Histology and histopathology Vol.23,nº11 (2008)

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http://hdl.handle.net/10201/177496

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Sarcomatoid acquired cystic disease-associated renal cell carcinoma
(Murcia : F. Hernández, 2008) Kuroda, Naoto; Tamura, Masato; Taguchi, Takahiro; Tominaga, Akira; Hes, Ondrej; Michal, Michal; Ohara, Masahiko; Hirouchi, Takashi; Mizuno, Keiko; Hayashi, Yoshihiro; Shuin, Taro; Lee, Gang-Hong
In this article, we report a rare case of hitherto undescribed acquired cystic disease (ACD)- associated renal cell carcinoma (RCC) with sarcomatoid change. A 78-year-old woman had been receiving hemodialysis for fourteen years at the time when a renal tumor was encountered on the follow-up examination of the kidney. Microscopically, oncocytic cuboidal cells proliferated with tubular, cribriform or papillary growth patterns, and atypical columnar cells with abundant cytoplasm proliferated with papillary configuration. Oxalate crystal deposition was observed in the stroma and the tumor focally resembled translocation type (TFE3) RCC. Sarcomatous neoplastic cells were also seen. The cytoplasm of oncocytic and sarcomatous neoplastic cells was diffusely positive for antimitochondrial antibody and the ultrastructural examination detected many mitochondria in the cytoplasm of oncocytic carcinoma cells and sarcomatous neoplastic cells. The loss of chromosomes 1p, 2q11-22, 9 and 14 was observed using comparative genomic hybridization analysis. We thus report here a case of hitherto undescribed ACD-associated RCC intermingled with oncocytic cells, translocation type RCC-like area and sarcomatoid change. This is the sixth case of sarcomatoid RCC arising in end-stage kidney disease.
Open Access
Epidemiology and molecular biology of gastrointestinal stromal tumors -GISTs- a population-based study in the South of Switzerland, 1999-2005
(Murcia : F. Hernández, 2008) Mazzola, Paola; Spitale, Alexandra; Banfi, Sara; Mazzucchelli, Luca; Frattini, Milo; Bordoni, Andrea
Introduction. Gastrointestinal stromal tumors (GISTs) are characterized at the molecular level by c-kit or PDGFRA oncogene mutations. Although GISTs raised major interest in past decades, population-based studies are still rare. Materials and Methods. All GISTs diagnosed in Southern Switzerland (1999-2005) were identified using Ticino Cancer Registry and analysed for c-kit and PDGFRA mutations. Clinical and molecular features were studied. Results. Annual incidence of GISTs was 1.47 cases/100,000 inhabitants (median age: 64 years; median size: 6.0 cm). Most GISTs arose in the stomach (60.5%). The malignancy risk was verylow/ low in 47% of patients. DNA sequences showed a gene alteration in either c-kit or PDGFRA genes in 72.5% of patients. Mutations occurred mostly in c-kit exon 11 (60%). No mutations in c-kit exons 13 or 17 were found. An equal number of alterations in exons 12 and 18, and no mutations in exon 14 were observed in the PDGFRA gene. Discussion. This is the first comprehensive population-based study of GISTs incidence and molecular biology characterization in Central Europe. Our incidence data showed higher agestandardized rates compared to other European countries. The gene mutation spectrum differed when compared to the literature. This is relevant to improve the molecular profile knowledge based on Cancer Registry data.
Open Access
Ets transcription factors in intestinal morphogenesis, homeostasis and disease
(Murcia : F. Hernández, 2008) Jedlicka, Paul; Gutierrez-Hartmann, Arthur
Ets transcription factors comprise a large family of sequence-specific regulators of gene expression with important and diverse roles in development and disease. Most Ets family members are expressed in the developing and/or mature intestine, frequently in a compartment-specific and temporally dynamic manner. However, with the exception of the highly expressed Elf3, involved in embryonic epithelial differentiation, little is known about Ets functions in intestinal development and homeostasis. Ets factors show altered expression in colon cancer, where they regulate pathways relevant to tumor progression. Ets factors also likely act as important modifiers of nonneoplastic intestinal disease by regulating pathways relevant to tissue injury and repair. Despite a large body of published work on Ets biology, much remains to be learned about the precise functions of this large and diverse gene family in intestinal morphogenesis, homeostasis, and both neoplastic and non-neoplastic pathology.
Open Access
Involvement of endoplasmic reticulum stress and activation of MAP kinases in B-lapachone-induced human prostate cancer cell apoptosis
(Murcia : F. Hernández, 2008) Lien, Yi-Chen; Kung, Hsiu-Ni; Lu, Kuo-Shyan; Jeng, Chung-Jiuan; Chau, Yat-Pang
ß-Lapachone, an o-naphthoquinone, induces various carcinoma cells to undergo apoptosis, but the mechanism is poorly understood. In the present study, we found that the ß-lapachone-induced apoptosis of DU145 human prostate carcinoma cells was associated with endoplasmic reticulum (ER) stress, as shown by increased intracellular calcium levels and induction of GRP-78 and GADD-153 proteins, suggesting that the endoplasmic reticulum is a target of ß-lapachone. ß- Lapachone-induced DU145 cell apoptosis was dosedependent and accompanied by cleavage of procaspase- 12 and phosphorylation of p38, ERK, and JNK, followed by activation of the executioner caspases, caspase-7 and calpain. However, pretreatment with the general caspase inhibitor, z-VAD-FMK, or calpain inhibitors, including ALLM or ALLN, failed to prevent ß-lapachone-induced apoptotic cell death. Blocking the enzyme activity of NQO1 with dicoumarol, a known NQO1 inhibitor, or preventing an increase in intracellular calcium levels using BAPTA-AM, an intracellular calcium chelator, substantially inhibited MAPK phosphorylation, abolished the activation of calpain, caspase-12 and caspase-7, and provided significant protection of ßlapachone- treated cells. These findings show that ßlapachone- induced ER stress and MAP kinase phosphorylation is a novel signaling pathway underlying the molecular mechanism of the anticancer effect of ßlapachone.
Open Access
Hepatocyte nuclear phenotype, the cross-talk between anabolic androgenic steroids and exercise in transgenic mice
(Murcia : F. Hernández, 2008) Fontana, Karina; Aldrovani, Marcela; Paoli, Flávia de; Oliveira, Helena C.F.; Campos Vidal, Benedicto de; da Cruz Hoflingl, M.A.
The growing and indiscriminate use of high doses of anabolic androgenic steroid (AAS) among youth and athletes has raised serious concerns about its hepatotoxic effects. Herein, the influence of AAS in the nuclear phenotype of hepatocytes was investigated in sedentary and trained mice heterozygous for the human CETP (cholesteryl ester transfer protein) transgene and for LDL-receptor null allele (CETP+/-LDLr+/-) by image analysis. Five groups were assayed comprising treadmill exercised (Ex) and sedentary (Sed) mice, administered mesterolone (AAS) or gum arabic (GA) and a sedentary blank control: G1(SedAAS), G2(SedGA), G3(ExAAS), G4(ExGA), and G5(SedBL). To assess nuclear phenotypes, the state of chromatin supraorganization, DNA content and fragmentation (TUNEL assay), area and perimeter of hepatocytes were determined in Feulgen-stained liver imprints. In addition, the activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) hepatic transaminases were measured. SedAAS-G1 showed the lowest chromatin condensation and highest Feulgen-DNA content, polyploid nuclei frequency, nuclear area and perimeter, suggesting gene activation. Contrarily, ExAAS-G3 showed a highest chromatin condensation, and a significant decrease of Feulgen-DNA content and decreased frequency of polyploid nuclei, which suggest gene silencing. Image analysis of the nuclear phenotype offered a coherent descriptive picture of the changing patterns of chromatin organization, which were shown to be congruent with the levels of Feulgen-DNA content, geometric nuclear parameters and hepatocyte activity. In this study, the image analysis permitted the monitoring of the nuclear response to mesterolone and physical exercise action in liver cells, the molecular mechanism of which is in prospect.

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