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Hyalinizing Spindle Cell Tumor With Giant Rosettes--A Soft Tissue Tumor With Mesenchymal and Neuroendocrine Features.

An Immunohistochemical, Ultrastructural, and Cytogenetic Analysis

Lane et al[1] recently described a distinctive neoplasm that they termed hyalizing spindle cell tumor with giant rosettes. It is a tumor characterized by 2 histologic components. One is cellular with spindle cell areas. The second component is represented by well-circumscribed almost acellular islands filled with hyalinized material that are characteristically surrounded by round-to-oval cells. These palisading cells display an unusual immunohistochemical profile, because they react with antibodies directed against antigens of neural differentiation, whereas the spindle cellular areas are negative for neural markers. The clinical information obtained by Lane et al indicated that these lesions occur predominantly in the extremities of young to middle-aged adults, and the behavior, in a limited follow-up, is benign.[1,2]

We present 2 additional cases, one of which arose in what appears to be an unusual location, the prestyloid parapharyngeal space. We applied a broad immunohistochemical panel to both specimens in an attempt to better elucidate the nature of these tumors. We also describe for the first time the ultrastructural and cytogenetic features of this tumor.

MATERIALS AND METHODS

The hematoxylin-eosin-stained slides of 2 tumors with the histopathologic features of spindle cell tumor with giant rosettes were reviewed. The specimens were fixed in 10% buffered formalin and embedded in paraffin. Eleven sections from the first case and 7 from the second were examined by light microscopy, and stains for trichrome, reticulin, and immunomarkers were also performed. Fresh tissue from one tumor was allocated for electron microscopic and cytogenetic studies.

Electron Microscopy

Tissue for ultrastructural analysis was fixed promptly after excision in 2.5% glutaraldehyde buffered with 0.1 mol/L cacodylate buffer, pH 4.3, postfixed in buffered 1% osmium tetroxide, block stained with 2% uranyl acetate, and embedded in spur resin. Thin sections were stained with lead citrate and examined with a Phillips 300 transmission electron microscope.

Immunohistochemistry

Sections 5 [micro]m thick were deparafinized in xylene and rehydrated through decreasing concentrations of ethanol to water. Application of microwave antigen retrieval and/or enzymatic treatment to enhance exposure of antigens before the incubation with primary antibodies and the characteristics and source of the antibodies are indicated in the Table. Negative controls were prepared by substituting the primary antibody with either nonimmune mouse immunoglobulin G (Sigma Laboratories, St Louis, Mo) or rabbit serum. The counterstain was Harris hematoxylin. An indirect biotin-avidin method was used with the Ventana 320 immunostainer (Ventana Medical Systems, Tucson, Ariz). Double immunostainings for HAM56/CD57 and factor XIIIa/CD57 were performed. HAM56 and factor XIIIa were primary antibodies with an incubation time of 32 minutes and were detected by using the Ventana peroxidase diaminobenzidine chromogen. CD57 was the second antibody applied for 30 minutes and was detected by using streptavidin alkaline phosphatase blue substrate (Kirkegaard & Perry Laboratory, Gaithersburg, Md).

Antibodies Used and Immunoreactivity in 2 Cases(*)
Antibody/Clone Source

S100 protein/Z0628 Dako, Carpinteria, Calif
Synapatophysin/SY38 Dako
CD57/HNK-1 Becton Dickinson, Mountainview,
 Calif
Protein gene product 9.5/1304 Ultraclone Limited, Isle of Wight,
 England
Neuron-specific enolase/ Zymed, San Francisco, Calif
 18-0042
Vimentin/34B Dako
Factor Xllla Calbiochem, La Jolla, Calif
HAM56/HAM56 Enzo Diagnostics, Farmingdale, NY
Collagen IV/CIV-22 Zymed
CD68/PG-M1 Dako
Ki-67/MIB1 Amac, Westbrook, Me
Glial acidic fibrillary Dako
 protein
Chromogranin/LK2H10 Boehringer
 Mannhein, Indianapolis, Ind
Neurofilament/NP57 Dako
Muscle-specific actin/HHF35 Dako
Smooth muscle actin/IA4 Sigma
Cytokerati n/Cam 5.2 Becton Dickinson
Cytokeratin/AE1/AE3 Boehringer
 Mannhein
Epithelial membrane Dako
 antigen/E29
CD45/RP2/18 Ventana
CD34/Q-Bend-10 Vector, Burlingame, Calif
Desmin Dako
Factor VIIIRA/AOO82 Dako
p53/DO-1 Calbiochem

Antibody/Clone Species Dilution

S100 protein/Z0628 R 1:800
Synapatophysin/SY38 R 1:400
CD57/HNK-1 M 1:20
Protein gene product 9.5/1304 R 1:20
Neuron-specific enolase/ R 1:100
 18-0042
Vimentin/34B M 1:40
Factor Xllla R 1:500
HAM56/HAM56 M 1:20
Collagen IV/CIV-22 R 1:20
CD68/PG-M1 M 1:50
Ki-67/MIB1 M 1:40
Glial acidic fibrillary R 1:100
 protein
Chromogranin/LK2H10 M 1:800

Neurofilament/NP57 M 1:700
Muscle-specific actin/HHF35 M 1:400
Smooth muscle actin/IA4 M 1:1500
Cytokerati n/Cam 5.2 M 1:25
Cytokeratin/AE1/AE3 M 1:400
Epithelial membrane M 1:20
 antigen/E29
CD45/RP2/18 M Prediluted
CD34/Q-Bend-10 M 1:30
Desmin M 1:10
Factor VIIIRA/AOO82 R 1:200
p53/DO-1 M 1:150

 Reactivity
 in
 Trypsin Rossette-Forming
Antibody/Clone Digestion Cells

S100 protein/Z0628 Protease +
Synapatophysin/SY38 Protease +
CD57/HNK-1 Protease +
Protein gene product 9.5/1304 ... +
Neuron-specific enolase/ ... +[dagger]
 18-0042
Vimentin/34B Protease +
Factor Xllla Protease -
HAM56/HAM56 Protease -
Collagen IV/CIV-22 Protease -
CD68/PG-M1 ... -
Ki-67/MIB1 Trypsin -
Glial acidic fibrillary Protease -
 protein
Chromogranin/LK2H10 ... -
Neurofilament/NP57 ... -
Muscle-specific actin/HHF35 Protease -
Smooth muscle actin/IA4 ... -
Cytokerati n/Cam 5.2 Protease -
Cytokeratin/AE1/AE3 Protease -
Epithelial membrane ... -
 antigen/E29
CD45/RP2/18 ... -
CD34/Q-Bend-10 ... -
Desmin ... -
Factor VIIIRA/AOO82 Protease -
p53/DO-1 ... -

 Reactivity
 in Spindle
Antibody/Clone Cells

S100 protein/Z0628 -
Synapatophysin/SY38 -
CD57/HNK-1 -
Protein gene product 9.5/1304 -
Neuron-specific enolase/ -
 18-0042
Vimentin/34B +
Factor Xllla +
HAM56/HAM56 +
Collagen IV/CIV-22 +
CD68/PG-M1 +
Ki-67/MIB1 LI:2.2[double dagger]
Glial acidic fibrillary -
 protein
Chromogranin/LK2H10 -
Neurofilament/NP57 -
Muscle-specific actin/HHF35 -
Smooth muscle actin/IA4 -
Cytokerati n/Cam 5.2 -
Cytokeratin/AE1/AE3 -
Epithelial membrane -
 antigen/E29
CD45/RP2/18 -
CD34/Q-Bend-10 -
Desmin -
Factor VIIIRA/AOO82 -
p53/DO-1 -


(*) Heat-induced epitope retrival was required for CD57, p53, and Ki-67. R indicates rabbit; M, mouse: plus sign, positive; and minus sign, negative.

(dagger) Immunoreactivity seen in only 1 case.

(double dagger) LI:MIB labeling index expressed as percentage of Ki-67-positive cells on the count of 1000 cells averaging both cases.

Cytogenetic Studies

The specimen for cytogenetic analysis consisted of a 1.5 X 0.5 cm pink homogeneous fragment from the prestyloid tumor. Cytogenetic analysis was performed according to standard in situ cell culture protocol.[3] Briefly, the tissue was minced with sterile scissors and digested with collagenase P for 1 hour at 37 [degrees] C. The resulting single cell suspension was seeded onto coverslips and cultured for 4 to 6 days in Chang D medium. Cytogenetic results were obtained from 4-day cultures.

Clinical Histories

Both patients presented within 8 months at Miami Valley Hospital in Dayton, Ohio, and were then referred to the University of Cincinnati Medical Center for surgical treatment and follow-up.

Case 1

A 22-year-old woman presented with a 2-month history of fullness in the neck. The patient did not complain of dysphagia or pain. She did have a history of anorexia nervosa and resection of a giant cell reparative granuloma of the right maxilla at the age of 2 years, with no recurrences. Physical examination revealed a firm mass located in the right posterior submandibular triangle. No cranial nerve deficits were identified. Computed tomography, magnetic resonance imaging, and magnetic resonance angiography scans revealed a nonvascular mass positioned in the prestyloid parapharyngeal space (Figure 1). This was resected via a transcervical approach. The tumor was located posterior to the external carotid artery but anterior to the internal carotid artery. It was well circumscribed, with no discernible origin from any cranial nerve and no obvious extension of tumor into the adjacent tissues. At intraoperative frozen section consultation, a diagnosis of a spindle cell proliferation without overt features of malignancy was rendered. However, the unusual histologic features described herein prompted the allocation of fresh tissue for ancillary studies. An enlarged regional lymph node that measured 2.1 cm in largest dimension was also removed, and its histologic examination showed benign reactive changes. There was no evidence of recurrence 8 months after surgery.

[Figure 1 ILLUSTRATION OMITTED]

Case 2

A 50-year-old woman presented with a mass in the quadriceps muscle of the left thigh. Preoperatively, the tumor was thought to be a sarcoma. It was removed with ample surrounding uninvolved tissue. Five months later she developed painful left inguinal lymphadenopathy. Three superficial lymph nodes were removed. Histologic examination revealed reactive benign changes. The swollen area in the inguinal region resolved spontaneously within the following days. Since then, she has been in good health, with no evidence of recurrence or disseminated disease at 16-month follow-up.

RESULTS

Gross Findings

Both tumors were well circumscribed and had an apparent capsule. The lesion from the neck was 4 X 3 X 3 cm, and the one from the thigh was 2.9 X 1.9 X 1.3 cm. On section, each tumor had a uniform firm consistency. The cut surfaces were white-tan with whorled areas. Their uniform appearance was disrupted by the presence of white specks, which in areas became confluent forming short streaks (Figure 2).

[Figure 2 ILLUSTRATION OMITTED]

Histologic Findings

Microscopically, both tumors were surrounded by a thin capsulelike fibrous band without peripheral infiltrating projections. The tumors had 2 main architectural components. The first and most prominent was represented by the giant rosettes described by Lane et al.[2] These are hyalinized acellular islands surrounded by round-to-oval plump cells in a palisading-like pattern (Figure 3). Some of these rosettes became confluent to form serpiginous connections. The core in these rosettes was birefringent under polarized light. In some of the rosettes, empty spaces within the collagen were observed. These spaces appear to be the result of vanishing cells leaving "ghostlike" lacunae. The second component was the interrosette spindle cells with a variable cell density. The hypercellular areas consisted of plump elongated cells located in a highly vascularized background, some of which were arranged in a storiform pattern. Occasionally, there were multinucleated cells within these cellular areas. In the less cellular areas, the spindle cells were slender and separated by conspicuous collagen. Necrosis was absent and mitotic activity was minimal, with 1 mitotic figure seen per 50 consecutive high-power fields in the tumor from the neck and none in the tumor from the thigh. No clear-cut myxoid component was observed. In both cases the surrounding soft tissue, including skeletal muscle, was not infiltrated by the tumor.

[Figure 3 ILLUSTRATION OMITTED]

Immunohistochemical Findings

The pattern of immunostaining was similar for both lesions. Both the spindle cells and the rosette-forming cells stained for vimentin. The hallmark of these tumors was established with antibodies to neural and endocrine antigens, since only the rosette-forming cells were immunoreactive for S100, CD57, protein gene product 9.5, and neuron-specific enolase (Figure 4), whereas the stromal spindle cells were negative for these 4 antibodies. Rare positive cells were seen among the spindle cells; however, they were located near the rosettes and probably represent entrapped rosette cells. The markers that frequently labeled spindle cells were antibodies associated with histiocytic differentiation, including HAM56, factor XIIIa, and, rarely, CD68. Factor XIIIa stained most spindle cells (Figure 5). The cells that reacted with this antibody had positivity in the nuclei and the cytoplasmic elongated projections, thus resembling dendritic cells. Double immunostain for factor XIIIa/CD57 and HAM56/CD57 revealed absence of simultaneous staining in either the rosette or the spindle cells. No positivity was observed to any of the other lineage of differentiation antibodies used in this study (Table). Collagen IV was present among the spindle cells, but it did not stain the core of the rosettes.

[Figure 4 and 5 ILLUSTRATION OMITTED]

Immunostaining with Ki-67 antibody showed scant nuclear positivity with a labeling index of 3.4% by counting 1000 consecutive nuclei of the cells from the parapharyngeal tumor and 1% for the tumor from the lower extremity. The average for both tumors was 2.2%.

Ultrastructural Findings

Electron microscopic examination performed on the tumor excised from the parapharyngeal region concentrated on cellular fields and at the periphery of the hyalinized nodules. There were 2 cell types with distinctly different ultrastructural morphologic configurations. The most numerous cells were spindle or fusiform shaped, with indented nuclei containing a prominent nucleolus and dense peripheral chromatin. The cytoplasm contained a varying amount of rough endoplasmic reticulum with often dilated cisternae. These cells were embedded in an extracellular matrix interspersed with dense bands of mature collagen fibrils and had the characteristics of fibroblasts. Cytoplasmic processes were observed.

The second cell type was frequently encountered in the periphery of the hyalinized rosettes. It was oval with a central smooth-contoured nucleus that contained dense chromatin but no nucleolus. Within the cytoplasm, there were membrane-limited dense granules measuring up to 400 nm, with a mean diameter of 340 nm. The granules were usually clustered near a prominent Golgi or at the cell periphery, with 5 to 15 granules per cell. However, only a few of the oval cells contained dense core granules. Some of the granules had fine stippled substructures more in accord with endocrine than neuroendocrine granules, reminiscent of those seen in paragangliomas (Figure 6).[4] Other features of the oval cells include a sparse RER occasionally arranged in small stacks in one area of the cytoplasm and rudimentary cellular junctions characterized by the presence of paired subplasmalemmal densities with focal thickening of adjacent cell membranes. The matrix around these cells and the hypocellular rosettes contain fibrils of periodically cross-striated collagen.

[Figure 6 ILLUSTRATION OMITTED]

Karyotypic Studies

Cytogenetic analysis of 20 metaphase spreads disclosed 2 cell lines, both containing a common, apparently balanced translocation between chromosomes 7 and 16. The karyotype is 46,XX,t(1;15;20)(q25;q22;q13.2),t(7;16)(q36;p13.1)[14]/ 46,XX,t(7;16)(q36;p13.1)[6]. Since no cells without the t(7;16) were identified in the tumor culture, chromosome analysis of peripheral blood lymphocytes was conducted to rule out a constitutional balanced translocation. Peripheral blood analysis of 20 metaphases disclosed normal female chromosomes, 46,XX, confirming that the changes observed in the tumor cells were acquired (Figure 7).

[Figure 7 ILLUSTRATION OMITTED]

COMMENT

Hyalinizing spindle cell tumor with giant rosettes is a tumor of distinctive and unusual histologic features described first in 1996 by Lane et al.[1] The rosettes are hyalinized islands embedded in a spindle cell proliferation and are spread throughout the tumor. These rosettes are lined by round-to-oval cells that contrast markedly with the intervening spindle cells, not only for their morphologic structure but also because the former express a neural phenotype by immunohistochemistry including S100, neuron-specific enolase, and CD57. The microscopic morphologic structure of the tumor is also reflected in the gross appearance, because the rosettes are evident as white specks. In fact, our report contains the first gross photograph of this unusual soft tissue tumor. Reinforcing the neuroendocrine phenotype of these cells, we show that protein gene product 9.5 also is present in the rosette-forming cells. Protein gene product 9.5 was originally isolated from brain and is present in neuroendocrine cells.[5] No immunostaining with neuroendocrine markers was seen in the spindle areas where cells stained only for vimentin, collagen IV, factor XIII, and HAM56. Epithelial, endothelial, and muscle markers were negative in all areas of the tumors. There was diffuse immunoreactivity for factor XIII in most spindle cells. This suggests that this type of tumor is rich in cells showing histiocytic differentiation. Factor XIII is a transglutaminase that is expressed in dendrophages that are spindled and dendritic tissue histiocytes. These dendrophages are mesenchymal cells that appear to be involved in morphogenesis, inflammation, stromal remodeling, and tissue repair and are possibly found in fibrohistiocytic and fibrovascular tumors.[6]

In the first 19 cases described by Lane et al, the tumors were located deeply or superficially in the extremities.[1,2] They indicated that a myxoid background was present in some of the 19 tumors, and these resembled the cases of another recently described entity, low-grade fibromyxoid sarcoma.[7] However, low-grade fibromyxoid sarcomas lack the characteristic rosettes and the cells with a neural immunophenotype around the rosettes. Neither of our 2 cases showed a myxoid component. It appears that low-grade fibromyxoid sarcoma is a fibroblastic neoplasm in contrast to hyalinizing spindle cell tumor with giant rosettes whose spindle cells are composed of a mixture of histiocytes and fibroblasts. The latter tumor expresses factor XIIIa, CD68, and HAM56, and the former lacks these markers but expresses only vimentin.

In a letter to the editor, Magro et al[8] described a patient with multiple lung nodules that showed identical histologic features to those presented herein and in the paper by Lane et al.[2] There was no clinical evidence of a primary neoplasm outside the lung. Their case, however, showed negative results for S100, CD57, neuron-specific enolase, CD34, epithelial membrane antigen, lysozyme, pan-cytokeratin, desmin, or [Alpha]-smooth muscle actin. Weiss, in response to the letter, acknowledged that the pulmonary lesions appeared to be an acceptable case of the entity she described, although the presence of multiple intraparenchymal nodules is a feature that would immediately suggest metastatic disease.[9] After a 1-year follow-up, the patient was well, with no enlargement of the lung lesions on computed tomography examination.

Why these tumors display the characteristic biphasic appearance is unknown. It is not clear yet if the cells surrounding the rosettes represent neoplastic cells with an altered phenotype, indicating neural differentiation, or whether the cells represent an influx of 1 or more normal cell types such as histiocytes occurring in response to collagen deposits.[2] Our ultrastructural studies and double immunostaining partially answer these questions. First, there are dense core granules in the cytoplasm of the oval cells surrounding the rosettes, thus explaining their immunoreactivity for the neuroendocrine markers. Some of the granules had fine stippled substructures instead of dense cores. The fine, light particulate granules have been associated with endocrine products rather than neuroendocrine in the adrenal medulla and paragangliomas. This is an observation encountered in tissues that are fixed in glutaraldehyde and postfixed in osmium tetroxide.[4] These neuroendocrine cells appeared primitive with sparse RER and rudimentary intracellular junctions more consistent with a neoplastic origin than entrapment or influx of normal cells. We saw no granules in the spindle cells that had a morphologic structure and phenotype more in accord with being fibrohistiocytic. Second, the neuroendocrine rosette-forming cells are not histiocytes, because they do not stain simultaneously for HAM56 and CD57 or CD68 and CD57. Third, we interpret the presence of empty spaces within the rosettes as ghosts of cells that degenerated and disappeared within the collagenous overgrowth in those particular areas. Moreover, the deposits within the core of the rosettes appear not to be type IV collagen, since the immunohistochemical stains failed to stain them (although it is strongly positive among the stromal spindle cells) and electron microscopy showed features more consistent with type I collagen rather than type IV.

This report presents for the first time to our knowledge the karyotypic findings of a hyalinizing spindle cell tumor with giant rosettes. The specific pattern of acquired cytogenetic aberrations seen here has not been previously reported for any type of malignancy and the individual rearrangements are likewise unique.[l0] Each of the specific breakpoints, however, has been observed in rearrangements or other chromosomal imbalances in a variety of neoplasms. Chromosome band 1q25 has been seen in tumor necrosis factor genes.[11] Band 15q22 is the site of PML, a gene commonly rearranged in acute myelogenous leukemia[12] Band 20q13 is frequently overrepresented in colon and ovarian cancers, suggesting the presence of 1 or more tumor suppressor genes. Band 7q36 is commonly disrupted or deleted in myeloid neoplasias.[10] Band 16p13 is also rearranged with some frequency in myeloid neoplasias.[13]

Soft tissue tumors that may display giant rosettes include leiomyoma of deep soft tissues,[14] neurilemoma[15] malignant peripheral nerve sheath tumor,[16] and osteosarcomas.[17] However, they can be differentiated from hyalinizing spindle cell tumors with giant rosettes by their location and their immunohistochemical characteristics.

The short follow-up of our 2 cases precludes a statement on their behavior. However, our cases differ from the tumors described previously[2] in that ours lacked infiltration of surrounding tissues, supporting the short-term observation of their indolent behavior. An additional support for a nonaggressive outcome is the low proliferating index seen in the nuclei of the cells with Ki-67.

In summary, the study of these 2 new cases of hyalinizing spindle cell tumor with giant rosettes serves to increase the awareness of this distinct soft tissue tumor and to indicate that they are spindle cell neoplasms composed of dendritic, histiocytic, and fibroblastic cells admixed with cells that have neuroendocrine differentiation.

We are thankful to Dr Yuri Nikiforov for making us aware of the existence of one of the cases.

References

[1.] Lane KL, Shannon RJ, Weiss SW. Hyalinizing spindle cell tumor with giant rosettes: a distinctive soft tissue tumor mimicking fibromatosis [abstract]. Mod Pathol. 1996;9:9.

[2.] Lane KL., Shannon RJ, Weiss SW. Hyalinizing spindle cell tumor with giant rosettes: a distinctive tumor closely resembling low-grade fibromyxoid sarcoma. Am J Surg Pathol. 1997;21:1481-1488.

[3.] Sheng WW, Soukup S, Bove K, Gotwals B, Lampkin B. Chromosome analysis of 31 Wilm's tumors. Cancer Res. 1990;50:2786-2793.

[4.] Tischler AS. Paraganglia. In: Sternberg SS, ed. Histology for Pathologists. 2nd ed. Philadelphia, Pa: Lippincott-Raven; 1997:1161-1163.

[5.] Rode J, Dhillon AP, Doran JF, Jackson RJ, Thompson RJ. PGP9.5, a new marker for human neuroendocrine tumours. Histopathology. 1985;9:147-158.

[6.] Derrick EK, Barker JNWN, Khan A, Price ML, Macdonald DM. The tissue distribution of factor XIIIa positive cells. Histopathology. 1993;22:157-162.

[7.] Evans HL. Low-grade fibromyxoid sarcoma. Am J Surg Pathol. 1993;17:595-600.

[8.] Magro G, Fraggetta F, Manusia M, Mingrino A. Hyalinizing spindle cell tumor with giant rosettes: a previously undescribed lesion of the lung [letter to the editor]. Am J Surg Pathol. 1998;22:1431-1433.

[9.] Weiss SW. Hyalinizing spindle cell tumor with giant rosettes: a previously undescribed lesion of the lung [letter to the editor, author's reply]. Am J Surg Pathol. 1998;22:1433.

[10.] Mitelman F, ed. Catalog of Chromosome Aberrations in Cancer '98. New York, NY: Wiley Liss; 1998.

[11.] Gruss HJ, Dower SK. Tumor necrosis factor ligand superfamily: involvement in the pathology of malignant lymphomas. Blood. 1995;85:3378-3404.

[12.] Goy A, Passalaris T, Xiao YH, Miller WH Jr, Siegel DS, Zelenetz AD. The PML gene is linked to a megabase-scale insertion/deletion restriction fragment length polymorphism. Genomics. 1995;26:327-333.

[13.] Campbell LJ, Challis J, Fok T, Garson OM. Chromosome 16 abnormalities associated with myeloid malignancies. Genes Chromosomes Cancer. 1991;3: 55-61.

[14.] Kilpatrick SE, Mentzel T, Fletcher CDM. Leiomyoma of deep soft tissue: clinicopathologic analysis of a series. Am J Surg Pathol. 1994;18:576-582.

[15.] Goldblum JR, Beals TF, Weiss SW. Neuroblastoma-like neurilemoma. Am J Surg Pathol. 1994;18:266-273.

[16.] Enzinger FM, Weiss SW. ,Soft Tissue Tumors. St Louis, Mo: Mosby; 1995.

[17.] Kim H, Park C, Lee YB, Jim SY, Ro JY, Ayala AG. Case report 643. Skeletal Radiol. 1990;19:609-612.

Accepted for publication February 4, 2000.

From the Department of Pathology, University of Miami School of Medicine, Miami, Fla (Dr Bejarano); Departments of Otolaryngology-Head and Neck Surgery (Drs Padhaya and Gluckman) and Pathology (Dr Smith), University of Cincinnati Medical Center, Cincinnati, Ohio, Human Genetics Laboratory, Children's Hospital, Cincinnati, Ohio; (Dr Blough); and Department of Pathology, Mercy Hospital, Hamilton, Ohio (Dr Devitt).

Reprints: Pablo A. Bejarano, MD, Department of Pathology, University of Miami School of Medicine, 1611 NW 12th Ave, East Tower, Room 2042, Miami, FL 33136.
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Author:Bejarano, Pablo A.; Padhya, Tapan A.; Smith, Roger; Blough, Ruthann; Devitt, James J.; Gluckman, Jac
Publication:Archives of Pathology & Laboratory Medicine
Date:Aug 1, 2000
Words:3883
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