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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 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>3</prism:number><prism:publicationDate>June 2012</prism:publicationDate><prism:copyright> © 2012 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/PIIS1092913411001456/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001468/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS109291341100147X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001481/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001493/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001547/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411001961/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411000116/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411000244/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411000256/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913411000281/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913412000044/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913412000469/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913412000470/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913412000482/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annalspathology.com/article/PIIS1092913412000494/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001456/abstract?rss=yes"><title>Absence of IDH1-R132H mutation predicts rapid progression of nonenhancing diffuse glioma in older adults</title><link>http://www.annalspathology.com/article/PIIS1092913411001456/abstract?rss=yes</link><description>Abstract: Advanced age and contrast enhancement portend a poor prognosis in diffuse glioma (DG). Diffuse glioma may present as nonenhancing tumors that rapidly progress in weeks to months to a pattern of ring enhancement, characteristic of glioblastoma (GBM). Mutations involving isocitrate dehydrogenase 1 (IDH1) have recently emerged as important diagnostic and prognostic markers in DG. R132H is the most common mutation, expressed in more than 80% of DG and secondary GBM but in less than 10% of primary GBM. Adults older than 50 years with nonenhancing, rapidly progressing DG were identified. A comparison group comprised randomly selected, age-matched patients with nonenhancing, nonprogressing DG. Isocitrate dehydrogenase 1 status was evaluated using anti–IDH1-R132H antibodies (Dianova, Hamburg, Germany). The results were correlated with the clinical outcomes. We identified 4 patients who presented with nonenhancing DG that rapidly progressed to ring-enhancing lesions that were subsequently diagnosed on surgical resection as GBM. This group showed absent IDH1-R132H expression, which is characteristic of primary GBM. The comparison group of 5 patients presented with nonenhancing, nonprogressing DG, and all 5 tumors showed IDH1-R132H expression. In conclusion, negative IDH1-R132H mutation status in nonenhancing DG of older adults is a poor prognostic factor associated with rapid progression to ring-enhancing GBM. The shorter interval of progression and negative IDH1-R132H mutation status suggest a similar molecular pathway as seen in primary GBM.</description><dc:title>Absence of IDH1-R132H mutation predicts rapid progression of nonenhancing diffuse glioma in older adults</dc:title><dc:creator>Adriana Olar, Aditya Raghunathan, Constance T. Albarracin, Kenneth D. Aldape, Daniel P. Cahill, Suzanne Z. Powell, J. Clay Goodman, Gregory N. Fuller</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.08.010</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-12-26</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-12-26</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>161</prism:startingPage><prism:endingPage>170</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001468/abstract?rss=yes"><title>Significance of Ki-67 and p53 immunoexpression in the differential diagnosis of oral necrotizing sialometaplasia and squamous cell carcinoma</title><link>http://www.annalspathology.com/article/PIIS1092913411001468/abstract?rss=yes</link><description>Abstract: Necrotizing sialometaplasia (NS) is a benign condition that usually involves the hard palate and can be mistaken for invasive squamous cell carcinoma (SCC). In this study, we have demonstrated that p53 and Ki-67 staining may assist in the differential diagnosis of NS from SCC. Thirteen cases of NS and 20 cases of oral cavity SCC were randomly selected from our surgical pathology archive from 1992 to 2009. Each case was additionally stained with Ki-67, p53, BCL-2, p16, and epidermal growth factor receptor (EGFR) antibodies. All 13 cases of NS were negatively stained for BCL-2, EGFR, and Ki-67. Three cases (23%) showed weak and focal positive nuclear staining for p53. Two cases (15%) showed positive staining for p16. In 16 well-differentiated SCC cases, p53 was positive in 12 cases (75%); BCL-2, p16, EGFR were positive in 3 cases (18%); and Ki-67 was positive in all cases (100%). In 4 moderately differentiated SCC cases, p53 expression was positive in all cases. Two tumors (50%) had a positive expression of BCL-2. Three cases (75%) had a positive p16 staining, and 1 (25%) had a positive EGFR staining. All cases were positive with high nuclear staining greater than 35% of cells for Ki-67. Ki-67 and p53 showed more intense staining and increased in moderately differentiated SCC comparing with well-differentiated SCC and NS. BCL-2, EGFR, and p16 had the same pattern of staining with the same extent in NS and SCCs. The diagnosis of NS may be difficult and may be supplemented via immunohistochemistry by demonstrating focal or absent p53, low to absent Ki-67 (&lt;10% of cells). Although Ki-67 and p53 staining are generally more intense and are increased in malignancy, these findings may be helpful adjuncts in the differential diagnosis of NS from SCC in appropriate clinical setting.</description><dc:title>Significance of Ki-67 and p53 immunoexpression in the differential diagnosis of oral necrotizing sialometaplasia and squamous cell carcinoma</dc:title><dc:creator>Tahereh Dadfarnia, Bassim S. Mohammed, Mahmoud A. Eltorky</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.08.011</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-12-26</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-12-26</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>171</prism:startingPage><prism:endingPage>176</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS109291341100147X/abstract?rss=yes"><title>Up-regulation of Notch-1 in psoriasis: an immunohistochemical study</title><link>http://www.annalspathology.com/article/PIIS109291341100147X/abstract?rss=yes</link><description>Abstract: The Notch pathway plays a key role in differentiation, proliferation, and influencing cell fate decision in multiple organisms and tissues including the epidermis and its appendages. The role of Notch-1 in psoriasis has not been widely evaluated; therefore, the current study aimed to evaluate its role in etiopathogenesis of this common skin disease. The current study used immunohistochemical technique to evaluate Notch-1 expression in 35 lesional biopsies of patients having chronic plaque psoriasis in comparison with normal skin biopsies, representing the control group. Notch-1 was expressed in the epidermis of both normal and psoriatic skins; however, the intensity was in favor of psoriatic lesion, and the nuclear form of Notch-1 was more frequently and diffusely seen in psoriasis. Exacerbation of psoriasis as assessed by the Psoriasis Area and Severity Index score was significantly associated with intense (P = .005) and nuclear form of Notch-1 expression (P = .0001). The nuclear form of Notch-1 was also correlated with female sex (P = .043). From this study, up-regulation and not down-regulation of Notch-1 may have a role in pathogenesis of psoriasis. The nuclear form is responsible for the exacerbation of symptoms, and it is the one that may disappear by the effect of psoralen and ultraviolet A radiation (PUVA) therapy.</description><dc:title>Up-regulation of Notch-1 in psoriasis: an immunohistochemical study</dc:title><dc:creator>Asmaa Gaber Abdou, Alaa Hassan Maraee, Amany Sharaf, Nada Farag Elnaidany</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.09.005</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-12-26</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-12-26</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>177</prism:startingPage><prism:endingPage>184</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001481/abstract?rss=yes"><title>Clinicopathologic and biomarker analysis of invasive pleomorphic lobular carcinoma as compared with invasive classic lobular carcinoma: an experience in our institution and review of the literature</title><link>http://www.annalspathology.com/article/PIIS1092913411001481/abstract?rss=yes</link><description>Abstract: Pleomorphic lobular carcinoma (PLC) is a distinct morphological variant of invasive lobular carcinoma (ILC). Although PLC retains the distinctive loosely cohesive and single-file growth pattern of ILC, it has specific distinguishable characteristics, including enlarged nuclei with greater nuclear irregularity, increased hyperchromasia, prominent nucleoli, increased mitotic activity, and abundant eosinophilic cytoplasm. We compared the clinicopathologic features and biomarker expression of PLC and ILC. Fifty-eight cases of classic ILC (5.3%) and 7 cases of PLC (0.6%) were identified from our file between January 2002 and December 2010. Histopathologic data and tumor biomarkers were recorded. Clinical follow-up information (3-93 months; median, 29 months) for distant metastasis and survival was also gathered. Fisher exact test was used, and results were considered statistically significant if P value is less than .05. Our results showed that compared with classic ILC, PLC was more frequently grade III (P &lt; .01), estrogen receptor negative (P &lt; .001), and has Ki-67 greater than 10% (P &lt; .002). In conclusion, PLC is more frequently higher grade and may exhibit an adverse biomarker profile (negative estrogen receptor and high Ki-67) as compared with classic ILC. However, no significant differences were found between PLC and classic ILC for axillary lymph node/distant metastases and survival.</description><dc:title>Clinicopathologic and biomarker analysis of invasive pleomorphic lobular carcinoma as compared with invasive classic lobular carcinoma: an experience in our institution and review of the literature</dc:title><dc:creator>Melissa Jacobs, Fang Fan, Ossama Tawfik</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.10.001</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-12-26</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-12-26</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>185</prism:startingPage><prism:endingPage>189</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001493/abstract?rss=yes"><title>Low local metastatic rate may widen indication of nephron-sparing surgery for renal cell carcinoma</title><link>http://www.annalspathology.com/article/PIIS1092913411001493/abstract?rss=yes</link><description>Abstract: To explore the rationale for renal-sparing surgery as an alternative method to radical nephrectomy in the treatment of renal cell carcinoma (RCC), we analyzed clinical data from 94 patients diagnosed as having RCC. They were divided into 3 groups based on the maximum diameter of their tumor specimens. Group A had tumors size ranging from 0 to 4 cm, group B had tumors size ranging from 4 to 7 cm, and group C had tumors size greater than 7 cm. Tissue samples (5 cm) were taken from the upper pole side, lower pole side, and renal pelvic side of the tumor pseudocapsule; if the tumor was located on 1 pole of the kidney, samples were collected from 2 directions. The specimens were then embedded in paraffin and cut serially at segments 0 to 1, 1 to 3, and 3 to 5 cm. Staining with hematoxylin and eosin, anti-pancytokeratin, and vimentin was performed to determine tumor type and tumor infiltration. From the 94 patients analyzed, 2 patients in group A had RCC metastasis within 1 cm of tissue around the pseudocapsule, and 4 patients in groups B and C had lymph node metastasis without metastasis in the tissue 1 cm outside the pseudocapsule in all 3 directions described. There was no statistical significant difference found between the incidence of local metastasis of the various tumor sizes, suggesting that local metastasis of RCC is not associated with the size of the tumor. Based on the observation that incidences of local metastasis were low in early-stage RCC, we came to the conclusion that pseudocapsule of RCC tumor might have growth-limiting effect on the tumor enclosed. It is theoretically a safer and better surgical option for patients with RCC with a smaller size of tumor and indications for radical nephrectomy to undergo renal-sparing surgery with an excision margin of 1 cm of normal tissue around the pseudocapsule of the tumor.</description><dc:title>Low local metastatic rate may widen indication of nephron-sparing surgery for renal cell carcinoma</dc:title><dc:creator>Zu-quan Xiong, Jie Zheng, Chen-chen Feng, Yun Bao, Qiang Ding, Zu-jun Fang</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.10.002</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-01-03</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-01-03</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Original Contributions</prism:section><prism:startingPage>190</prism:startingPage><prism:endingPage>195</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001547/abstract?rss=yes"><title>Microcalcifications of the breast: a mammographic-histologic correlation study using a newly designed Path/Rad Tissue Tray</title><link>http://www.annalspathology.com/article/PIIS1092913411001547/abstract?rss=yes</link><description>Abstract: The introduction of screening mammography has brought about a greater knowledge of early breast cancer characteristics. These improvements have led to a reduction in size of suspicious lesions and a shift from surgical to image-guided core needle biopsies (CNBs). Establishing correlation between histologic and imaging findings is required for accurate diagnosis. Currently, there are no standardized multidisciplinary protocols for evaluating such lesions. We correlated histologic and radiologic findings in mammographically detectable calcified lesions in CNBs using specially designed Path/Rad Tissue Trays (patent pending, University of Kansas). Evidence of calcification was analyzed in 440 with and without the use of tissue trays. After mammographic identification of the lesion, CNBs are harvested, placed in tissue trays, and x-rayed to confirm sampling of the lesion. Images of CNBs with calcifications are marked by the radiologists and sent to the pathologist along with the biopsies. Trays with CNBs are then placed into cassettes and sent to the laboratory where they are embedded without disturbing orientation. Identification and localization of targeted microcalcifications were accomplished by radiologists and pathologists in 68 of 71 cases when using the tissue trays compared with 292 of 369 without tissue trays. Confirmation of microcalcifications was accomplished after deeper sectioning into tissue blocks from discordant cases. In conclusion, a systematic approach is recommended to standardize reporting of calcifications. The use of Path/Rad Tissue Trays has created a level of concordance between pathologists and radiologists that previously did no exist. It improved diagnostic reliability, encouraged communication between pathologists and radiologists, and minimized false diagnoses and/or delays in cancer diagnosis.</description><dc:title>Microcalcifications of the breast: a mammographic-histologic correlation study using a newly designed Path/Rad Tissue Tray</dc:title><dc:creator>Ryan Gallagher, Grant Schafer, Mark Redick, Marc Inciradi, William Smith, Fang Fan, Ossama Tawfik</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.10.007</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-01-06</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-01-06</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Radiologic-Pathologic Correlation</prism:section><prism:startingPage>196</prism:startingPage><prism:endingPage>201</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411001961/abstract?rss=yes"><title>How much formalin is enough to fix tissues?</title><link>http://www.annalspathology.com/article/PIIS1092913411001961/abstract?rss=yes</link><description>Abstract: A total of sixty samples from human breast, uterus, liver, skin and abdominal fat were fixed for 8; 24 and 48 hours at a room temperature of 20 to 22°C with neutral buffered formalin (NBF) with volume to tissue ratios of 1:1; 2:1; 5:1 and 10:1 and manually processed with isopropyl alcohol and mineral oil mixtures. All the slides prepared were evaluated as suitable for diagnostic purposes by nine pathologists from three different Russian histopathology institutions. The microtomy quality differences between the samples was not statistically significant for the different fixation volume ratios tested, but the differences between fixation periods and tissues types were, with 48 hours being the optimum fixation period, with skin and fat the most difficult to infiltrate. Neither the time and volume ratio combinations affected the pH of NBF or the immunostaining for vimentin in uterus or the histochemical periodic acid reaction or reticular demonstration fibers in liver. Fixing tissues with a ratio of NBF volume to tissue volume of 2:1 for 48 hours at 20-22°C was enough to assure a proper fixation and infiltration of the tested tissues and there is no objective reason to expect that other tissues will not behave similarly. It is suggested that in order to obtain good fixation and paraffin wax infiltration in around 10 hours, the fixation with NBF at 2:1 should be at 45°C with pressure and agitation.</description><dc:title>How much formalin is enough to fix tissues?</dc:title><dc:creator>René J. Buesa, Maxim V. Peshkov</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.12.003</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-04-09</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-04-09</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Methods in Pathology</prism:section><prism:startingPage>202</prism:startingPage><prism:endingPage>209</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411000116/abstract?rss=yes"><title>Tubulovillous adenoma of the anal canal: report of 2 rare cases with review of literature</title><link>http://www.annalspathology.com/article/PIIS1092913411000116/abstract?rss=yes</link><description>Abstract: Adenomatous polyps of the colon are common lesions; however, involvement of anal canal by these lesions is extremely rare. Anal canal adenomas may rarely develop in the setting of familial adenomatous polyposis. Herein we describe 2 unique cases of tubulovillous adenoma of the anal canal with review of the literature. The diagnosis of these lesions is clinically important as they may undergo malignant transformation.</description><dc:title>Tubulovillous adenoma of the anal canal: report of 2 rare cases with review of literature</dc:title><dc:creator>Deepali Jain, Shashi Dhawan</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.01.002</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-03-30</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-03-30</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>210</prism:startingPage><prism:endingPage>213</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411000244/abstract?rss=yes"><title>Malacoplakia of the tongue complicating the site of irradiation for squamous cell carcinoma with review of the literature</title><link>http://www.annalspathology.com/article/PIIS1092913411000244/abstract?rss=yes</link><description>Abstract: Malacoplakia is a benign and uncommon inflammatory response that develops most frequently in the genitourinary tract but has been reported at other sites. We report the case of 67-year-old man who presented with a lesion at the base of the tongue 7 months after chemoradiation for biopsy-proven invasive squamous cell carcinoma of the tongue. The lesion showed intense avidity by positron emission tomography and was biopsied with the putative clinical diagnosis of recurrent malignancy. Histologically, the lesion showed the characteristics of malacoplakia as well as abundant intracellular gram-negative bacilli. Ultrastructural analysis revealed giant lysosomes, intracytoplasmic calcific concretions (Michaelis-Gutman bodies), and partially digested gram-negative bacilli within vacuolated lysosomes of macrophages. To our knowledge, this is the seventh reported case of malacoplakia of the tongue and the first to develop at the site of prior radiation treatment of a carcinoma. The clinical features of this case, a review of previously reported cases, and a consideration of pathogenesis are presented.</description><dc:title>Malacoplakia of the tongue complicating the site of irradiation for squamous cell carcinoma with review of the literature</dc:title><dc:creator>Richard L. Kradin, Thomas A. Sheldon, Petur Nielsen, Martin Selig, Jennifer Hunt</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.02.001</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-04-29</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-04-29</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>214</prism:startingPage><prism:endingPage>218</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411000256/abstract?rss=yes"><title>Plasmablastic lymphoma clinically presenting in the urinary tract</title><link>http://www.annalspathology.com/article/PIIS1092913411000256/abstract?rss=yes</link><description>Abstract: Plasmablastic lymphoma is a high-grade B-cell lymphoma that poses major diagnostic problems and carries an extremely poor prognosis. This tumor was first described in the oral cavity of HIV+ patients but has since been identified in other sites and in seronegative patients. We describe 2 cases of plasmablastic lymphoma of the urinary tract that both presented with hydronephrosis. One occurred in an HIV+ patient and harbored a MYC translocation; the other, in an HIV− patient with no translocation detected.</description><dc:title>Plasmablastic lymphoma clinically presenting in the urinary tract</dc:title><dc:creator>Jean-Christophe Tille, Marie-Françoise Pelte, Julien Schwartz, Pierre-Yves Dietrich, Thomas A. McKee</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.02.002</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-05-02</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-05-02</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>219</prism:startingPage><prism:endingPage>223</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913411000281/abstract?rss=yes"><title>Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue type arising in the pleura with pleural fibrous plaques in a lathe worker</title><link>http://www.annalspathology.com/article/PIIS1092913411000281/abstract?rss=yes</link><description>Abstract: Our patient was an 86-year-old man who had worked as a lathe operator for 40 years. He had no history of tuberculosis, pyothorax, or autoimmune disease. He had not been exposed to asbestos. He was asymptomatic, but an imaging study showed gradually increasing pleural plaques. A biopsy specimen of a pleural lesion showed sclerosis of the pleura and diffuse infiltration of small- to medium-sized B lymphocytes. Polymerase chain reaction–based analysis detected monoclonal rearrangement of immunoglobulin heavy-chain genes. Histologic diagnosis was extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue type (MALT lymphoma). The lymphoma was negative for Epstein-Barr virus. We report a rare case of a metal worker with MALT lymphoma arising in the pleura with pleural fibrous plaques. It is speculated that MALT lymphoma might develop in the background of pneumoconiosis. Inflammatory and/or immunologic reactions to metal particles might contribute to the oncogenesis of this tumor.</description><dc:title>Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue type arising in the pleura with pleural fibrous plaques in a lathe worker</dc:title><dc:creator>Shin-ichi Nakatsuka, Teruaki Nagano, Hayato Kimura, Shoji Hanada, Hidetoshi Inoue, Takashi Iwata</dc:creator><dc:identifier>10.1016/j.anndiagpath.2011.02.003</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2011-05-05</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2011-05-05</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>224</prism:startingPage><prism:endingPage>229</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913412000044/abstract?rss=yes"><title>Chondroid lipoma: an update and review</title><link>http://www.annalspathology.com/article/PIIS1092913412000044/abstract?rss=yes</link><description>Abstract: Chondroid lipoma is a rare, benign soft tissue tumor with features of both embryonal fat and embryonal cartilage that most often arises in the proximal limb and limb girdles of adult women. Histologically, it comprises nests and cords of rounded cells with granular eosinophilic or multivacuolated, lipid-containing cytoplasm within prominent myxohyaline stroma and may be morphologically confused with some sarcomas. Correct diagnosis is crucial to avoid overtreatment because it does not recur or metastasize, and simple excision is curative. The etiology of chondroid lipoma remains unknown, but it appears genetically distinct, with a reciprocal t(11;16)(q13;p13) translocation identified in an increasing number of cases. We review the literature on chondroid lipoma, discussing tumor histology, immunohistochemistry, ultrastructure, and differential diagnosis, and summarize the molecular genetic features so far known.</description><dc:title>Chondroid lipoma: an update and review</dc:title><dc:creator>Khin Thway, Rashpal Singh Flora, Cyril Fisher</dc:creator><dc:identifier>10.1016/j.anndiagpath.2012.01.002</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Review Article</prism:section><prism:startingPage>230</prism:startingPage><prism:endingPage>234</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913412000469/abstract?rss=yes"><title>Masthead</title><link>http://www.annalspathology.com/article/PIIS1092913412000469/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(12)00046-9</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A1</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913412000470/abstract?rss=yes"><title>Editorial Board</title><link>http://www.annalspathology.com/article/PIIS1092913412000470/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(12)00047-0</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A2</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913412000482/abstract?rss=yes"><title>Table of Contents</title><link>http://www.annalspathology.com/article/PIIS1092913412000482/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(12)00048-2</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A4</prism:endingPage></item><item rdf:about="http://www.annalspathology.com/article/PIIS1092913412000494/abstract?rss=yes"><title>Instructions for Authors</title><link>http://www.annalspathology.com/article/PIIS1092913412000494/abstract?rss=yes</link><description></description><dc:title>Instructions for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1092-9134(12)00049-4</dc:identifier><dc:source>Annals of Diagnostic Pathology 16, 3 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Annals of Diagnostic Pathology</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1092-9134(12)X0003-0</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A5</prism:startingPage><prism:endingPage>A6</prism:endingPage></item></rdf:RDF>
