[Show abstract][Hide abstract] ABSTRACT: Chondroblastoma is a benign bone tumor with a relatively high incidence in older children and adolescents during the period of active epiphyseal growth. It is generally regarded as a benign neoplasm, but sometimes it grows aggressively or recurs. To prevent recurrence, complete curettage is important; however, such an approach can be extremely difficult to perform precisely when the chondroblastoma arises deep in the epiphysis. In our patient's case, we used a computed tomography-based navigation system with registration technique involving skin marker fiduciaries and endoscopic curettage of the lesion.
A 16-year-old Japanese girl presented to our facility with left knee joint pain, which started nine months before her initial examination. Computed tomography and magnetic resonance imaging studies of the left knee showed a radiolucent lesion with marginal sclerosis and lobular homogeneous hypo-intensity and hyper-intensity signals in the distal epiphysis of the left femoral epiphysis, carried through to the growth plate. To prevent recurrence of chondroblastoma and growth disturbance, we used a computed tomography-based navigation system with registration technique involving skin marker fiduciaries and endoscopic curettage of the lesion. Wide excision with total removal of the chondroblastoma in the distal femur often requires large exposure with associated drawbacks, where a wide excision near the growth plate can potentially lead to growth disturbance. Therefore, in an accessible location in the distal femur, endoscopic excision of chondroblastoma under navigation system guidance can be performed with minimal operative damage.
In the setting of a benign intra-osseous lesion infiltrating the growth plate, arthroscopic retrieval or excision under a computed tomography-based navigation system should be considered before proceeding with open surgery.
Journal of Medical Case Reports 06/2013; 7(1):164. DOI:10.1186/1752-1947-7-164
[Show abstract][Hide abstract] ABSTRACT: Background:
Expression profiles of some microRNAs (miRNAs) were associated with clinicopathological findings in human prostate cancer (PC), but the relative expression of miRNAs among Gleason patterns (GPs) remains unclear. In this study, we investigated the expression of several known microRNAs in each GP of PC.
Formalin-fixed, paraffin embedded (FFPE) tissue samples were obtained from radical prostatectomy (RP) (patient set 1, n = 43, including (GP 3) n = 22, (GP 4) n = 35, and (GP 5) n = 12) and needle biopsy (patient set 2, n = 10, (GP 4) n = 10). Cancer tissues from each GP and adjacent normal counterparts were separately collected using laser-captured microdissection (LCM). Real-time RT-PCR was performed to determine the relative expression of miRNAs, including miR-31-5p, -34c-5p, -96-5p, -182-5p, -183-5p, -205-5p, -221-3p, and -222-3p, which were currently reported to be involved in PC progression.
In radical prostatectomy samples, relative expression of miR-31-5p, miR-34c-5p, and miR-205-5p in any GP was significantly decreased compared to normal counterpart. However, no significant difference was detected among GP 3, GP 4, and GP 5. Meanwhile, in the same GP4, expression of miR-31-5p miR-182-5p, and miR-205-5p in cancer tissues obtained from high grade cancer was significantly higher than those obtained from intermediate grade cancer. Validation study using biopsy samples revealed that the relative expression of miR-182-5p was statistically higher in high grade cancer even in same GP4.
We confirmed the expression of miR-182-5p depended on the cancer grade even in same GP 4. Expression of miRNA associated with Gleason grading system may contribute to more accurate preoperative cancer risk evaluation.
The Prostate 06/2013; 73(8). DOI:10.1002/pros.22626 · 3.57 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background
Cutaneous squamous cell carcinoma (SCC) of the hands and fingers are sometimes locally aggressive; with higher rates of regional metastasis than other cutaneous SCC, although distant metastasis is rare.
We present the case of a 62–year-old Japanese man with double cancers: a tongue SCC and a cutaneous SCC. Swelling of the finger lesion developed gradually around the entire remaining middle finger after accidental amputation at the proximal interphalangeal joint. Histopathological examination of the tumor on the stump of the amputated finger indicated a well-differentiated SCC. The past history indicated surgery for SCC of the tongue 3 years earlier; with histopathology of moderately-differentiated SCC.
Since dedifferentiation is unlikely in metastatic tumors, the cutaneous SCC of the finger is unlikely to have originated from the tongue SCC. Alternatively, the double cancer may be two unrelated lesions or the tongue tumor could have originated from the cutaneous SCC.
BMC Research Notes 10/2012; 5(1):595. DOI:10.1186/1756-0500-5-595
[Show abstract][Hide abstract] ABSTRACT: Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive forms of squamous cell carcinomas. Common genetic lesions in ESCC include p53 mutations and EGFR overexpression, both of which have been implicated in negative regulation of Notch signaling. In addition, cyclin D1 is overexpressed in ESCC and can be activated via EGFR, Notch and Wnt signaling. To elucidate how these genetic lesions may interact during the development and progression of ESCC, we tested a panel of genetically engineered human esophageal cells (keratinocytes) in organotypic 3D culture (OTC), a form of human tissue engineering. Notch signaling was suppressed in culture and mice by dominant negative Mastermind-like1 (DNMAML1), a genetic pan-Notch inhibitor. DNMAML1 mice were subjected to 4-Nitroquinoline 1-oxide-induced oral-esophageal carcinogenesis. Highly invasive characteristics of primary human ESCC were recapitulated in OTC as well as DNMAML1 mice. In OTC, cyclin D1 overexpression induced squamous hyperplasia. Concurrent EGFR overexpression and mutant p53 resulted in transformation and invasive growth. Interestingly, cell proliferation appeared to be regulated differentially between those committed to squamous-cell differentiation and those invading into the stroma. Invasive cells exhibited Notch-independent activation of cyclin D1 and Wnt signaling. Within the oral-esophageal squamous epithelia, Notch signaling regulated squamous-cell differentiation to maintain epithelial integrity, and thus may act as a tumor suppressor by preventing the development of a tumor-promoting inflammatory microenvironment.
American Journal of Cancer Research 08/2012; 2(4):459-75. · 4.17 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To investigate whether grade II oligodendroglioma was transformed to glioblastoma or not, histopathological evaluation of recurrent oligodendrogliomal tumors (OG) and diffuse astrocytomas (DA) was performed. The OG group was composed of ten patients with OG, including seven oligodendrogliomas and three oligoastrocytomas. The DA group was composed of ten patients with DA, including eight fibrillary astrocytomas and two gemistocytic astrocytomas. The histopathological parameters of glioblastoma including nuclear atypia, multinucleated giant cells, glomeruloid tufts (GT) as a marker of microvascular proliferation, necrosis, and the Ki-67 staining index were investigated. Evaluation of these parameters was scored as follows: 0, none; 1, sporadic; 2, partial; 3, extensive. There were no cases of transformation to glioblastoma in the OG group. There were five cases of transformation to secondary glioblastoma in the DA group. In recurrent tumors, scores of GT and necrosis in the OG group were significantly lower than those in the DA group (p < 0.005). Nuclear atypia and high proliferative activity (Ki-67 index) were identified in recurrent tumors of the OG group. Our study suggested that the extent of GT and necrosis in recurrent OG was less than that in recurrent DA, and transformation to glioblastoma from oligodendroglial tumor was exceptional.
[Show abstract][Hide abstract] ABSTRACT: There have been some recent reports about glioblastoma with oligodendroglial (OG) components and malignant glioma with primitive neuroectodermal tumor (PNET)-like components. We investigated whether the presence and extent of OG components and PNET-like components influenced the prognosis in patients with glioblastoma. Eighty-six patients with glioblastoma were divided into an OG group (28 %), which revealed areas with a honeycomb appearance, and a non-OG group (72 %) without a honeycomb appearance. Patients with glioblastoma were also divided into a PNET group (27 %), which revealed areas with PNET-like features defined as neoplastic cells with high N/C ratios and hyperchromatic oval-carrot-shaped nuclei, and lacked the typical honeycomb appearance, and a non-PNET group (73 %) without PNET features. There were no significant differences in overall survival among the OG, the non-OG, the PNET, and the non-PNET groups. Two patients who survived longer than 36 months had both OG and PNET components with 1p or 19q loss of heterozygosity. Perinuclear halo, which is a characteristic feature of oligodendrogliomas, is an artifact of tissue fixation. Therefore, we should not readily use the term glioblastoma with OG components. PNET-like components, which are considered rare in malignant gliomas, may be frequently identified in glioblastomas.
[Show abstract][Hide abstract] ABSTRACT: We report a case of advanced sarcomatoid renal cell carcinoma (RCC) effectively treated with sunitinib. A 77-year-old female who had gross hematuria and left lower abdominal pain was found to have a left renal tumor by computed tomography (CT) and was referred to our hospital. CT revealed a poorly enhanced mass in the left kidney and an enlarged paraaortic lymph node. The patient underwent laparoscopic left nephrectomy, and the tumor was histologically diagnosed as a sarcomatoid RCC. Sunitinib was administered to treat lymph node metastasis, postoperatively, and a partial response was observed after 4 courses. Sunitinib administration has been continued without tumor re-growth.
[Show abstract][Hide abstract] ABSTRACT: Hepatocyte growth factor (HGF) is a multifunctional molecule that acts as mitogen, motogen, and/or morphogen in a variety of cells. MET, a specific receptor tyrosine kinase for HGF, is upregulated in various tumors including squamous cell carcinoma of the human head and neck (HNSCC), but how HGF affects the expression of downstream functional genes has not yet been elucidated in detail. In the present study, we examined the expression of microRNA (miRNA), non-coding small RNA that regulate cell proliferation and functions by interfering with the translation of target mRNA, with or without HGF stimulation in HNSCC cell line HSC3. Among several miRNAs, in which the expression was altered after HGF stimulation, we focused on miR-200c and miR-27b, both of which were drastically downregulated after HGF stimulation. Expression of ZEB1, a target mRNA for miR-200c, was upregulated 3 and 6 h after HGF stimulation, and that of E-cadherin, a downstream molecule of ZEB1, was downregulated 12 h after HGF stimulation. Expression of ST14/matriptase, an enzyme for extracellular matrix (ECM) degradation and HGF activation and a target mRNA for miR-27b, was drastically upregulated in the protein level after HGF stimulation, although it was not statistically altered in the mRNA level. These results suggest that miR-200c and miR-27b downregulated by HGF might play an important role in epithelial-mesenchymal transition mediated by ZEB1/E-cadherin and ECM degradation and HGF autoactivation mediated by ST14/matriptase, respectively. Altered expression of miRNA directly regulated by HGF might contribute enhanced progressive and invasive characteristics of HNSCC by regulating the translation of HGF-induced functional molecules.
Cancer Science 09/2011; 102(12):2164-71. DOI:10.1111/j.1349-7006.2011.02096.x · 3.52 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Zinc finger E-box-binding (ZEB) proteins ZEB1 and ZEB2 are transcription factors essential in TGF-β-mediated senescence, epithelial-to-mesenchymal transition (EMT), and cancer stem cell functions. ZEBs are negatively regulated by members of the miR-200 microRNA family, but precisely how tumor cells expressing ZEBs emerge during invasive growth remains unknown. Here, we report that NOTCH3-mediated signaling prevents expansion of a unique subset of ZEB-expressing cells. ZEB expression was associated with the lack of cellular capability of undergoing NOTCH3-mediated squamous differentiation in human esophageal cells. Genetic inhibition of the Notch-mediated transcriptional activity by dominant-negative Mastermind-like 1 (DNMAML1) prevented squamous differentiation and induction of Notch target genes including NOTCH3. Moreover, DNMAML1-enriched EMT-competent cells exhibited robust upregulation of ZEBs, downregulation of the miR-200 family, and enhanced anchorage-independent growth and tumor formation in nude mice. RNA interference experiments suggested the involvement of ZEBs in anchorage-independent colony formation, invasion, and TGF-β-mediated EMT. Invasive growth and impaired squamous differentiation were recapitulated upon Notch inhibition by DNMAML1 in organotypic three-dimensional culture, a form of human tissue engineering. Together, our findings indicate that NOTCH3 is a key factor limiting the expansion of ZEB-expressing cells, providing novel mechanistic insights into the role of Notch signaling in the cell fate regulation and disease progression of esophageal squamous cancers.
Cancer Research 09/2011; 71(21):6836-47. DOI:10.1158/0008-5472.CAN-11-0846 · 9.33 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A 60-year-old man presented with icterus and stomachache. Enhanced CT showed dilatation of both the main pancreatic duct and bile duct, enhanced wall thickening in the lower bile duct, and minute linear calcification along the pancreatic duct in the pancreatic head. ERCP showed redness of the main papilla and bile duct-duodenum fistula. Biopsy of papilla and fistula did not reveal malignancy. FDG-PET showed strong accumulation in the pancreatic head. Because malignant disease of the lower bile duct or pancreatic head could not be denied, we performed pylorus-preserving pancreatoduodenectomy though the tumor markers were not elevated. A pathologic diagnosis of pancreatic abscess caused by actinomycosis was estalished. Actinomycosis in the pancreas is extremely rare. The fistulous opening of the bile duct to the duodenum may be one cause.
[Show abstract][Hide abstract] ABSTRACT: Mucinous cystic neoplasm (MCN) of the pancreas is characterized by mucin-producing columnar epithelium and an ovarian-type stroma. It occurs almost exclusively in women and is almost always located in the pancreatic body or tail. Here, we report a case of large MCN located in the pancreatic head but not in the body nor tail in a 32-year-old pregnant woman, which was thought to have grown rapidly during pregnancy. It was ruptured at 34 weeks of gestation and the patient was admitted to the emergency department of the University of Fukui Hospital with an acute abdomen. Emergency cesarean section followed by pancreaticoduodenectomy was performed. The tumor consisted of many small cysts lined by a single-layer of mucinous epithelium with papillary growth and partial solid parts showing invasive growth and sarcomatoid changes, indicating mucinous cystic neoplasm with an associated invasive carcinoma (previously referred as mucinous cystadenocarcinoma). Thickened septa revealed ovarian-type stroma strongly positive for α-inhibin and partly positive for progesterone receptor immunohistochemically. We also review and discuss previous reports of MCNs including those with an associated invasive carcinoma in pregnant patients.
Pathology International 01/2011; 61(1):28-33. DOI:10.1111/j.1440-1827.2010.02609.x · 1.69 Impact Factor