Case Reports

Passive Seeding in Metanephric Adenoma A Review of Pseudometastatic Lesions in Perinephric Lymph Nodes

Gladell P. Paner, MD; Thomas M. Turk, MD; Joseph I. Clark, MD; Valerie Lindgren, PhD; Maria M. Picken, MD, PhD

● Lymph node involvement derived from a discrete neo- longs to the spectrum of putatively nephrogenic rest-de- plastic process fundamentally implies tumor malignancy. rived tumors, which also include Wilms tumor (WT), However, rarely, inconsequential passive transport of be- metanephric adenofibroma (MAF), and metanephric stro- nign neoplastic cells to the lymph node can occur and may mal tumor.1–3 Although WT, or nephroblastoma, is thought cause confusion as to the nature of the neoplasm (ie, ma- to represent the malignant end of this spectrum, the other lignant vs benign). We describe a 10-cm right renal meta- metanephric neoplasms are generally regarded as benign, nephric adenoma incidentally discovered in a 30-year-old and thus far, only a few reports have suggested that a woman during cesarean section for a triplet pregnancy. small subset of these tumors can have atypical histologic Subsequent nephrectomy following an equivocal needle bi- features and behavior.3–6 Recently,acaseofMAina7- opsy diagnosis showed histologic features classic for meta- year-old child was reported with lymph node involvement nephric adenoma, including the lack of cytologic atypia that was interpreted as metastasis.7 and mitoses. Necrosis present in this lesion appeared to be Some cells indigenous to the lymph node could be mis- secondary to tumor physical disruption. The tumor cells taken for metastatic carcinoma, such as lymphoid follicles were positive for Wilms tumor 1 (WT1) antigen, pankera- or germinal centers protruding into sinuses, histiocytic tin, and CD57, focally positive for epithelial membrane an- granulomas, thick endothelial cells of postcapillary ve- tigen, and negative for cytokeratin 7, cytokeratin 34␤E12, nules, and rarely, nodal megakaryocytes.8 Moreover, be- and CD56. Electron microscopy confirmed the tumor’s ep- nign cellular inclusions not native to the lymph node, such ithelial nature, and cytogenetics revealed a diploid 46XX as epithelial and hyaline or Tamm-Horsfall protein (THP)– karyotype. The tumor proliferation index with Ki-67 was associated epithelial inclusions, mesothelial inclusion cysts only 3% to 5% and the proliferating cell nuclear antigen (MICs), and rarely, mature squamous cells, have been de- index was 0%. A single, concurrently resected hilar lymph scribed in the perinephric lymph nodes of pediatric renal node contained scattered subcapsular, sinusoidal, and fo- patients from the National Wilms Tumor Study.8 The be- cally intralymphovascular psammoma bodies along with nign MICs, which are small cysts lined by a serous (mu¨l- occasional adherent epithelial cells. These cells were high- lerian)–type epithelium, have long been recognized in the lighted by pankeratin but were nonreactive to WT1 anti- abdominal and pelvic lymph nodes of female patients gen, similar to the nonviable cells in the primary tumor. with gynecologic tumors.9 Clinical surveillance and follow-up showed no disease re- Herein, we describe an MA in a woman with multiple currence 4 years after nephrectomy. We postulate that the psammoma body–associated epithelial cells in the peri- lymph node inclusions found in this case represent passive nephric lymph node. Diagnosis of the primary kidney tu- transport of neoplastic cells to the lymph node following mor was supported by ancillary studies, including im- manipulation of the renal mass. We conclude that this phe- munohistochemical, cytogenetic, and electron microscopic nomenon is understudied and underrecognized and can studies. easily be mistaken for metastasis. (Arch Pathol Lab Med. 2005;129:1317–1321) REPORT OF A CASE A 30-year-old woman with a triplet pregnancy at 33 weeks of etanephric adenoma (MA) is an uncommon renal ep- gestation was admitted to Loyola University Medical Center fol- ithelial neoplasm of primitive appearance that be- lowing the premature rupture of membranes. She had an uncom- M plicated prenatal course and class D diabetes mellitus with a 23- year history of insulin use. There was no prior diagnosis of ma- lignancy, and her family history was unremarkable. She had no Accepted for publication May 31, 2005. history of blood polycythemia. Laboratory examination showed From the Departments of Pathology (Drs Paner, Lindgren, and Pick- mild leukocytosis with a white blood cell count of 11 900/␮L en), Urology (Dr Turk), and Medicine (Dr Clark), Loyola University ␮ Medical Center, Maywood, Ill. Dr Paner is now with the Department (reference range, 4000–10 000/ L); the rest of the complete blood of Pathology, Emory University, Atlanta, Ga. Dr Lindgren is now with cell count findings were normal. The patient’s other laboratory the Department of Pathology, University of Illinois, Chicago. findings were as follows: glucose, 184 mg/dL (reference range, The authors have no relevant financial interest in the products or 70–110 mg/dL) (10.21 mmol/L [reference range, 3.89–6.11 companies described in this article. mmol/L]); blood urea nitrogen, 19 mg/dL (reference range, 7– Reprints: Maria M. Picken, MD, PhD, Department of Pathology, Loy- 22 mg/dL) (6.78 mmol/L [reference range, 2.50–7.85]); and cre- ola University Medical Center, 2160 S First Ave, Bldg 110, Room 2242, atinine, 0.9 mg/dL (reference range, 0.7–1.5 mg/dL) (79.56 Maywood, IL 60153 (e-mail: [email protected]). ␮mol/L [reference range, 61.88–132.60 ␮mol/L]). A primary, low Arch Pathol Lab Med—Vol 129, October 2005 Passive Seeding in Metanephric Adenoma—Paner et al 1317 Figure 1. Metanephric adenoma. A, The metanephric adenoma cells form papillary structures and tubuloacinar clusters in an eosinophilic acellular stroma (hematoxylin-eosin, original magnification ϫ200). B, There are wide areas of necrosis associated with granulation tissue formation (he- matoxylin-eosin, original magnification ϫ40). C, An abortive glomerular structure composed of monomorphic metanephric adenoma cells with absent mitosis (hematoxylin-eosin, original magnification ϫ400). D, There is strong diffuse nuclear expression of Wilms tumor 1 (WT1) by the viable tumor cells, and the necrotic tumor ghost cells are showing no immunoreactivity (WT1, original magnifications ϫ200 and ϫ400 [inset]). E, An area showing moderate membranous expression of CD57 by the tumor cells (CD57, original magnification ϫ400). F, Ultrastructurally, the tumor cells are closely apposed, with intercellular junctions, focally present basement membrane, and occasional microvilli projecting into the lumina. transverse cesarean section with the patient under epidural an- (CK7; prediluted, K72, Cell Marque, Hot Springs, Ark), esthesia was performed, and initially the postpartum recovery CK34␤E12 (prediluted, Cell Marque), epithelial membrane anti- was uncomplicated. However, 4 days after the pregnancy delivery gen (EMA; prediluted, Mc5, Zymed, San Francisco, Calif), vi- procedure, the patient complained of dysuria followed by a spik- mentin (prediluted, 3B4, Ventana), WT1 (1:100, 6F-H2, Dako- ing fever. Urine culture test results were positive for Escherichia Cytomation, Carpinteria, Calif), CD56 or neural cell adhesion coli, and she was treated with an antibiotic regimen. Two days molecule (1:100, 123C3, Zymed), CD57 (prediluted, NK1, Cell later, she complained of right flank pain, and subsequent ultra- Marque), estrogen receptor (prediluted, 6F11, Ventana), proges- sound revealed a large mass that measured approximately 10 cm terone receptor (prediluted, 1A6, Zymed), proliferating cell nu- in diameter located at the midlower pole of the right kidney. clear antigen (1:20, PC10, Dako), and Ki-67 (prediluted, 7B11, Scattered calcifications within the renal mass with high attenua- Zymed). An electron microscopic study was performed as pre- tion were seen on computed tomography (CT). A CT-guided fine- viously described.6 For cytogenetic analysis, a fresh sample from needle aspiration (FNAB) biopsy specimen was suggestive of the tumor was disaggregated with collagenase (Sigma-Aldrich MA, but a low-grade papillary renal cell carcinoma (PRCC) could Co, St Louis, Mo), physically disrupted, and put into culture with not be ruled out. The results of subsequent radiologic surveys for Eagle minimal essential medium. Harvesting and staining fol- metastatic lesions were negative. Based on the equivocal FNAB lowed standard cytogenetic techniques. A total of 20 tumor cells diagnosis, a right radical nephrectomy was performed 6 weeks were examined. after the cesarean section and 1 week after the FNAB. During nephrectomy, an enlarged 2.5-cm hilar lymph node was noted, PATHOLOGIC FINDINGS which was also resected. The specimen submitted for pathologic examination was the entire right kidney, including the surround- The kidney had a bulging intraparenchymal mass lo- ing perinephric fat and Gerota fascia, attached proximal segment cated in the inferior renal pole. On sectioning, the mass of the ureter and hilar vessels, and the resected hilar lymph node. was well defined and fairly circumscribed, measured 10 The patient tolerated the surgery well and had an unremarkable cm in diameter, and involved both the renal cortex and postoperative recovery. Subsequently, she underwent interleukin medulla. The cut surface was solid brown with foci of 2 therapy, which was also well tolerated. The patient is alive with hemorrhages and necrosis. The renal pelvis was not in- no clinical evidence of disease recurrence (regular radiological volved by the tumor. A stretched renal capsule covered survey) 48 months after the nephrectomy procedure. the portion of the mass that bulged into the perinephric MATERIALS AND METHODS fat. No gross infiltration of the perinephric fat outside the For light microscopic evaluation, tissue was fixed in 10% buff- capsule was seen. ered neutral formalin and paraffin sections were stained with Histologically, the tumor was not encapsulated but well hematoxylin-eosin. Immunohistochemistry was performed as demarcated from the uninvolved renal parenchyma. The previously described6 with the following antibodies: pankeratin tumor was cellular, and the neoplastic cells were arranged (prediluted, AE1/AE3, Ventana, Tucson, Ariz), cytokeratin 7 in tubulopapillary formations and acini (Figure 1, A). 1318 Arch Pathol Lab Med—Vol 129, October 2005 Passive Seeding in Metanephric Adenoma—Paner et al Figure 2. Lymph node involvement by metanephric adenoma. A, The psammoma bodies in the lymph node are scattered mostly in the subcapsular area and the sinuses (hematoxylin-eosin, original magnifications ϫ40 and ϫ200 [inset]). B, Only rarely are cells closely associated with the psammoma bodies identified by hematoxylin-eosin stain. Notice the nuclear groove in one of the cells (hematoxylin-eosin, original magnification ϫ400). C, Keratin stain highlights a cell cluster associated with a psammoma body (hematoxylin-eosin, original magnification ϫ400). D, A single larger cluster of psammoma bodies at the capsular areas, surrounded by lymphoplasmacytic infiltrate and fibrosis, lodge within a lymphovascular channel. This cluster disappeared on deeper cutting performed for immunohistochemical studies (hematoxylin-eosin, original magnifications ϫ40 and ϫ200 [inset]).

There were expanses of coagulative necrosis and hemor- mor cell nuclei to be diffusely positive with WT1 stain; rhage (Figure 1, B). The tumor cells were monotonous however, the nonviable ghost tumor cells in the area of and, usually, the tubular spaces and papillae were lined necrosis were nonreactive (Figure 1, D). There was cyto- by a single cell layer, although, occasionally, multiple cell plasmic reactivity of the tumor cells with pankeratin stain layers, a slight degree of cell crowding, and overlapping and varied (light to moderate) membranous reactivity to were seen. The acini were variably arranged, relatively CD57 (Figure 1, E) and focally (5%) with EMA stain. The dense to loosely scattered in some areas amid an inter- tumor cells were nonreactive for CK7, CK34␤E12, vimen- vening acellular light pink stroma. Occasionally, the small tin, CD56, estrogen receptor, and progesterone receptor tubules contained luminal papillary formations that re- stains. The proliferation index of the tumor was 3% to 5% sembled abortive glomerular structures (Figure 1, C). The by Ki-67 count and 0% by proliferating cell nuclear anti- tumor cells had a small amount of cytoplasm and were gen. Electron microscopic studies showed closely apposed round to ovoid and slightly irregular, with darkly staining tumor cells with intercellular junctions, focally present nuclei with even to open chromatin, as well as occasional basement membrane, and occasional microvilli projecting inclusions, an occasional nuclear groove, and inconspicu- into the lumina (Figure 1, F). Cytogenetic analysis re- ous nucleoli. Mitoses were virtually absent. Psammoma vealed a normal 46,XX karyotype. bodies were scattered within the tumor. A spindle cell The hilar lymph node contained scattered psammoma component was not appreciated, and no blastemal or dis- bodies singly and in small clusters (Figure 2, A). These tinct stromal components were present in the tumor. The psammoma bodies were distributed throughout the renal pelvis and ureter urothelium were not involved by lymph node and were more easily detectable in the sinus- the tumor and did not show any cytologic atypia. No es and subcapsular areas but never within the capsule. nephrogenic rests were identified in the adjacent benign There were epithelial cells associated with these psam- renal parenchyma. Immunohistochemistry showed the tu- moma bodies, but these were only rarely apparent by he- Arch Pathol Lab Med—Vol 129, October 2005 Passive Seeding in Metanephric Adenoma—Paner et al 1319 Summary of Various Inclusions Mimicking Metastases Reported in Perinephric Lymph Nodes* Morphologic Location in Reactive Concurrent Kidney Inclusions Putative Origin Features Lymph Node Immunostain Lesions Source, y THP-associated Benign renal tubular Small tubular ar- Subcapsular, sinus- Cytokeratin WT, cystic nephro- Weeks et al,8 inclusions cells rangement, es, intralym- ma, clear cell sar- 1990; sometimes single phatic† coma, congenital Zanetti,12 or irregular clus- mesoblastic ne- 1986 ter of cells em- phroma, reflux ne- bedded in pro- phropathy tein matrix MICs Mu¨llerian derived Single of small tub- Connective tissue WT, cystic nephro- Weeks et al,8 ulelike structure septa ma 1990 lined by cuboi- dal cells Mature squamous Squamous metaplas- Mature squames Sinuses Cytokeratin WT Weeks et al,8 cells tic urothelial cells 1990 from renal calyces Passive seeding Nonviable MA cells Single or irregular Subcapsular, sinus- Cytokeratin MA Current case cluster of cells es, intralympho- associated with vascular pasammoma bodies * THP indicates Tamm-Horsfall protein; WT, Wilms tumor; MICs, mesothelial inclusion cysts; and MA, metanephric adenoma. † Lymphatic channel of renal sinus. matoxylin-eosin (Figure 2, B). Pankeratin staining high- is evolving and that rare malignant tumors have been re- lighted these cells that varied from 1 to 10 epithelial cell ported, such as MAF with carcinomatous foci,3 metaneph- clusters (Figure 2, C). The largest of these lymph nodal ric adenocarcinoma,4 mixed MA and PRCC,5 and meta- cell deposits, as measured in the pankeratin slide, was less nephric adenosarcoma.6 However, we strongly believe that than 0.1 mm in diameter. The lymph node paraffin block the current tumor represents an otherwise classic MA, was entirely sectioned and showed similar findings. In ad- which is a benign tumor, with unusual features such as dition, a single focus of a small collection of psammoma wide areas of necrosis within the tumor and the presence bodies with few epithelial cells was noted within a lym- of inclusions in a regional lymph node. We would like to phovascular space in the lymph node capsule (Figure 2, propose that both of these features may be secondary to D). This intralymphovascular cluster disappeared on the mechanical manipulation of the tumor as explained here- next subsequent level. Only stain for pankeratin was pos- in. itive in these psammoma body–associated cells; stains for Admittedly, the lymph node inclusions were small and CK7 and WT1 were negative. could have been easily missed if not for the presence of the more conspicuous psammoma bodies associated with COMMENT them. A summary of various previously reported inclu- The differential diagnosis for the presented tumor in- sions that mimic active metastases in perirenal lymph cludes MA, solid variant of PRCC, and the epithelial pre- nodes is presented in the Table. The differential diagnosis dominant WT.7,10 The morphologic overlap between MA of the current inclusions includes THP-associated epithe- and the basophilic type (type I) of PRCC has long been lial cells, MICs, or tumor cells that represent passive trans- recognized. Both these tumors feature tubulopapillary fer versus active metastases. In contrast to THP-associated structures and psammoma bodies. However, there are im- epithelial inclusions, in our case, no hyaline-like matrix munophenotypic and cytogenetic differences that aid in material was present. The presence of psammoma bodies, the differential diagnosis. Like the current tumor, MA is seen in our case, has never been reported to be associated positive for WT1 and is usually negative for CK7 and with these inclusions.8,12 The MICs are detected in 1% of EMA, although a focal expression of CK7 has been re- abdominal and pelvic lymph nodes of gynecologic pa- ported.2,3,11 In contrast, PRCC diffusely expresses CK7 and tients and mostly involve the lymph nodes along the usually EMA but is negative for WT1.11 Cytogenetically, drainage route from the ovary.9 A small subset of MICs MA, like the current tumor, has a diploid karyotype, are bland-appearing metastases of serous borderline tu- whereas PRCC shows gains of several chromosomes, most mors of the ovary.9 The MICs were previously described notably of 7 and 17.2 The WT occurs predominantly in in regional lymph nodes of pediatric WT.8 Psammoma young children, although rare adult cases have been re- bodies can rarely be associated with the benign MICs.9 ported; in contrast, MA affects mostly adults (mean age, However, in contrast to the current nodal inclusion, MICs 41 years).1 Nephroblastoma is usually triphasic, with epi- are almost exclusively glandular in appearance and most thelial, blastemal, and stromal components present.10 commonly located in the intracapsular or subcapsular However, on rare occasions, a monophasic WT can occur, area and are rare in the intrafollicular zone of the lymph and when the epithelial component predominates, neph- node.9 Being derived from the mesothelial lining, MICs roblastoma may be difficult to distinguish morphological- are expected to be positive for the WT1 antigen antibody, ly from MA.10 The presence of cytologic atypia, mitoses, thus making the differential diagnosis based on immu- and anaplastic foci favors the diagnosis of WT, features nophenotypic expression challenging. that were not present in the current tumor. The phenomenon of passive seeding of both tumor and We recognize that the spectrum of metanephric tumors benign, nonneoplastic epithelial cells into the regional 1320 Arch Pathol Lab Med—Vol 129, October 2005 Passive Seeding in Metanephric Adenoma—Paner et al lymph nodes has long been recognized in various areas review of this tumor, by the same group of authors, em- of pathology, such as breast, gastrointestinal, and gyne- phasized the morphologic atypicality brought about by the cologic pathology.13 In urologic laparoscopy, tumor dis- encapsulation of the ‘‘primary’’ tumor, which would favor semination was reported following nephroureterectomy an epithelial predominant WT, a valid argument consid- and nephrectomy for transitional cell carcinoma and fol- ering the young age of the patient.3 It would be interesting lowing adrenalectomies and retroperitoneal and pelvic to see a follow-up of this case published, possibly with lymph node dissections.14 With other types of lymph node additional immunostains, emphasizing the differential di- inclusions ruled out, we believed that in the current case, agnosis. lymph node epithelial inclusion resulted from a similar In conclusion, we present a case of MA in an adult pa- phenomenon (ie, passive seeding of the renal tumor). This tient characterized by what we believe represents a passive hypothesis is based on the following grounds. First, the mechanical seeding of tumor cells into the paranephric tumor compression by the triplet pregnancy and physical lymph node consequent to preresection physical distur- disturbance brought about by the cesarean section and bance of the main necrotic kidney tumor and mimicking a preresection FNAB may have caused break-up and seed- true metastatic process. Awareness of this phenomenon is ing of the tumor cells. Second, the expanses of necrosis in important, because it may cause critical diagnostic confu- MA made the nonviable tumor cells less resistant to dis- sion that may affect diagnosis and staging of benign neo- lodgement by agitation. These factors may have led to pas- plasms with malignant mimicry. sive embolic transport of tumor cells into the lymphatic The authors are grateful to John N. Eble, MD, MBA, for his channels, some of which may have settled in the hilar expert opinion regarding this case. lymph node as scattered minute deposits. Although the References psammoma bodies could have traveled with the dislodged 1. Davis CJ, Barton JH, Sesterhenn IA, Mostofi FK. Metanephric adenoma: clin- cells, some calcifications may have formed in the lym- icopathological study of fifty patients. Am J Surg Pathol. 1995;19:1101–1114. 2. Jones EC, Pins M, Dickersin GR, Young RH. Metanephric adenoma of the phatic channels around nonviable cells that served as a kidney: a clinicopathological, immunohistochemical, flow cytometric, cytoge- nidus (as suggested in papillary carcinomas of the thy- netic, and electron microscopic study of seven cases. Am J Surg Pathol. 1995;19: roid).15 Interestingly, although the inclusion cells in the 615–626. 3. Arroyo MR, Green DM, Perlman EJ, Beckwith JB, Argani P. The spectrum of lymph nodes stained for pankeratin, they did not stain for metanephric adenofibroma and related lesions: clinicopathologic study of 25 cas- CK7 or WT1 antigen. We believe that the lack of WT1 stain es from the National Wilms Tumor Study Group Pathology Center. Am J Surg may have been secondary to necrosis. Although keratin, Pathol. 2001;25:433–444. 4. Pins MR, Jones EC, Martul EV, Kamat BR, Umlas S, Renshaw Al. Meta- which is a structural protein (unlike the WT1 antigen) can nephric adenoma-like tumors of the kidney: report of 3 malignancies with em- frequently be detected in various ghost tumor cells, stain phasis on discriminating features. Arch Pathol Lab Med. 1999;123:415–420. 5. Drut R, Drut RM, Ortolani C. Metastatic metanephric adenoma with foci of for the other markers is usually negative in necrotic papillary carcinoma in a child. Int J Surg Pathol. 2001;9:241–247. 10,16 cells. Thus, in our opinion, the negativity to WT1 an- 6. Picken MM, Curry JL, Lindgren V, Clark JL, Eble JN. Metanephric adeno- tigen antibody does not argue against the tumor origin of sarcoma in a young adult: morphologic, immunophenotypic, ultrastructural, and fluorescence in situ hybridization analyses: a case report and review of the lit- the nodal inclusions. Rather, it corroborates our notion that erature. Am J Surg Pathol. 2001;25:1451–1457. the cells in the lymph node are not proliferating (as one 7. Renshaw AA, Freyer DR, Hammers YA. Metastatic metanephric adenoma would expect in actively metastasizing cells) but represent in a child. Am J Surg Pathol. 2000;24:570–574. 8. Weeks DA, Beckwith JB, Mierau GW. Benign nodal lesions mimicking me- dead or dying cells incapable of surviving outside the con- tastases from pediatric renal neoplasms: a report of the National Wilms’ Tumor fines of the main tumor. However, the presence of psam- Study Pathology Center. Hum Pathol. 1990;21:1239–1244. moma bodies in both the renal tumor and the nodal de- 9. Moore WF, Bentley RC, Berchuck A, Robboy SJ. Some mullerian inclusion cysts in the lymph nodes may sometimes be metastases from serous borderline posits underscores the similarity between these 2 lesions. tumors of the ovary. Am J Surg Pathol. 2000;24:710–718. We would like to recommend the exercise of caution in the 10. Argani P, Beckwith JB. Renal neoplasms of childhood. In: Mills SE, Carter interpretation of nodal inclusions as frank metastases and, D, Greenson JK, Oberman HA, Reuter V, Stoler MH. Sternberg’s Diagnostic Sur- gical Pathology. 4th ed. New York, NY: Lippincott Williams & Wilkins; 2004: consequently, of the associated tumor as malignant. 2001–2033. We did not consider the possibility that the primary re- 11. Muir TE, Cheville JC, Lager DJ. Metanephric adenoma, nephrogenic rests, nal tumor was malignant. There were no cytologic atypia and Wilm’s tumor: a histologic and immunophenotypic comparison. Am J Surg Pathol. 2001;25:1290–1296. or brisk mitoses observed in the metastasizing metaneph- 12. Zanetti G. Epithelial inclusions and Tamm-Horsfall protein in paranephric ric ‘‘adenocarcinoma’’ reported by Pins et al.4 The low tu- lymph nodes: a light microscopy and immunohistochemical study. Virchows Arch 1986;408:593–601. mor proliferation index in the current tumor also favors 13. Carter BA, Jensen RA, Simpson JF, Page DL. Benign transport of breast its benign nature. Finally, and most significantly, the ab- epithelium into axillary lymph nodes after biopsy. Am J Clin Pathol. 2000;113: sence of disease recurrence after 4 years of follow-up 259–265. 14. Micali S, Celia A, Bove P, et al. Tumor seeding in urological laparoscopy: strongly supports the contention that both the renal tumor an international study. J Urol. 2004;171:2151–2154. and the nodal epithelial inclusions were not biologically 15. LiVolsi VA. Surgical Pathology of the Thyroid. Philadelphia, Pa: WB Saun- malignant. The only other case of MA with concomitant ders Co; 1990. 16. Judkins AR, Montone KT, LiVolsi VA, van de Rijn M. Sensitivity and spec- nodal involvement, interpreted as metastases, was report- ificity of antibodies on necrotic tumor tissue. Am J Clin Pathol. 1998;110:641– ed by Renshaw et al.7 However, a subsequently published 646.

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