autocrine/paracrine pathway links protein aggregates to cell death in this keratinocyte EBS cellular model. Furthermore, mutation in K14 reduced its affinity to TNFalpha receptor-associated death domain (TRADD), suggesting that the susceptibility of keratinocytes to caspase-8-mediated apoptosis is increased in mutated K14 because of impairment of the cytoprotective mechanism mediated by K14-TRADD interaction.

Annexin A5↗
PubMed2003

Keratinocyte-specific Pten deficiency results in epidermal hyperplasia, accelerated hair follicle morphogenesis and tumor formation.

PTEN is a tumor suppressor gene mutated in many human cancers. We used the Cre-loxP system to generate a keratinocyte-specific null mutation of Pten in mice (k5Pten(flox/flox) mice). k5Pten(flox/flox) mice exhibit wrinkled skin because of epidermal hyperplasia and hyperkeratosis and ruffled, shaggy, and curly hair. Histological examination revealed that skin morphogenesis is accelerated in k5Pten(flox/flox) mice. Within 3 weeks of birth, 90% of k5Pten(flox/flox) mice die of malnutrition possibly caused by hyperkeratosis of the esophagus. All k5Pten(flox/flox) mice develop spontaneous tumors within 8.5 months of birth, and chemical treatment accelerates the onset of tumors. k5Pten(flox/flox) keratinocytes are hyperproliferative and resistant to apoptosis and show increased activation of the Pten downstream signaling mediators Akt/protein kinase B (PKB) and extracellular signal-regulated kinase. Pten is thus an important regulator of normal development and oncogenesis in the skin.

Animals↗
PubMed2003

Mucinous carcinoma of the skin with apocrine-type differentiation: immunohistochemical studies.

We investigated the pathway of differentiation in a case of mucinous carcinoma of the skin (MCS) arising on the right temple of a 70-year-old man. Histopathologic findings of the tumor showed evidence of apocrine-type differentiation such as distinctive decapitation secretion. Additionally, by employing a panel of antibodies, the immunohistochemical staining pattern of tumor cells was shown to be compatible with that of apocrine glands. Although the differentiation of this neoplasm remains controversial, the findings in our case suggest apocrine differentiation.

Adenocarcinoma, Mucinous↗
PubMed2002

Genetic epidemiology of hereditary hemorrhagic telangiectasia in a local community in the northern part of Japan.

Hereditary hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber syndrome) is an autosomal dominant disorder characterized by aberrant vascular development. We report here a genetic epidemiologic study in a county, A, in the Akita prefecture (population 1.2 million) located in northern Japan. Nine HHT patients who had been referred to tertiary-care hospitals were located in and near the study county. A total of 137 pedigree members were traced of which 81 were alive and 32 were affected by HHT. Complications associated with cerebral or pulmonary arteriovenous malformations were proven in six out of seven families. Linkage analysis in two large families revealed a weak yet suggestive linkage to the HHT1 locus (encoding endoglin; ENG). Three novel mutations were found in four families, all of which led to a frameshift: a G to C transversion at the splicing donor site of intron 3 (Inv3+1 G>C) in one family, one base pair insertion (A) at nucleotide 828 (exon 7) of the endoglin cDNA in two large families (c.828-829 ins A), and a four base pair deletion (AAAG) beginning with nucleotide 1120 (exon 8) of the endoglin cDNA (c.1120-1123 delAAAG) in one family. The insertion of A in exon 11 (c.1470-1471 insA) mutation found in one family has also been reported in a European family. No endoglin gene mutations were found in two families. The population prevalence of HHT in the county was estimated to be 1:8,000 approximately 1:5,000, roughly comparable with those reported in European and U.S. populations, which is contradictory to the traditional view that HHT is rare among Asians. We recommend that families with HHT be screened for gene mutations in order that high-risk individuals receive early diagnosis and treatment initiation that will substantially alter their clinical course and prognosis.

Adult↗
PubMed2002

Alteration of mast cell proliferation/apoptosis and expression of stem cell factor in the regression of mastocytoma--report of a case and a serial immunohistochemical study.

BACKGROUND: Spontaneous regression of solitary mastocytoma is a well-described phenomenon, but its mechanism is unknown. METHODS: Serial-section immunohistochemical analyses were performed on biopsies of a mastocytoma from a Japanese child during the proliferation stage (PS, 7 months of age) and the regression stage (RS, 5 years old). RESULTS: Mast cell (MC) density in RS was markedly decreased (406 cells/mm2) compared to that in PS (3554 cells/mm2). MCs in RS were larger than those in PS. With proliferative cell nuclear antigen (PCNA) staining, 1.7% MCs were positive in PS, whereas no positive MCs were seen in RS. TUNEL-labeling index (LI) in RS (2.8%) increased 1.5-fold in PS (1.9%). With stem cell factor (SCF) staining, 57% of lesional MCs in RS revealed strong cytoplasmic immunoreactivity, whereas only 9% of MCs were positive in PS. Epidermal SCF reactivity was found as intracellular and intercellular patterns in both PS and RS. CONCLUSIONS: Loss of MC proliferating activity, an increase in apoptotic MCs, and increased expression of SCF in remaining MCs in RS may play a role in the involution of mastocytomas.

Apoptosis↗
PubMed2002

Activation of mast cells within a tumor of angiosarcoma: ultrastructural study of five cases.

The accumulation of mast cells around tumors is a well-recognized phenomenon in a number of malignancies, including basal cell carcinoma, melanoma, and breast cancer. However, little information exists regarding mast cells within tumor nests. To clarify the role of mast cells infiltrating in skin cancers, we examined the morphological features of mast cells within tumors of five cases of angiosarcoma, including two patients with Stewart-Treves syndrome, by electron microscopy. In light microscopy, mast cells were observed within tumor nests at various densities and exhibited weak staining intensity with toluidine blue. By electron microscopy, most of the tumor-infiltrating mast cells exhibited anaphylactic or piecemeal degranulation, indicating that the mast cells had been activated in situ. Some mast cells were noted in close apposition to tumor cells, suggesting the existence of direct cell-to-cell interactions. Tumor cells adjacent to mast cells showed no degenerative changes. In conclusion, these results suggest that careful histologic examination in combination with electron microscopy should enable us to identify more mast cells within cancer lesions with greater sensitivity than in a number of prior reports. Furthermore, the close proximity of mast cells and surrounding tumor cells suggests some biologically significant role of mast cells in the development of angiosarcoma, including tumor growth as well as host immunity and stromal reaction.

Aged↗