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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.annalspathology.com/?rss=yes"><title>Annals of Diagnostic Pathology</title><description>Annals of Diagnostic Pathology RSS feed: Current Issue.    A peer-reviewed journal devoted to the publication of articles dealing with traditional morphologic studies using standard diagnostic 
techniques and stressing clinicopathological correlations and scientific observation of relevance to the daily practice of pathology. 
Special features include pathologic-radiologic correlations and pathologic-cytologic correlations.   </description><link>http://www.annalspathology.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:issn>1092-9134</prism:issn><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:publicationDate>January 2012</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001808/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001043/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001067/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001080/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001110/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001122/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001146/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913410001899/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001079/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913410001759/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913410001784/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913410001802/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913410001814/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913410001917/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001717/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001821/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS109291341100181X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001791/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001808/abstract?rss=yes"><title>Editorial Board</title><link>http://www.annalspathology.com/article/PIIS1092913411001808/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(11)00180-8</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001043/abstract?rss=yes"><title>Association of mast cells with microvessel density in urothelial carcinomas of the urinary bladder</title><link>http://www.annalspathology.com/article/PIIS1092913411001043/abstract?rss=yes</link><description>Abstract: This study aims to investigate the relation of mast cell (MC) accumulation with tumor grade and stage in urothelial carcinomas of the urinary bladder and to determine its relationship with angiogenesis. A total of 78 urothelial carcinomas obtained by transurethral resection were investigated immunohistochemically by using c-Kit (CD117) and anti-CD34. The correlation between MC counts and microvessels was evaluated and compared with histopathologic parameters including tumor stage and grade. There were significant correlations between MC counts, grade, and stage (P &lt; .05; r = 0.69 and 0.63, respectively). However, MC counts in adjacent nontumoral bladder mucosa significantly were higher than the MC counts in tumoral zone (P &lt; .001). On the other hand, significant correlation was found between the number of MCs in tumoral zone and the microvessel density (P &lt; .05, r = 0.56). The results of our study suggest that c-Kit positive MCs in tumoral zone may contribute to tumor angiogenesis and play a significant role in tumor growth and invasion. Further studies are needed to support these observations.</description><dc:title>Association of mast cells with microvessel density in urothelial carcinomas of the urinary bladder</dc:title><dc:creator>Aysegul Sari, Aylin Calli, Fulya Cakalagaoglu, Aysegul Aksoy Altınboga, Kaan Bal</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.07.001</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-10-24</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-10-24</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>6</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001067/abstract?rss=yes"><title>Changing trends in human papillomavirus–associated head and neck squamous cell carcinoma</title><link>http://www.annalspathology.com/article/PIIS1092913411001067/abstract?rss=yes</link><description>Abstract: Head and neck squamous cell carcinoma (HNSCC) continues to be a significant disease with varying rates of incidence and mortality worldwide. Numerous studies have demonstrated that human papillomavirus (HPV) is etiologically linked with a subset of HNSCC, independent of tobacco and alcohol use. This subset of tumor shows increased sensitivity to radiation therapy and association with better outcomes. The study aims to determine the HPV burden and trend among patients with HNSCC in the southern region of the United States over the past 10 years. Of 142 cases from 2000 to 2004, 18 (13%) were positive for high-risk HPV. Nine of these were oropharyngeal tumors, including 4 cases from the tonsil. These constitute 38% (9/24) of all oropharyngeal tumors and 57% (4/7) of tonsillar tumors. Of 35 cases from 2009 to 2010, 14 (40%) were positive for high-risk HPV. Thirteen of these were oropharyngeal tumors, including 9 cases from the tonsil. These constitute 59% (13/23) of oropharyngeal tumors and 64% (9/14) of tonsillar tumors. When data from the 2 periods are combined, the results show that African American patients are less likely to have HPV-associated disease compared with white patients (9% vs 22%). Human papillomavirus–positive and oropharyngeal HNSCC are more likely to be nonkeratinizing (P &lt; .0001). In conclusion, the HPV detection rate in oropharyngeal squamous cell carcinoma increased from 38% to 59% between the 2000-to-2004 and 2009-to-2010 periods.</description><dc:title>Changing trends in human papillomavirus–associated head and neck squamous cell carcinoma</dc:title><dc:creator>Xiaohong Iris Wang, Jaiyeola Thomas, Songlin Zhang</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.07.003</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-10-17</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-10-17</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>7</prism:startingPage><prism:endingPage>12</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001080/abstract?rss=yes"><title>Correlation between the endoscopic and histologic diagnosis of gastritis</title><link>http://www.annalspathology.com/article/PIIS1092913411001080/abstract?rss=yes</link><description>Abstract: Our aims were to determine the rate of concordance between endoscopic and pathologic diagnoses of gastritis and to determine if there was any common factor in discordant cases. A retrospective analysis of data from 400 patients was performed. The endoscopic diagnoses were compared with the pathologic diagnoses, and histologic slides from discordant cases were reviewed. Of the 400 patients, there was discordance between endoscopy and histology in 136 (34%; κ statistic, 0.31). These discordant cases comprised 56 with normal endoscopy but abnormal histology and 80 with abnormal endoscopy but normal histology. In 13 patients, there was normal histology, although erosions had been diagnosed endoscopically. No consistent histologic features were found in the discordant cases. These findings show that standard endoscopy is a poor predictor of pathologic changes. Biopsies are required for accurate diagnosis of gastritis.</description><dc:title>Correlation between the endoscopic and histologic diagnosis of gastritis</dc:title><dc:creator>Norman John Carr, Hannah Leadbetter, Alexandra Marriott</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.08.002</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-11-14</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-11-14</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>13</prism:startingPage><prism:endingPage>15</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001110/abstract?rss=yes"><title>Distinct immunophenotype of early T-cell progenitors in T lymphoblastic leukemia/lymphoma may predict FMS-like tyrosine kinase 3 mutations</title><link>http://www.annalspathology.com/article/PIIS1092913411001110/abstract?rss=yes</link><description>Abstract: FMS-like tyrosine kinase 3 (FLT3) mutation in T lymphoblastic leukemia/lymphoma (T-LL) is rare (∼4%) and reported only in cases with CD117 expression. This study aimed to identify the immunophenotypic features that may predict FLT3 mutations. We report 3 (43%) of 7 CD117+ T-LL cases harboring FLT3-internal tandem duplication mutation. Compared with 4 FLT3-unmutated cases, all 3 FLT3-mutated cases had a distinct immunophenotype (CD1a−/CD2+/CD7+/CD34+/CD117uniform+/Tdt+) corresponding to the stage of earliest thymic T-cell progenitors possessing myeloid lineage potential. Indeed, all FLT3-mutated T-LL cases expressed myeloperoxidase on a very small subset of blasts and, thus, may be further considered a mixed phenotype acute leukemia, T/myeloid, by the 2008 World Health Organization classification scheme. We conclude that this unique immunophenotype (CD1a−/CD2+/CD7+/CD34+/CD117+/Tdt+) is a better predictor of FLT3 mutation than sole CD117 expression.</description><dc:title>Distinct immunophenotype of early T-cell progenitors in T lymphoblastic leukemia/lymphoma may predict FMS-like tyrosine kinase 3 mutations</dc:title><dc:creator>Charles M. Zaremba, Dwight Oliver, Maryellen Cavalier, Franklin Fuda, Nitin J. Karandikar, Weina Chen</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.07.005</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-11-04</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-11-04</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>16</prism:startingPage><prism:endingPage>20</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001122/abstract?rss=yes"><title>Florid reactive lymphoid hyperplasia (lymphoma-like lesion) of the uterine cervix</title><link>http://www.annalspathology.com/article/PIIS1092913411001122/abstract?rss=yes</link><description>Abstract: Lymphoma-like lesion (LLL) of the female genital tract is an older term in the literature that describes a florid reactive lymphoid proliferation that can be misinterpreted as lymphoma. Multiple causes of LLL have been suggested but most cases remain unexplained. We describe the clinicopathologic features of 6 patients with LLL involving the uterine cervix. Five patients presented with abnormal Papanicolaou test (Pap smear), and 3 patients had a biopsy procedure performed prior to detection of LLL in a loop electrosurgical excision procedure (LEEP). In each specimen, surface epithelial erosion was associated with a superficial, polymorphous lymphoid infiltrate with numerous scattered large cells, without cellular necrosis or sclerosis. Squamous dysplasia was present in 4 patients. Immunohistochemical studies revealed a mixed population of B- and T-lymphoid cells. T-cells were more numerous but B-cells and formed aggregates or sheets in areas. The large cells were predominantly B-cells positive for CD20 and negative for CD3 in all cases. CD30 was positive 3 cases, and Epstein-Barr virus-encoded RNA was positive in 3 cases. Assessment for clonality in 1 patient using polymerase chain reaction (PCR) methods revealed monoclonal immunoglobulin heavy chain (IgH) gene rearrangements. At last clinical follow-up there was no evidence of progressive or systemic disease. We conclude that LLL of the cervix has a number of etiologies and that a prior surgical procedure, present in 3 patients in this study, is another possible etiology. As has been reported by others, monoclonal IgH gene rearrangements can be detected in this entity which has a benign clinical course.</description><dc:title>Florid reactive lymphoid hyperplasia (lymphoma-like lesion) of the uterine cervix</dc:title><dc:creator>Preetha Ramalingam, Pablo Zoroquiain, José R. Valbuena, Bonnie L. Kemp, L. Jeffrey Medeiros</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.08.004</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-11-07</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-11-07</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>21</prism:startingPage><prism:endingPage>28</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001146/abstract?rss=yes"><title>Pathologic complete response to neoadjuvant therapy in patients with pancreatic ductal adenocarcinoma is associated with a better prognosis</title><link>http://www.annalspathology.com/article/PIIS1092913411001146/abstract?rss=yes</link><description>Abstract: In patients with pancreatic ductal adenocarcinoma (PDA) who received neoadjuvant therapy and pancreatectomy, pathologic complete response (pCR) is rarely observed and the prognostic significance of pCR is not clear. In this study, we identified 11 patients with pCR (2.5%) from 442 patients with PDA who received neoadjuvant treatment and pancreatectomy from 1995 to 2010. There were 6 men and 5 women, with a median age of 61 years. Four patients had either synchronous or history of extrapancreatic cancer. Five patients received neoadjuvant chemotherapy followed by chemoradiation, and 6 received chemoradiation alone. Ten patients had pancreaticoduodenectomy, and 1 had distal pancreatectomy. Scar and chronic pancreatitis consistent with therapy effect were present in all cases (100%). Pancreatic intraepithelial neoplasia (PanIN) 3/carcinoma in situ was present in 5 cases, and PanIN1 and PanIN2 in 5 cases. However, no residual invasive carcinoma or lymph node metastasis was identified in all cases. Follow-up information was available in 10 patients. Follow-up time ranges from 6 to 194 months (median, 63 months). During the follow-up, 3 patients died of other causes, and 1 developed a second primary PDA in the tail of the pancreas at 84 months after the initial pancreaticoduodenectomy and died at 105 months after the initial diagnosis of PDA. The other 6 patients were alive with no evidence of disease. Patients with pCR had a better survival than did those who had posttherapy stage I or IIA disease (P &lt; .001). Patients with PDA who received neoadjuvant therapy and had pCR in pancreatectomy are rare but have a better prognosis.</description><dc:title>Pathologic complete response to neoadjuvant therapy in patients with pancreatic ductal adenocarcinoma is associated with a better prognosis</dc:title><dc:creator>Qing Zhao, Asif Rashid, Yun Gong, Matthew H. Katz, Jeffrey E. Lee, Robert Wolf, Aparna Balachandran, Gauri R. Varadhachary, Peter W. Pisters, Hua Wang, Henry F. Gomez, James L. Abbruzzese, Jason B. Fleming, Huamin Wang</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.08.005</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-11-04</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-11-04</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>29</prism:startingPage><prism:endingPage>37</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913410001899/abstract?rss=yes"><title>Multilocular thymic cyst with epithelioid granulomata of unknown etiology: a radiologic and histopathologic correlation</title><link>http://www.annalspathology.com/article/PIIS1092913410001899/abstract?rss=yes</link><description>Abstract: Thymic cysts (congenital or acquired) are believed to account for 3% to 5% of all mediastinal masses. Multilocular thymic cysts are an acquired reactive inflammatory process arising within the thymus gland and are less common than the congenital unilocular type. Multilocular cysts have been reported in association with a variety of neoplastic, autoimmune, and infectious conditions. We report a case of a 23-year-old white man who presented with a 2-week history of progressive right-sided shoulder and chest pain. He was found to have an anterior mediastinal mass involving the thymus. This case of multilocular thymic cyst is particularly unique due to the presence of abundant epithelioid granulomata within the cyst, a finding that has not previously been emphasized as a histologic feature of these lesions, and one that expands the histopathologic differential diagnosis, warranting exclusion of infectious and autoimmune etiologies.</description><dc:title>Multilocular thymic cyst with epithelioid granulomata of unknown etiology: a radiologic and histopathologic correlation</dc:title><dc:creator>Yusuf Kasirye, Stephen Talsness, Matthew P. Walters, John W.E. Douglas-Jones, Jeffrey M. Resnick, Joseph J. Mazza, Steven H. Yale</dc:creator><dc:identifier>10.1016/j.anndiagpath.2010.11.009</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-03-11</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-03-11</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Radiologic-Pathologic Correlations</prism:section><prism:startingPage>38</prism:startingPage><prism:endingPage>42</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001079/abstract?rss=yes"><title>Multicentric epithelioid hemangioendothelioma of bone. Report of a case with radiologic-pathologic correlation</title><link>http://www.annalspathology.com/article/PIIS1092913411001079/abstract?rss=yes</link><description>Abstract: Epithelioid hemangioendothelioma (EHE) is a rare vascular tumor of uncertain biologic behavior. Most cases come out as a single lesion of the soft tissue but also may appear in the lung, liver, and other locations. Epithelioid hemangioendothelioma of bone is an extremely rare tumor and more prevalent in the second and third decades of life; its behavior is uncertain, it most commonly is unifocal, and it affects preferentially lower extremities. In this work, we present the clinical, radiologic, and pathologic findings of a 19-year-old man with a multicentric EHE of bone that involved 3 vertebrae and developed lung metastasis.</description><dc:title>Multicentric epithelioid hemangioendothelioma of bone. Report of a case with radiologic-pathologic correlation</dc:title><dc:creator>Luisa I. Gómez-Arellano, Tabare Ferrari-Carballo, Hugo R. Domínguez-Malagón</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.08.001</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-12-09</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-12-09</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Radiologic-Pathologic Correlations</prism:section><prism:startingPage>43</prism:startingPage><prism:endingPage>47</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913410001759/abstract?rss=yes"><title>Extraoral plasmablastic lymphoma with intravascular component and MYC translocation</title><link>http://www.annalspathology.com/article/PIIS1092913410001759/abstract?rss=yes</link><description>Abstract: Plasmablastic lymphoma (PBL) is an uncommon, clinically aggressive, Epstein-Barr virus–driven B-cell lymphoma that was initially described in tumors of relatively young human immunodeficiency virus–positive men. Subsequent to initial reports, the clinical and pathological spectrum of this disease has been expanded such that, now, PBL is recognized to be a heterogeneous disease entity. Plasmablastic lymphoma has been seen in clinical settings outside those initially reported and has been shown to demonstrate a variety of morphologic patterns. We describe a case of extraoral PBL in an human immunodeficiency virus–infected patient with a computed tomography–identified heterogeneously enhancing mass in the stomach. Histologically, a prominent intravascular component was identified. Fluorescent in situ hybridization analysis for MYC/IGH (immunoglobulin heavy chain) rearrangement t(8;14) identified fusion signals, confirming the presence of MYC rearrangement. The presence of a prominent intravascular in our case is unique. To our knowledge, these findings have not been observed in the previous reports of PBL. The observation of this vascular component supports the heterogeneity of PBL and may be an indicator of tumor aggressiveness. We were able to demonstrate the MYC/IGH rearrangement in our case of PBL. The interplay between Epstein-Barr virus and this MYC rearrangement may be similar to what is observed in Burkitt lymphoma, another clinically aggressive non–Hodgkin lymphoma.</description><dc:title>Extraoral plasmablastic lymphoma with intravascular component and MYC translocation</dc:title><dc:creator>Jennifer Chapman-Fredricks, Naomi Montague, Ikechukwu Akunyili, Offiong Ikpatt</dc:creator><dc:identifier>10.1016/j.anndiagpath.2010.11.002</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-01-18</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-01-18</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>48</prism:startingPage><prism:endingPage>53</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913410001784/abstract?rss=yes"><title>Kocher-Debré-Sémélaigne syndrome diagnosed by autopsy associated with disseminated intravascular coagulation</title><link>http://www.annalspathology.com/article/PIIS1092913410001784/abstract?rss=yes</link><description>Abstract: Kocher-Debré-Sémélaigne syndrome is a rare disease with little literature, which develops with myopathy in infancy associated with neuromuscular alterations, polymyositis with symmetrical proximal muscle weakness, pseudohypertrophy, muscular rigidity and spasms, exercise intolerance, myxoedema, short stature, and cretinism. Male patient aged 18 years old, 1.52 m in height, admitted in the General Hospital of Triângulo Mineiro Federal University on November 11, 2003, complaining of intense diffuse abdominal pain like severe cramps, without triggering factors, associated with asthenia and hyporexia. This seems to be one of the few reports of KDS syndrome diagnoses by autopsy, where alterations in the thyroid gland connected with hypotrophy and probable congenital hypothyroidism were described and resulted in complications such as disseminated intravascular coagulation and hemophagocytic syndrome with fast progression to death of an 18-year-old patient.</description><dc:title>Kocher-Debré-Sémélaigne syndrome diagnosed by autopsy associated with disseminated intravascular coagulation</dc:title><dc:creator>Natália Dias B. Guimarães, Ana Paula Espindula, Laura Penna Rocha, Janaínna Grazielle Pacheco Olegário, Débora Tavares Resende Silva Abate, Renata Calciolari Rossi e Silva, Camila Lourencini Cavellani, Marlene Antônia dos Reis, Vicente de Paula Antunes Teixeira, Eumenia Costa da Cunha Castro, Rosana Rosa Miranda Corrêa</dc:creator><dc:identifier>10.1016/j.anndiagpath.2010.11.004</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-02-14</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-02-14</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>54</prism:startingPage><prism:endingPage>58</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913410001802/abstract?rss=yes"><title>Mucin poor mucinous tubular and spindle cell carcinoma of the kidney, with nonclassic morphologic variant of spindle cell predominance and psammomatous calcification</title><link>http://www.annalspathology.com/article/PIIS1092913410001802/abstract?rss=yes</link><description>Abstract: Mucinous tubular and spindle cell carcinoma (MTSCC) is a rare type of kidney tumor that has only been recently described. The classic MTSCCs are polymorphic renal neoplasms characterized by small, elongated tubules lined by cuboidal cells and/or cords of spindled cells separated by pale mucinous stroma. Nonclassic morphologic variants and features of MTSC have not been well studied and rarely been reported. We report a challenging case of mucin-poor MTSCC with marked spindle cell predominance and focal psammomatous calcification in a 39-year-old man and describe its histologic and immunohistochemical features. Pathologists must be aware of the histologic spectrum of MTSCCs to ensure their accurate diagnosis.</description><dc:title>Mucin poor mucinous tubular and spindle cell carcinoma of the kidney, with nonclassic morphologic variant of spindle cell predominance and psammomatous calcification</dc:title><dc:creator>Hanan Farghaly</dc:creator><dc:identifier>10.1016/j.anndiagpath.2010.10.001</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-02-10</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-02-10</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>59</prism:startingPage><prism:endingPage>62</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913410001814/abstract?rss=yes"><title>Metastatic gastric adenocarcinoma primarily presenting in the fallopian tube</title><link>http://www.annalspathology.com/article/PIIS1092913410001814/abstract?rss=yes</link><description>Abstract: We report a 48-year-old woman presenting with gastric adenocarcinoma metastatic only to the left fallopian tube. In addition to invasive, poorly differentiated adenocarcinoma, there were areas simulating intraepithelial carcinoma, suggesting a primary fallopian tube lesion. The differential diagnosis included a metastatic process, based on unusual morphologic patterns with occasional signet-ring cells, single-cell linear pattern of infiltration, and abundant lymphvascular space invasion. Metastasis from an upper gastrointestinal primary was confirmed by immunostains (cytokeratin 7, CDX-2, and p53 positive in the tumor cells and cytokeratin 20, WT-1, estrogen, and progesterone receptors negative). Imaging studies and a posterior biopsy demonstrated primary gastric adenocarcinoma with similar histology and immunoprofile. We report an unusual case of primary gastric adenocarcinoma presenting only in the fallopian tube and discuss its mimics and differential diagnosis.</description><dc:title>Metastatic gastric adenocarcinoma primarily presenting in the fallopian tube</dc:title><dc:creator>Andres A. Roma</dc:creator><dc:identifier>10.1016/j.anndiagpath.2010.12.002</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-02-10</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-02-10</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>63</prism:startingPage><prism:endingPage>66</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913410001917/abstract?rss=yes"><title>A uterine leiomyoma in which a leiomyosarcoma with osteoclast-like giant cells and a metastasis of a ductal breast carcinoma are present</title><link>http://www.annalspathology.com/article/PIIS1092913410001917/abstract?rss=yes</link><description>Abstract: Leiomyosarcoma of the uterus is a rare tumor, and the presence of osteoclast-like giant cells in this tumor is even rarer. A leiomyosarcoma arising in a leiomyoma is also quite unique. Breast cancer metastasizing to the uterus is seldom seen as well. A 70-year-old woman presented with metastasized breast cancer to the bones. An evaluation of the computed tomographic scan was made, which showed an enlarged uterus with a tumor. The tumor was a leiomyoma in which a leiomyosarcoma with osteoclast-like giant cells as well as a metastasis of a ductal breast carcinoma was present. To our knowledge, this is the first report of a leiomyosarcoma containing osteoclast-like giant cells, present in a leiomyoma, in a uterus also containing a ductal breast cancer metastasis present in the leiomyoma and myometrium.</description><dc:title>A uterine leiomyoma in which a leiomyosarcoma with osteoclast-like giant cells and a metastasis of a ductal breast carcinoma are present</dc:title><dc:creator>Hannah S. van Meurs, Jan J. Dieles, Herbert V. Stel</dc:creator><dc:identifier>10.1016/j.anndiagpath.2010.11.010</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2011-01-10</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-01-10</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>67</prism:startingPage><prism:endingPage>70</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001717/abstract?rss=yes"><title>Histochemistry as a tool in morphological analysis: a historical review</title><link>http://www.annalspathology.com/article/PIIS1092913411001717/abstract?rss=yes</link><description>Abstract: Histochemistry has an interesting history, extending back to ancient times, in some ways. Man has long had a desire to understand the workings of the human body and the roles that various “humors” or chemicals have in those processes. This review traces the evolution of histochemistry as an investigative and diagnostic discipline, beginning with the efforts of medicinal chemists and extending through a period in which histology was increasingly paired with biochemistry. Those developments served as the underpinnings for an eventual marriage of microscopy, chemistry, immunology, and molecular biology, as realized in the current practice of anatomical pathology.</description><dc:title>Histochemistry as a tool in morphological analysis: a historical review</dc:title><dc:creator>Mark R. Wick</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.10.010</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>History of Pathology</prism:section><prism:startingPage>71</prism:startingPage><prism:endingPage>78</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001821/abstract?rss=yes"><title>Instructions for Authors</title><link>http://www.annalspathology.com/article/PIIS1092913411001821/abstract?rss=yes</link><description></description><dc:title>Instructions for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(11)00182-1</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>B5</prism:startingPage><prism:endingPage>B6</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS109291341100181X/abstract?rss=yes"><title>Table of Contents</title><link>http://www.annalspathology.com/article/PIIS109291341100181X/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(11)00181-X</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001791/abstract?rss=yes"><title>Masthead</title><link>http://www.annalspathology.com/article/PIIS1092913411001791/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(11)00179-1</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1092-9134(11)X0007-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A3</prism:endingPage></item></rdf:RDF>
