: A Morphologic and Immunohistochemical Study of 13 Cases. Miyamoto H, Montgomery EA, Epstein JI. Am J Surg Pathol. 2010 Mar 4. PMID: 20216379
Departments of *Pathology daggerOncology double daggerOrthopedics section signUrology, The Johns Hopkins University School of Medicine, Baltimore, MD.
Paratesticular fibrous pseudotumor is a rare intrascrotal fibrous proliferation for which numerous synonyms have been proposed. Immunohistochemical staining was done in 13 cases identified by a database search (2000 to 2008) at our institution. All men (19 to 75 y old, mean 41.9 y) presented with scrotal masses, 6 patients also had hydroceles. Six men were treated by orchiectomy, whereas the remaining 7 men underwent excisional biopsy. Histologically, lesions were subdivided into 3 types: (1) "plaque-like" consisting of dense fibrous tissue with clefts without significant inflammation identical to a pleural plaque (5 cases); (2) "inflammatory sclerotic" with dense fibrous tissue containing lymphocytes (diffusely or aggregates or germinal centers), plasma cells, and an increased capillary network (6 cases); and (3) "myofibroblastic" consisting of reactive looking tissue-culture-like spindle cells with numerous capillaries and sparse chronic inflammation (2 cases). Stains for smooth muscle actin were positive in 11/13 (84.6%) cases, whereas desmin was positive in 4/13 (30.8%) cases. Stains for cytokeratin AE1/AE3, calretinin, and CD34 were positive in 7/13 (53.8%), 6/13 (46.2%), and 7/13 (53.8%) cases, respectively. All cases were negative for beta-catenin and ALK-1. Ki-67 showed a proliferation index of <1% in all but 2 cases, which had 5% labeling. Although there were 3 distinct histologic patterns seen in paratesticular fibrous pseudotumors, their immunohistochemical profile had overlapping features. Paratesticular fibrous pseudotumor looks histologically distinct from fibromatosis and inflammatory myofibroblastic tumor (IMT) seen in other organs, an assertion supported by negative stains for beta-catenin and ALK-1, respectively. However, as not all IMTs react with ALK and we had only 2 cases with a myofibroblastic appearance, we cannot definitively exclude the possibility that this subtype of paratesticular fibrous pseudotumor is related to IMT. Although this lesion has different histologic patterns, presently it is not warranted to split it into 3 separate entities as all share the same clinical presentation, are biologically benign, and lack consistent immunohistochemical differences.
PMID: 20216379
http://www.humpath.com/paratesticular-fibrous-pseudotumor
Saturday, March 13, 2010
Friday, March 12, 2010
ETS Gene Aberrations in Atypical Cribriform Lesions of the Prostate
: Implications for the Distinction Between Intraductal Carcinoma of the Prostate and Cribriform High-grade Prostatic Intraepithelial Neoplasia. Han B, Suleman K, Wang L, Siddiqui J, Sercia L, Magi-Galluzzi C, Palanisamy N, Chinnaiyan AM, Zhou M, Shah RB. Am J Surg Pathol. 2010 Mar 8. PMID: 20220513
Am J Surg Pathol. 2010 Mar 8. [Epub ahead of print]
ETS Gene Aberrations in Atypical Cribriform Lesions of the Prostate: Implications for the Distinction Between Intraductal Carcinoma of the Prostate and Cribriform High-grade Prostatic Intraepithelial Neoplasia.
Han B, Suleman K, Wang L, Siddiqui J, Sercia L, Magi-Galluzzi C, Palanisamy N, Chinnaiyan AM, Zhou M, Shah RB.
*Michigan Center for Translational Pathology daggerDepartment of Pathology section signHoward Hughes Medical Institute parallelDepartment of Urology paragraph signComprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI double daggerDepartment of Anatomic Pathology, Cleveland Clinic, Cleveland, OH.
BACKGROUND: Atypical cribriform lesions (ACLs) of the prostate consist of cribriform glands lined with cytologically malignant cells with partial or complete basal cell lining. It may represent cribriform "high-grade prostatic intraepithelial neoplasia" (HGPIN) or "intraductal carcinoma of the prostate" (IDC-P), which is almost always associated with clinically aggressive prostate carcinoma (PCa). Distinction between these 2 lesions has profound clinical significance, especially on needle biopsies. However, there are lesions that do not fully satisfy the criteria for IDC-P yet are worse than typical HGPIN and are difficult to distinguish based on morphologic criteria alone. METHODS: To better understand the biologic and molecular basis of distinction between cribriform HGPIN and IDC, we used break-apart fluorescence in-situ hybridization assay to assess ETS gene aberrations, a specific and commonest molecular alteration involving PCa, in a cohort of 16 isolated ACL, presumed to be an isolated cribriform HGPIN, and 45 carcinoma-associated ACL (ACL-PCa) on radical prostatectomy specimens, presumed to be spectrum of IDC-P. The latter was further divided into 2 groups: group A with marked nuclear atypia (nuclear size 6xnormal or larger) and/or comedonecrosis (n=21) and group B that did not fulfill these criteria (n=24). RESULTS: Overall, ERG rearrangement was absent (0 of 16) in isolated cribriform HGPIN, whereas present in 75% (36 of 48) of IDC-P, of which 65% (23 of 36) were through deletion and 35% (13 of 36) through insertion. Notably, 17% (6 of 36) of the IDC-P showed duplication of ERG rearrangement in combination with deletion of 5'-ERG. Hundred percent (34 of 34) of the IDC-P showed concordance of ERG rearrangement status with adjacent invasive carcinoma. There was no difference between the 2 groups of IDC-P lesions regarding prevalence of ERG rearrangement (group A 79% vs. group B 74%) and EDel2+ (20% vs. 15%). No case with ETV1, ETV4, or ETV5 rearrangement was identified. CONCLUSIONS: Our molecular data suggest that isolated cribriform HGPIN and IDC-P are biologically distinct lesions. Majority of ACL-PCa most likely represent intraductal spread of PCa. There is a significant overlap between IDC-P and HGPIN at the lower grade morphologic spectrum. ERG break-apart fluorescence in-situ hybridization assay provides insight into understanding the molecular basis of cribriform HGPIN and IDC-P and has potential clinical implications in their distinction on needle biopsies.
PMID: 20220513
Am J Surg Pathol. 2010 Mar 8. [Epub ahead of print]
ETS Gene Aberrations in Atypical Cribriform Lesions of the Prostate: Implications for the Distinction Between Intraductal Carcinoma of the Prostate and Cribriform High-grade Prostatic Intraepithelial Neoplasia.
Han B, Suleman K, Wang L, Siddiqui J, Sercia L, Magi-Galluzzi C, Palanisamy N, Chinnaiyan AM, Zhou M, Shah RB.
*Michigan Center for Translational Pathology daggerDepartment of Pathology section signHoward Hughes Medical Institute parallelDepartment of Urology paragraph signComprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI double daggerDepartment of Anatomic Pathology, Cleveland Clinic, Cleveland, OH.
BACKGROUND: Atypical cribriform lesions (ACLs) of the prostate consist of cribriform glands lined with cytologically malignant cells with partial or complete basal cell lining. It may represent cribriform "high-grade prostatic intraepithelial neoplasia" (HGPIN) or "intraductal carcinoma of the prostate" (IDC-P), which is almost always associated with clinically aggressive prostate carcinoma (PCa). Distinction between these 2 lesions has profound clinical significance, especially on needle biopsies. However, there are lesions that do not fully satisfy the criteria for IDC-P yet are worse than typical HGPIN and are difficult to distinguish based on morphologic criteria alone. METHODS: To better understand the biologic and molecular basis of distinction between cribriform HGPIN and IDC, we used break-apart fluorescence in-situ hybridization assay to assess ETS gene aberrations, a specific and commonest molecular alteration involving PCa, in a cohort of 16 isolated ACL, presumed to be an isolated cribriform HGPIN, and 45 carcinoma-associated ACL (ACL-PCa) on radical prostatectomy specimens, presumed to be spectrum of IDC-P. The latter was further divided into 2 groups: group A with marked nuclear atypia (nuclear size 6xnormal or larger) and/or comedonecrosis (n=21) and group B that did not fulfill these criteria (n=24). RESULTS: Overall, ERG rearrangement was absent (0 of 16) in isolated cribriform HGPIN, whereas present in 75% (36 of 48) of IDC-P, of which 65% (23 of 36) were through deletion and 35% (13 of 36) through insertion. Notably, 17% (6 of 36) of the IDC-P showed duplication of ERG rearrangement in combination with deletion of 5'-ERG. Hundred percent (34 of 34) of the IDC-P showed concordance of ERG rearrangement status with adjacent invasive carcinoma. There was no difference between the 2 groups of IDC-P lesions regarding prevalence of ERG rearrangement (group A 79% vs. group B 74%) and EDel2+ (20% vs. 15%). No case with ETV1, ETV4, or ETV5 rearrangement was identified. CONCLUSIONS: Our molecular data suggest that isolated cribriform HGPIN and IDC-P are biologically distinct lesions. Majority of ACL-PCa most likely represent intraductal spread of PCa. There is a significant overlap between IDC-P and HGPIN at the lower grade morphologic spectrum. ERG break-apart fluorescence in-situ hybridization assay provides insight into understanding the molecular basis of cribriform HGPIN and IDC-P and has potential clinical implications in their distinction on needle biopsies.
PMID: 20220513
Friday, March 5, 2010
High-resolution array CGH of metanephric adenomas: lack of DNA copy number changes
Szponar A, Yusenko MV, Kovacs G. Histopathology. 2010 Jan;56(2):212-6. PMID: 20102400
Laboratory of Molecular Oncology, Medical Faculty, Ruprecht-Karls-University, Heidelberg, Germany.
AIMS: Previous karyotyping and fluorescence in situ hybridization analysis of metanephric adenomas (MAs) has yielded controversial data. The aim of this study was to detect small genomic alterations, if any, specific to MAs by applying high-resolution oligoarrays.
METHODS AND RESULTS: DNA extracted from paraffin blocks of six metanephric adenomas was hybridized onto Agilent oligoarrays with approximately 43,000 in situ synthesized 60-mer oligonucleotide probes that span coding and non-coding sequences with an average spatial resolution of approximately 35 kb. None of the metanephric adenomas showed DNA copy number changes. To confirm our results, DNA extracted from the paraffin block of a chromophobe renal cell carcinoma (RCC) was simultaneously hybridized to one of the four arrays on the same slides as an internal control. The chromophobe RCC showed loss of several chromosomes but no alteration was seen in MAs. We have confirmed the negative results by dye-swap and sex mismatch hybridization experiments.
CONCLUSIONS: Our high-resolution oligoarray analysis indicates that metanephric adenomas lack DNA copy number alterations. This finding may help to differentiate between metanephric adenomas from Wilms' tumour and papillary renal cell adenoma with overlapping phenotype.
PMID: 20102400
humpath.com #6815
Laboratory of Molecular Oncology, Medical Faculty, Ruprecht-Karls-University, Heidelberg, Germany.
AIMS: Previous karyotyping and fluorescence in situ hybridization analysis of metanephric adenomas (MAs) has yielded controversial data. The aim of this study was to detect small genomic alterations, if any, specific to MAs by applying high-resolution oligoarrays.
METHODS AND RESULTS: DNA extracted from paraffin blocks of six metanephric adenomas was hybridized onto Agilent oligoarrays with approximately 43,000 in situ synthesized 60-mer oligonucleotide probes that span coding and non-coding sequences with an average spatial resolution of approximately 35 kb. None of the metanephric adenomas showed DNA copy number changes. To confirm our results, DNA extracted from the paraffin block of a chromophobe renal cell carcinoma (RCC) was simultaneously hybridized to one of the four arrays on the same slides as an internal control. The chromophobe RCC showed loss of several chromosomes but no alteration was seen in MAs. We have confirmed the negative results by dye-swap and sex mismatch hybridization experiments.
CONCLUSIONS: Our high-resolution oligoarray analysis indicates that metanephric adenomas lack DNA copy number alterations. This finding may help to differentiate between metanephric adenomas from Wilms' tumour and papillary renal cell adenoma with overlapping phenotype.
PMID: 20102400
humpath.com #6815
Friday, February 26, 2010
Smooth Muscle Neoplasms of the Urinary Bladder
A Clinicopathologic Study of 51 Cases. Lee TK, Miyamoto H, Osunkoya AO, Guo CC, Weiss SW, Epstein JI. Am J Surg Pathol. 2010 Feb 11. PMID: 20154594
Smooth Muscle Neoplasms of the Urinary Bladder: A Clinicopathologic Study of 51 Cases. Lee TK, Miyamoto H, Osunkoya AO, Guo CC, Weiss SW, Epstein JI. Am J Surg Pathol. 2010 Feb 11.
Departments of *Pathology section signUrology parallelOncology, The Johns Hopkins Medical Institutions, Baltimore, MD daggerDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA double daggerDepartment of Pathology, University of Texas M.D. Anderson Cancer Center, Houston, TX.
Smooth muscle neoplasms of the urinary bladder are relatively rare. We report the largest series to date examining the clinicopathologic features of leiomyomas and leiomyosarcomas of the bladder.
This study sought to clarify several issues relating to smooth muscle neoplasms of the urinary bladder: (1) How to distinguish leiomyomas of the bladder from normal muscularis propria on transurethral resection (TUR) specimens; (2) Whether symplastic leiomyomas can be diagnosed in the bladder; (3) Can leiomyoma be definitively diagnosed on biopsy or TUR without the risk of there being unsampled leiomyosarcoma; and (4) Is the grade of leiomyosarcoma seen on biopsy or TUR heterogeneous and hence possibly not representative of the true grade. Thirty-one leiomyomas and 20 leiomyosarcoma cases of urinary bladder from 3 tertiary care medical centers were examined.
Leiomyosarcoma cases were subdivided into low-grade and high-grade based on mitotic count (>/=5/10 HPF) and nuclear atypia. The mean age of the patients with leiomyoma and leiomyosarcoma was 52 and 58, respectively. The M:F ratio was significantly higher in patients with leiomyosarcoma (2:1) compared with leiomyoma (1:3), p<0.005.
The specimen consisted of 20 TUR and 11 transurethral biopsies (TUBx) for leiomyomas, and 10 TUR, 3 TUBx, 5 cystectomies (Cyst), and 2 partial cystectomies (pCyst) for leiomyosarcomas. LEIOMYOMAS: Notable features in leiomyomas were hyalinization (7/31), degenerative atypia (7/31), necrosis (4/31), myxoid changes (2/31), and focal fatty metaplasia (1/31); although no surface ulceration was identified.
Clinical follow-up was available for 24 patients (12 to 108 mo; mean 36 mo); 4 lost to follow-up and 3 recent cases. Two patients had repeat TUR within a year of the initial diagnosis with the same bland leiomyoma on histology, probably reflecting persistence of earlier unresected tumor as opposed to recurrent tumor. None of the patients were diagnosed with leiomyosarcoma on follow-up, including 7 cases with degenerative atypia.
LEIOMYOSARCOMA: Of the 20 leiomyosarcomas, 8 were classified as low-grade and 12 as high-grade sarcomas.
Histologic features included epithelioid morphology (5/20; 1 entirely epithelioid), tumor cell necrosis (11/20), and mucosal ulceration (7/20). Infiltration into the muscularis propria was seen predominantly as a nodular growth pattern with some cases exhibiting an irregular infiltrative pattern (6/10 with evaluable borders); an infiltrative pattern was not restricted to high-grade lesions.
Lesional heterogeneity was present in only 1 case on the same specimen, which showed both low-grade and high-grade areas. Another case was low grade on TUR, yet high grade at cystectomy. None of the cases of leiomyosarcomas had areas histologically resembling leiomyoma.
Clinical follow-up was available for 15 patients with leiomyosarcoma (11 to 144 mo; mean 47 mo); 3 lost to follow-up and 2 recent cases. Only 1 patient with low-grade sarcoma experienced 2 local recurrences treated only by TUR and is currently free of disease. Disease-related mortality was significantly higher in patients with high-grade compared with low-grade leiomyosarcomas (50% vs. none, respectively; P<0.001).
Leiomyoma (including symplastic leiomyoma) may be diagnosed on TUR without risk of underdiagnosing unsampled leiomyosarcoma. High-grade leiomyosarcomas are highly aggressive neoplasms compared with low-grade leiomyosarcomas; in most cases grade can be accurately determined on TUR.
PMID: 20154594
Smooth Muscle Neoplasms of the Urinary Bladder: A Clinicopathologic Study of 51 Cases. Lee TK, Miyamoto H, Osunkoya AO, Guo CC, Weiss SW, Epstein JI. Am J Surg Pathol. 2010 Feb 11.
Departments of *Pathology section signUrology parallelOncology, The Johns Hopkins Medical Institutions, Baltimore, MD daggerDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA double daggerDepartment of Pathology, University of Texas M.D. Anderson Cancer Center, Houston, TX.
Smooth muscle neoplasms of the urinary bladder are relatively rare. We report the largest series to date examining the clinicopathologic features of leiomyomas and leiomyosarcomas of the bladder.
This study sought to clarify several issues relating to smooth muscle neoplasms of the urinary bladder: (1) How to distinguish leiomyomas of the bladder from normal muscularis propria on transurethral resection (TUR) specimens; (2) Whether symplastic leiomyomas can be diagnosed in the bladder; (3) Can leiomyoma be definitively diagnosed on biopsy or TUR without the risk of there being unsampled leiomyosarcoma; and (4) Is the grade of leiomyosarcoma seen on biopsy or TUR heterogeneous and hence possibly not representative of the true grade. Thirty-one leiomyomas and 20 leiomyosarcoma cases of urinary bladder from 3 tertiary care medical centers were examined.
Leiomyosarcoma cases were subdivided into low-grade and high-grade based on mitotic count (>/=5/10 HPF) and nuclear atypia. The mean age of the patients with leiomyoma and leiomyosarcoma was 52 and 58, respectively. The M:F ratio was significantly higher in patients with leiomyosarcoma (2:1) compared with leiomyoma (1:3), p<0.005.
The specimen consisted of 20 TUR and 11 transurethral biopsies (TUBx) for leiomyomas, and 10 TUR, 3 TUBx, 5 cystectomies (Cyst), and 2 partial cystectomies (pCyst) for leiomyosarcomas. LEIOMYOMAS: Notable features in leiomyomas were hyalinization (7/31), degenerative atypia (7/31), necrosis (4/31), myxoid changes (2/31), and focal fatty metaplasia (1/31); although no surface ulceration was identified.
Clinical follow-up was available for 24 patients (12 to 108 mo; mean 36 mo); 4 lost to follow-up and 3 recent cases. Two patients had repeat TUR within a year of the initial diagnosis with the same bland leiomyoma on histology, probably reflecting persistence of earlier unresected tumor as opposed to recurrent tumor. None of the patients were diagnosed with leiomyosarcoma on follow-up, including 7 cases with degenerative atypia.
LEIOMYOSARCOMA: Of the 20 leiomyosarcomas, 8 were classified as low-grade and 12 as high-grade sarcomas.
Histologic features included epithelioid morphology (5/20; 1 entirely epithelioid), tumor cell necrosis (11/20), and mucosal ulceration (7/20). Infiltration into the muscularis propria was seen predominantly as a nodular growth pattern with some cases exhibiting an irregular infiltrative pattern (6/10 with evaluable borders); an infiltrative pattern was not restricted to high-grade lesions.
Lesional heterogeneity was present in only 1 case on the same specimen, which showed both low-grade and high-grade areas. Another case was low grade on TUR, yet high grade at cystectomy. None of the cases of leiomyosarcomas had areas histologically resembling leiomyoma.
Clinical follow-up was available for 15 patients with leiomyosarcoma (11 to 144 mo; mean 47 mo); 3 lost to follow-up and 2 recent cases. Only 1 patient with low-grade sarcoma experienced 2 local recurrences treated only by TUR and is currently free of disease. Disease-related mortality was significantly higher in patients with high-grade compared with low-grade leiomyosarcomas (50% vs. none, respectively; P<0.001).
Leiomyoma (including symplastic leiomyoma) may be diagnosed on TUR without risk of underdiagnosing unsampled leiomyosarcoma. High-grade leiomyosarcomas are highly aggressive neoplasms compared with low-grade leiomyosarcomas; in most cases grade can be accurately determined on TUR.
PMID: 20154594
Sunday, January 3, 2010
Renal tubulocystic carcinoma is closely related to papillary renal cell carcinoma
: Implications for pathologic classification. Zhou M, Yang XJ, Lopez JI, Shah RB, Hes O, Shen SS, Li R, Yang Y, Lin F, Elson P, Sercia L, Magi-Galluzzi C, Tubbs R. Am J Surg Pathol. 2009 Dec;33(12):1840-9.PMID: 19898225
Cleveland Clinic, Cleveland, OH, USA. zhoum@ccf.org
Tubulocystic carcinoma of the kidney (TC-RCC) is a rare renal tumor with unique gross and microscopic features unlike other types of renal cell carcinoma (RCC). Several recent studies recommend that it should be classified as a distinct RCC subtype. In this study, we provide pathologic and cytogenetic evidence supporting that TC-RCC is closely related to papillary RCC (PRCC).
This study included 20 cases of renal tumors that partially or exclusively comprised a TC-RCC component. Pathologic examination documented the gross and microscopic features of TC-RCC, including multicentricity and the presence of concomitant PRCC and papillary adenoma. Formalin-fixed, paraffin-embedded sections from 12 TC-RCC and 20 PRCC were subjected to a multicolor fluorescence in situ hybridization assay containing probes for chromosomes 7, 17, and Y. One hundred nuclei were examined to enumerate the copy numbers of chromosomes in each tumor and its corresponding normal kidney tissue. A tumor with a percentage of cells harboring a chromosomal change > or = mean+3 SD of normal tissue was considered to harbor that chromosomal change, and a tumor with a percentage of cells with null Y chromosome count (loss of Y chromosome) > or = mean+3 SD of normal tissue was considered to harbor Y chromosome loss. Four of the 20 TC-RCCs were multicentric. Ten had associated PRCC or papillary adenoma within the same kidney as the TC-RCC. In 4 cases, the tubulocystic and papillary components were admixed together within the same lesion. The tumor cells lining both the tubulocystic and papillary components had similar cytologic features. Ten of 12 TC-RCCs had a chromosome 7 gain, 8 of 12 cases had a chromosome 17 gain, and 8 of 9 cases had a loss of Y chromosome. Six of 9 cases with all 3 chromosomes studied had a gain of chromosomes 7 and 17 and a loss of Y chromosome.
Our study shows that TC-RCCs and PRCCs are closely related entities. With its distinctive gross and microscopic features, TC-RCC may be considered a unique "morphologic entity." However, before it is accepted as a distinct renal cell carcinoma subtype, further studies are needed to document a characteristic molecular signature associated with this tumor.
PMID: 19898225
Cleveland Clinic, Cleveland, OH, USA. zhoum@ccf.org
Tubulocystic carcinoma of the kidney (TC-RCC) is a rare renal tumor with unique gross and microscopic features unlike other types of renal cell carcinoma (RCC). Several recent studies recommend that it should be classified as a distinct RCC subtype. In this study, we provide pathologic and cytogenetic evidence supporting that TC-RCC is closely related to papillary RCC (PRCC).
This study included 20 cases of renal tumors that partially or exclusively comprised a TC-RCC component. Pathologic examination documented the gross and microscopic features of TC-RCC, including multicentricity and the presence of concomitant PRCC and papillary adenoma. Formalin-fixed, paraffin-embedded sections from 12 TC-RCC and 20 PRCC were subjected to a multicolor fluorescence in situ hybridization assay containing probes for chromosomes 7, 17, and Y. One hundred nuclei were examined to enumerate the copy numbers of chromosomes in each tumor and its corresponding normal kidney tissue. A tumor with a percentage of cells harboring a chromosomal change > or = mean+3 SD of normal tissue was considered to harbor that chromosomal change, and a tumor with a percentage of cells with null Y chromosome count (loss of Y chromosome) > or = mean+3 SD of normal tissue was considered to harbor Y chromosome loss. Four of the 20 TC-RCCs were multicentric. Ten had associated PRCC or papillary adenoma within the same kidney as the TC-RCC. In 4 cases, the tubulocystic and papillary components were admixed together within the same lesion. The tumor cells lining both the tubulocystic and papillary components had similar cytologic features. Ten of 12 TC-RCCs had a chromosome 7 gain, 8 of 12 cases had a chromosome 17 gain, and 8 of 9 cases had a loss of Y chromosome. Six of 9 cases with all 3 chromosomes studied had a gain of chromosomes 7 and 17 and a loss of Y chromosome.
Our study shows that TC-RCCs and PRCCs are closely related entities. With its distinctive gross and microscopic features, TC-RCC may be considered a unique "morphologic entity." However, before it is accepted as a distinct renal cell carcinoma subtype, further studies are needed to document a characteristic molecular signature associated with this tumor.
PMID: 19898225
The basaloid cell is the best tissue marker for human papillomavirus in invasive penile squamous cell carcinoma: a study of 202 cases from Paraguay. Cubilla AL, Lloveras B, Alejo M, Clavero O, Chaux A, Kasamatsu E, Velazquez EF, Lezcano C, Monfulleda N, Tous S, Alemany L, Klaustermeier J, Muñoz N, Quint W, de Sanjose S, Bosch FX. Am J Surg Pathol. 2010 Jan;34(1):104-14.PMID: 20035150
Instituto de Patología e Investigación, Asunción, Paraguay. acubilla@institutodepatologia.com.py
Human papillomavirus (HPV) has been reported in 12-82% of penile squamous cell carcinomas (SCC). There is an association of the virus with basaloid and warty carcinomas but the reported prevalence is variable. The causes of these variations are not clear. They may be owing to geographic differences, the use of different techniques to detect HPV, the status of the original paraffin blocks, or to variable criteria in tumor classification. The aims of the study were to determine the prevalence of HPV in penile SCC and subtypes using a sensitive technique, to investigate genotypes involved, and to search for other morphologic features associated with the virus from a series of cases from Paraguay. HPV detection was done by SPF-10 polymerase chain reaction followed by DNA enzyme-immunoassay and genotyping by LIPA 25 (version 1). Samples were tested at Catalan Institute of Oncology, Barcelona, and cross testing was carried out at the Delft Diagnostic Laboratories in The Netherlands. HPV was detected in 64 of 202 cases (32%). Thirteen tumors had multiple HPV genotypes. Most prevalent genotypes were HPV-16 (46 cases), HPV-6 (6 cases), and HPV-18 (4 cases), either in single or in multiple infections. HPV was preferentially associated with warty-basaloid (82%), basaloid (76%), and warty (39%) carcinomas and not detected in verrucous, mixed verrucous-papillary, pseudohyperplastic, and pseudoglandular SCCs. There was a strong association between HPV and higher histologic grade. Basaloid cells were more frequently found in HPV positive tumors (72%) and this association was statistically significant in univariate and multivariate analyses. Cells with koilocytotic features and keratinizing squamous cells were also present but to a much lesser degree (47% and 19%, respectively). In summary, HPV was found in a third of the cases and the most common genotype was HPV-16. Low-risk genotypes were rarely found in single infections, representing 4 cases among all analyzed (2%). There was an association between HPV presence and higher histologic grade and with basaloid, warty-basaloid, and warty carcinomas. Our results also suggest that, in penile SCC, the basaloid cell is the best tissue marker for oncogenic HPV infection.
PMID: 20035150
Instituto de Patología e Investigación, Asunción, Paraguay. acubilla@institutodepatologia.com.py
Human papillomavirus (HPV) has been reported in 12-82% of penile squamous cell carcinomas (SCC). There is an association of the virus with basaloid and warty carcinomas but the reported prevalence is variable. The causes of these variations are not clear. They may be owing to geographic differences, the use of different techniques to detect HPV, the status of the original paraffin blocks, or to variable criteria in tumor classification. The aims of the study were to determine the prevalence of HPV in penile SCC and subtypes using a sensitive technique, to investigate genotypes involved, and to search for other morphologic features associated with the virus from a series of cases from Paraguay. HPV detection was done by SPF-10 polymerase chain reaction followed by DNA enzyme-immunoassay and genotyping by LIPA 25 (version 1). Samples were tested at Catalan Institute of Oncology, Barcelona, and cross testing was carried out at the Delft Diagnostic Laboratories in The Netherlands. HPV was detected in 64 of 202 cases (32%). Thirteen tumors had multiple HPV genotypes. Most prevalent genotypes were HPV-16 (46 cases), HPV-6 (6 cases), and HPV-18 (4 cases), either in single or in multiple infections. HPV was preferentially associated with warty-basaloid (82%), basaloid (76%), and warty (39%) carcinomas and not detected in verrucous, mixed verrucous-papillary, pseudohyperplastic, and pseudoglandular SCCs. There was a strong association between HPV and higher histologic grade. Basaloid cells were more frequently found in HPV positive tumors (72%) and this association was statistically significant in univariate and multivariate analyses. Cells with koilocytotic features and keratinizing squamous cells were also present but to a much lesser degree (47% and 19%, respectively). In summary, HPV was found in a third of the cases and the most common genotype was HPV-16. Low-risk genotypes were rarely found in single infections, representing 4 cases among all analyzed (2%). There was an association between HPV presence and higher histologic grade and with basaloid, warty-basaloid, and warty carcinomas. Our results also suggest that, in penile SCC, the basaloid cell is the best tissue marker for oncogenic HPV infection.
PMID: 20035150
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