Sabato 27 ottobre 2012 - Pacini Editore

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414 references 1 Seethala RR, Barnes EL, Hunt JL. Am J Surg Pathol. 2007;31:44-57. Erratum in: Am J Surg Pathol 2008;32:1923. 2 Shinozaki A, Nagao T, Endo H, et al. Am J Surg Pathol 2008;32:913-23. UrInArIO PCA3 ribo probe costruction for ISH analysis on tumoral prostatic samples G. Aquino1 , M. Cerrone1 , E. La Mantia1 , V. Gigantino1 , A. Marra1 , R. Sabatino1 , S. Perdonà2 , C. Santonastaso, R. Franco1 , G. Botti1 1 Pathology Department, National Cancer Institute “Fondazione G. Pascale”, Naples, Italy; 2 Urology Department, National Cancer Institute “Fondazione G. Pascale”, Naples, Italy Prostate cancer (PCa) is the most commonly diagnosed cancer in men and the second leading cause of death. The etiology of PCa is uncertain, several factors are involved: environmental, hormonal and hereditary. New diagnostic methods have been developed in recent years, the one that has had a greater clinical impact is a non-invasive diagnosis of urine, which detects the expression of the PCA3 gene. This diagnostic method, based RT-PCR, allows us to reveal the ‘overexpression of PCA3 RNA (mRNA) in the urine. This indicator would allow to discriminate patients who should undergo biopsy from patients who only need a close follow-up. The concentration of PCA3, in fact, is related to the risk of cancer. PCA3 is a non-coding RNA whose gene is located on chromosome 9, locus: 9q21-q22, there is no corresponding protein and possibly detectable by immunohistochemistry. Aim. The identification of PCA3 expression in urine represents a rapid and non-invasive screening method for PC detection, thus derives the interest in the practice of using histological routine to enable the identification of borderline lesions. The purpose of this study was development of a technique capable of detecting the presence of PCA3 RNA on histological sections. For this, we have built a digoxigenin-labeled probe for detecting several PCA3 isoforms. Methods. ISH was performed initially using a 350-bp digoxigenin-labelled ribo probe generated by PCR from RNA isolated and retro-transcripted from cell line LnCaP, subsequently to overcome the problem of RNA degradation we have built a smaller probe, respectively 139 bp. We used like a positive control Beta actin antisense probe while like negative control we use pca3 and beta actin sense probe. Experiments were performed on both positive and negative controls. ISH was realized both on LnCaP cells that on 7-micrometer-thick frozen tissue sections. The efficiency of the marking and the quantization of the probe was performed by direct evaluation by Dot Blot. Results. Preliminary results show a successful hybridization both on LnCaP cells and on prostate frozen sections. PCA3 and Beta Actin Antisense Probe show a diffuse cytoplasmic signals while PCA3 and Beta Actin sense probe don’t show any signals. The use of PCA3 on histological samples could permit the applications on routine samples in order to identify critical lesions of ambiguous interpretation, such as atypical small acinar proliferation. Extraprostatic infiltration and vascular invasion in prostate cancer: evaluation by proteomic analysis S. Bergamini1 , L. Reggiani Bonetti2 , E. Monari1 , E. Bellei1 , A. Maiorana2 , T. Ozben3 , A. Tomasi1 1 Department of Laboratories, Pathologic Anatomy and Legal Medicine, Section of Toxicology and Clinical Pharmacology and 2 Section of Pathologic Anatomy, Medical Faculty, University Hospital of Modena and Reggio Emilia, Modena, Italy; 3 Department of Biochemistry, Medical Faculty, Akdeniz University, Antalya, Turkey CONGRESSO aNNualE di aNatOmia patOlOGiCa SiapEC – iap • fiRENzE, 25-27 OttOBRE 2012 Background. Prostate adenocarcinoma (PCa) is one of the tumors showed an increased risk, which is still growing, in the male population. Of this cancer are known more or less aggressive forms that can be distinguished: organ confined PCa (tumor confined within the gland), locally advanced PCa (cancer that invades beyond the capsule and surrounding structures), metastatic PCa (tumor spreading distance generating metastases). The main mechanisms through which occurs the progression of the disease are extraprostatic infiltration (EPI) and lymph-vascular invasion (LVI). EPI occurs when the PCa infiltrates and exceeds the prostatic capsule and spreads to the extra-prostatic nervous structures, periprostatic soft tissue or seminal vesicles. The LVI occurs when cancer cells penetrate into the blood and lymphatic systems and reach locations generally distant from the primary tumor, in which generate the metastasis. Material and methods. In our study, proteomic analysis was performed using Surface Enhanced Laser Desorption/Ionization – Time of Flight – Mass Spectrometry (SELDI-ToF-MS) technology, which allowed us to detect differences in serum protein expression between the less aggressive forms of PCa (PCa organ confined) and the more aggressive (PCa locally advanced), studying in particular the EPI and the LVI. The SELDI-ToF- MS is an innovative technology derived from a combination of MS with the ProteinChip technology. The ProteinChip are thin strips of aluminum with 8 small wells on which is deposited serumsample. There are several types of ProteinChip which differ in the physico-chemical characteristics of their chromatographic surface and therefore for the ability to bind proteins with different characteristics. Results. The SELDI-ToF-MS analysis of serum profiles revealed peaks differentially expressed in PCa with LVI and PCa with EPI respected to PCa without ILV and PCa without IEP. Were also detected peaks closely related to the Gleason grade. Conclusions. Our study is a preliminary SELDI-ToF-MS analysis that need to confirm its results through a larger number of patients. Additionally will be very important to identify the differentially expressed peaks that may be useful serum biomarkers to detect, at the time of diagnosis, the presence of ILV and IEP, to define the aggressiveness of the tumor, the prognosis and the most appropriate treatment. Mixed adeno-neuroendocrine carcinoma (MAnEC) of the urinary bladder: a case report V. Bertolini1 , G. D’Ambrosio1 , P. Consonni2 , S. La Rosa3 , F. Sessa1,4 1 2 Dipartimento di Anatomia Patologica, Multimedica, Milano; Divisione di Urologia, Multimedica; 3 UO Anatomia Patologica, Ospedale di Circolo, Varese; 4 Dipartimento di Scienze Chirurgiche e Morfologiche, Università dell’Insubria, Varese. Introduction. Primary adenocarcinoma (AC) of the urinary bladder is an uncommon neoplasm accounting for 1-2 % of all malignant vesical tumours occurring more commonly in males. AC of the bladder could show different histologic patterns: enteric (colonic), mucinous, signet ring cell, clear cell, hepatoid and adenocarcinoma not otherwise specified. The enteric type closely resembles adenocarcinoma of the colon 1-3 . Neuroendocrine (NE) cells are uncommon in primary AC of the bladder, with only few studies concerning its biologic significance 4-6 . In a series of 16 primary bladder AC by Bollito et al, 60 % of cases showed NE cells 4 . Materials and methods. We report a case of primary AC of the bladder with a component of NE differentiation fulfilling the criteria of WHO 2010 for MANEC 7 . In addition, for comparison, we investigated 6 primary bladder enteric type AC. Results. A 42-year old male presented with gross haematuria and disuria for 2 months. CT scan revealed a 4.5 cm mass arising from the dome and projecting into the lumen of the bladder.
PoStER Fig. 1. EE primary intestinal adenocarcinoma of the bladder: glandular component (a), solid areas (B) (Original magnification 10x) A B Fig. 2. iHC in primary intestinal adenocarcinoma of the bladder for CdX2 (a) (Original magnification 10x), Chromogranin a(B) (Original Magnification 20x). A B First a cystoscopy with transurethral resection was carried out. Histopathological examination revealed an adenocarcinoma with enteric differentiation. So the The patient underwent partial cystectomy with pelvic lymphoadenectomy Even the surgical specimen showed an adenocarcinoma of enteric type, with predominantly well formed mucinous glands, a signet ring cell component (10%) and solid areas (30%). The tumor infiltrated the bladder wall, with diffuse lymphatic invasion but metastases was present in only one pelvic lymph node. Both the biopsy and the specimen showed the same overlapping immunohistochemical profile (IHC): a diffuse intense positivity CDX2 and MUC2 and CK20 in the mucinous component; cytoplasmic positivity for chromogranin A in about 30 % of tumour cells in the solid areas. Any stained cell was observed for CK7. The surrounding bladder mucosa was unremarkable, with no evidence of in situ carcinoma or cystitis glandularis In addition, no urachal remnants or urothelial tumoural elements were identified even on extensive sampling of the tumor. The final diagnosis was primary intestinal type mixed adeno-neuroendocrine carcinoma of the urinary bladder. The same IHC panel was performed on all cases of vesical intestinal adenocarcinoma. While CK20 and MUC2 showed an analogous expression; chromogranin stained few scattered cells in only 1 out of 6 cases. Conclusions. NE tumours are extremely rare and are generally small or large cells type 8 9 . Endocrine cells could possibly be present in an adenocarcinoma of the bladder but they are preferentially sparse not grouped or clustered togheter. This pattern reflects the gastrointestinal counterpart where few endocrine cells are found in up to 41% cases. The presence of a conspicuous component of endocrine cells (at least 30%) shift the diagnosis towards a mixed adeno-neuroendocrine carcinoma. This is the first description, of our knowledge, of an adenocarcinoma with a endocrine differentiation. references 1 Bostwick DG, Cheng L. Neoplasm of the urinary bladder. In: Urologic Surgical Pathology 2 nd ed. Philadelphia, PA: Mosby 2008, pp. 300-7. 2 Somak R, Parwani AV. Adenocarcinoma of the urinary bladder. Arch Pathol Lab Med 2011;135:1601-5. 3 Shanks JS, Iczkowski KA. Divergent differentiation in urothelial carcinoma and other bladder subtypes with selected mimics. Histopathology 2009;54:885-900. 4 Bollito ER, Pacchioni D, Lopez-Beltran A. Immunohistochemical 415 study of neuroendocrine differentiation in primary glandular lesions and tumors of the urinary bladder. Anal Quant Cytol Histol 2005;27:218-24. 5 Abenoza P, Manival C, Sibley RK. Adenocarcinoma with neuroendocrine differentiation of the urinary bladder. Clinicopathologic, immunohistochemical, and ultrastructural study. Arch Pathol Lab Med 1986;110:1062-6. 6 Hom JD, King EB, Fraenkel R. Adenocarcinoma with a neuroendocrine component arising in the Urachus. A case report. Acta Cytologica 1990;34:269-74. 7 th WHO Classification of Tumours of the Digestive System 4 ed. Lyon: IARC 2010. 8 Abrahams NA, Moran C, Reyes AO. Small cell carcinoma of the bladder: a contemporary clinicopathological study of 51 cases. Histopathology 2005;46:57-63. 9 Cheng L, Pan CX, Yang XJ. Small cell carcinoma of the bladder: a clinicopathologic analysis of 64 patients. Cancer 2004;101:957-62. Prognostic role of the receptor tyrosine kinase AXL and its ligand Gas6 in renal cell carcinoma F. Collina, L. Cindolo, L. La Sala, G. Scognamiglio, G. Aquino, G. Gaudioso, C. D’Alterio, S. Scala, M. Cantile, R.M. Melillo, R. Franco, G. Botti Background and aim. Renal Cell Carcinomas (RCC) is characterized by a complex molecular biology, a variable course and an unpredictable behavior. The only curative treatment of RCC is surgery and in cases of metastatic RCC, are performed systemic therapies such as immunotherapy (IFNα or IL-2). Since 2005, a series of tyrosine kinase inhibitors have been approved by the FDA for the treatment of advanced stage RCC. The Axl proto-oncogene is a receptor tyrosine kinase member of TAM receptors family. Some reports indicated that Axl and its ligand growth arrest-specific gene-6 (Gas6) might be involved in tumor progression of several human cancers. In fact, recently, it has been shown that aberrant expression of Axl and Gas6 mRNA are strongly correlated with the outcome of patients. Little information is available in the literature on the role of AXL and Gas6 in RCC, for this reason the aim of our work was to evaluate the expression of these markers on a series of 156 RCC samples, included in a prognostic TMA, and evaluate their potential association to clinicopathological features and outcome of patients. Methods. We used microarray technology comprising 156 renal cell carcinoma. Axl and Gas6 expression were valued by immunohistochemistry using monoclonal antibodies. Results and conclusions. Preliminary results show that Axl protein expression correlates with the Furhman grade (p value = 0.03), histological subtype (p value = 0.04) and disease progression (p value = 0.008). Moreover, there is a trend of statistical association with tumor size (p value = 0.07) and with Gas6 expression (p value = 0.078). Our data suggest that Axl might be used as a valid prognostic factor in RCC. Tubulocystic carcinoma of the kidney: case report of a rare subtype of renal cell carcinoma A. Ginori1 , D. Tacchini1 , L. Vassallo1 , M.G. Mastrogiulio1 , A. Barone1 , M.A.G.M. Butorano1 , S.F. Carbone2 , S. Tripodi1 1 Department of Human Pathology and Oncology, Pathological Anatomy Section, University of Siena, Siena, Italy; 2 Department of Radiology, University of Siena, Siena, Italy Background. A distinctive tumor once described under the term low-grade collecting duct carcinoma has recently been classified as tubulocystic renal cell carcinoma (TC-RCC). This subtype of renal cell carcinoma is not recognized in the World Health Organization 2004 classification. The tumor occurred in adults (mean age, 54 years) with a strong male predominance (7:1). TC-RCC is asymptomatic with low potential for metastasis. Up to now, less than 60 cases of TC-RCC have been reported in literature.
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212 Key words: EGC, Prognosis, Trea
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214 Tab. VI. univariate analysis: 5
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236 mas and leukemias, whereas the
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238 Patobiologia della parete aorti
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240 10 Luo BH, Carman CV, Springer
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242 zienti asintomatici, la sede pi
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patHOlOGiCa 2012;104:267-358 COMUnI
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COmuNiCaziONi ORali Solitary T-cell
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COmuNiCaziONi ORali differences in
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COmuNiCaziONi ORali Tab. I. CYTOLOG
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COmuNiCaziONi ORali BrAF mutation a
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COmuNiCaziONi ORali The aim of the
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COmuNiCaziONi ORali Tab. I. R-MSFTs
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COmuNiCaziONi ORali Fig. 1. skin us
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COmuNiCaziONi ORali complications.
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COmuNiCaziONi ORali Immunohistochem
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COmuNiCaziONi ORali advanced pathol
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COmuNiCaziONi ORali Fig. 4. tCRGd+c
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COmuNiCaziONi ORali LOH analysis of
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COmuNiCaziONi ORali in the leading
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COmuNiCaziONi ORali Conclusions. Sp
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COmuNiCaziONi ORali kidney) is unpr
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COmuNiCaziONi ORali A case of intra
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COmuNiCaziONi ORali progress, recur
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COmuNiCaziONi ORali Results. Expres
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COmuNiCaziONi ORali GEnITALE MASCHI
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COmuNiCaziONi ORali agnostic challe
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Pathologica 2012;104:359-420 POSTEr
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PoStER references 1 Gerber DE, Minn
Page 173 and 174: PoStER In our case the endofibrotic
Page 175 and 176: PoStER Fig. 1. Kaplan-meier surviva
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Page 179 and 180: PoStER references 1 Goepel JR. Beni
Page 181 and 182: PoStER MALT lymphoma of the rectum:
Page 183 and 184: PoStER 3 Ciulla A, Castronovo G, To
Page 185 and 186: PoStER for protein expression of PA
Page 187 and 188: PoStER the better one because the m
Page 189 and 190: PoStER Grossly, an irregular villou
Page 191 and 192: PoStER Expression of ror-1 in pancr
Page 193 and 194: PoStER (see Fig. 1) placental site
Page 195 and 196: PoStER Tissue were fixed in 10% for
Page 197 and 198: PoStER invaded focally adjacent tun
Page 199 and 200: PoStER bination chemotherapy the pr
Page 201 and 202: PoStER 21 to 55 years in age, the l
Page 203 and 204: PoStER Results and conclusion. We a
Page 205 and 206: PoStER Identification of cancer ste
Page 207 and 208: PoStER Epidemiological and biomolec
Page 209 and 210: PoStER Fig. 1. ductal invasive Brea
Page 211 and 212: PoStER Fig. 2. Fig. 3. Fig. 4. Conc
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Page 215 and 216: PoStER haematoxylin and eosin and V
Page 217 and 218: PoStER Fig. 4. High mitotic rate (a
Page 219 and 220: PoStER Fig. 6. focal sebaceous and
Page 221 and 222: PoStER Results. At gross examinatio
Page 223: PoStER strated that HPV is present
Page 227 and 228: PoStER Introduction. Angiosarcoma i
Page 229 and 230: PoStER 9 Klein KA, Stephens DH, Wel
Page 231 and 232: Pathologica 2012;104:421-423 InDICE
Page 233: iNDicE DEgli aUtoRi Orsaria M., 319
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Sabato 27 ottobre 2012 - Pacini Editore

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