HUMAN PATHOLOGY
Volume 22, No. 10 (October
10. Cottrill CM, Davis D, McMillen M. et al: Anomalous left coronaq’ artery from the pulmonary artery: Sigt%carlce of associated intracardiac defects. J Am Coil Cardioi 6:237-242, 1985 11. Esterly JR. Oppenheimer EH: Some aspects of cardiac pathology in infancy and childhood. I. Neonatal myocardial necrosis. Bull Hopkins Hospital 119:191-199, 1966 12. Donnelly WH. Bucclarelli RL, Nelson KM: Ischemir papillatry muscle necrosis in stressed newborn infattts. J Pediatr 96:295-300. 1980
ADENOSQUAMOUS
CARCINOMA
DEIRDKE M. DEVANEY. MRCPK~H,
OF THE PROSTATE:
A 70-year-old man presented with obstructive urinary symptoms in March 1980. A transurethral prostatectomy was performed and 70 g of tissue was removed. Histologic examination of the tissue revealed a prostatic adenocarcinoma (Gleason grade 3) (Fig 1). The patient had stage B disease and was treated with stilbestrol. 1 mg daily for 9 years. In March 1988, a repeat transurethral resection of the prostate was performed due to recurrence of symptoms. Biopsy specimens showed adenocarcinoma and focal squamous metaplasia of prostatic ducts (Fig 2). Serum prostatic acid phosphatase was normal and diagnostic imaging was negative for skeletal or visceral metastases. Stilbestrol therapy was continued. The patient underwent another biopsy in September 1988 for persistent obstructive urinary symptoms; specimens showed adenosquamous carcinoma (Fig 3). Stilbestrol therapy was discontinued in February 1989 following another resection, which demonstrated persistence of adenosquamous carcinoma. AND
13. Anderson KA. Burtwk JA. Fenton LJ. et al: Idiopathic arterial calcihc:ttion ,,f itlfanry in rlewbom siblings with unusual light and electron microscopic martifestations. Arch Pathol Lab Med 109:X38-840. 1985 14. Emmanouilide~ CC. Moss A,J, Duffie ER, et al: Pulmonary arterial pressure charlges irr human newborn infants from birth to 3 days of age. J Pediatr 55:327-333. 1964 1.5.Levm DC, Fellows KE, Abl-ams I-1L: Hemodynamically significant primary ;mo!nalies 01.the ~OII~IIV at-tet-iea. Circulation 58:25-34. 1978
A CASE REPORT
ANTHONY DORMAN, MB, ANI)Mary IXADEK, MD
Mixed ty!es of carcinoma of the jnostote are rure. The majority of those described (22 cases) are examples of mixed adenocarcinoma and transitional cell carcinoma. Much more unusual is the mixed adenosquamous carcinoma, of which only three cases have been described. This report presents an additional case of the rare actenosquamous carcinoma of the prostate. It discusses the cliGc@athologic features and the possible histogenesis of this tumor and suggests a role for stilbestrol in its development. HUM P.STMX 22:10461050. Copyright 0 1991 by W.H. Saunders Contpay
MATERIALS
1991)
METHODS
Pathology Light microscopy. Routinely processed paraffin blocks and hematoxylin-eosin-stained sections were available for study. The tissue specimen from 1980 showed a prostatic adenocarcinema (Gleason grade 3) with no evidence of squamous dif-
ferentiation (Fig 1). The March 1988 biopsy specimen also showed adenocarcinoma (Gleason grade 4); however, in addition, squamous metaplasia of prostatic ducts was also seen (Fig 2). In the biopsy material from September 1988 and February 1989 there was histologic evidence of an adenosquamous carcinoma (Fig 3). Both components were distinct and separate and. although closely juxtaposed, there was no obvious transition. The bulk of tumor now consisted of well-differentiated squamous carcinoma and the glandular component showed poorly differentiated adenocarcinoma (Gleason grade 4).
Immunohistochemisty The adenocarcinomatous component was positive for prostatic specific antigen (PSA; Dakopatts), prostatic acid phosphatase (PAP; Dakopatts). and the cytokeratin markers AEl/AE3 (Hybritech), and was negative for epithelial membrane antigen (EMA; Dakopatts). The malignant squamous component was positive for EMA and AEl/AEJ but negative for PSA and PAP. Squamous metaplasia showed only cytokeratin (AEl/AE3) positivity.
Electron Microscopy For ultrastructural studies, selected tissue specimens from 1989 were recovered from a paraffin wax block and sections were examined in a Jeol 1200EX transmission electron microscope. Ultrastructurally, the malignant squamous component lacked tight junctions, desmosomes, and tonofibrils and showed microvilli lining the intercellular spaces. Mucus granules were not seen.
DNA Analysis Selected areas of adenocarcinoma and squamous cell carcinoma were extracted from 1980 and 1989 blocks, respectively. Five-micrometer sections were cut and stained with Feulgen and were examined by an image analyzer (Cell Analysis System CAS 100, Becton Dickinson). Cytospin preparations of 50-Km sections were examined by image analysis (Fig 4) and by an EPICS Profile Flow Cytometer (Coulter). Diploid peaks were seen in the adenocarcinomatous component (Fig 4, top) and the malignant squamous component (Fig 4. bottom) by both methods of DNA analysis. No aneuploid stem lines were identified.
From the Departrrtent of Histopathology, Beaumont Hospital, Dublin. Ireland. and The Royal College of Surgeons in Ireland, Dublin, Ireland. Accepted for publication December 4. 1990. Key wordr: adenosquamous carcinoma, prostate, squamous metaplasia, stilbestml. Address correspondence and reprint requests to Mary Leader, MD, Department of Pathology, Beaumont Hospital, Dublin 9. Republic of Ireland. Copyright 0 1991 by W.B. Saunders Company 0046-8177/91/2210-0014$5.00/O
1046
CASE STUDIES
FIGURE
1.
Infiltrating adenocarcinoma
of the prostate from the 1980 biopsy. (Hematoxylin-eosin
I)ISCIiSSIOI\I
Adenoscluamous carcinoma of the prostate is a rare neoplasm. A review of the literature revealed three well-documented cases.‘.” Bainhorough,” in a 1952 review of scluarnous melaplasia of the prostate following estrogen therapy, referred to a single case showing a transition from adenocarcinoma to sclu;~mous cell carcinoma, but further details are scanty. In the three well-documented cases,‘.” a tissue di&osis of adellocarc11IioIiia was Inade initially and treatment included Tither radiotllerapy OI- estrogen therapy. or both (Table 1). Estrogrn was given in cx)mhination with radiotherapy for 9 to 4 years in two of the three reported cases.‘, In our case. estrogen was administered for 9 vears. In all foiir cases. adeIIc,sqI;a*Ilous carcinoma of the pros-
stain; magnification
= 348.)
tale appeared aftei- a variable nuIIIt~~r OF \carh (-4 IO !I vc3rs). SquaInous metaplasia was seen 011ly in the crihc pi-esenied. All four cases wcrc siIIIilaI- in presentation IO conventional prostatic aderlo~ar~inorna in term5 of agv group attected. clinical presentation, and mode of spread of Iun101. Two of the previousI\ reported patients died after 1 years; the third patient was alive and well at a .5-nlonth follo~up. In our crIse. the patient was alive at 9 months follow-up. Serum prostatic acid phosphatase was normal in two casts and elrvatrtl in IWO cases. The histogenesis of this uriusual tuniot‘ is still a matter of speculation. Saito et al’ have suggested that the imniunoreactivity of both the glandular and squamous c~oinpon~nts foI prostatic acid phosphatase provides e\ it1enc.e that the quamous elements were derivrd from the ;IdeIIo(.al.(.itIOIrl.I. HoweveI.. Bennett and hdgerron” hvl)ottIc=+i/rd Ih;II the aderIc)-
1047
Volume 22, No. 10 (October 1991)
HUMAN PATHOLOGY
FIGURE 2.
TABLE 1.
Squamous metaplasia of prostatic ducts from the 1988 biopsy
Cases of Adenosquamous
C;IW No. 2: Bennett and Edgerton
Case No. 1 : Sail0 et al’ Original tissue Age at original diagnosis (yr) Radiotherapy Estrogen therapy Ckmotherapy Time between diagnosis of conventional adenocal-cinema to ASCP Clinical symptoms Stage of disease of AXP at presentation Srrmm prostatir acid phosphatasc Response to estrogen therap! Dmation of follow-up period aftcl diagnosis of .ASCP Abhreviarion:
AXE’. adenosquamous
Adenocarcinoma 66 + _ 4 yt Urinary frequency dysuria C: Nor~mal No estrogens 5 mo, died
carcinoma
Carcinoma of the Prostate
and
given
Case No. 3: Present
Adenocarcintrma 58 + 4 yr-
I\demr-ar2r:::li 77 + 2 yt _
!I Vf _
-4 yt
10 yr
8 yr
Bone pain
Obstructive prostatism and hone pain D”
Obstructive
Raised Inadequately 5 mo. alive
Normal Poor I) mu, alive
DL’ Raised Poet Diagnosis autopsy
of the prostate.
1048
made at
Case
Adenocarcinoma 70 _
administered
I3
prostatism
CASE STUDIES
FIGURE 3. (Left) Infiltrating squamous cell carcinoma biopsy. (Hernatoxylin-eosin stain; magnification ~312.)
from the 1988 biopsy. (Right) infiltrating adenocarcinoma
from the 1988
FIGURE 4. (Top) Histogram of DNA distribution by image analysis of a cytospin preparation derived from a 50-pm section from the areas of a paraffin block containing c’nly the 1980 adenocarcinoma. The inset (arrow) is a histogram of DNA distribution of 40 lymphocytes (control population) from the same paraffin block. Cell count is shown on the x axIs and DNA mass on the y axis of each histogram. No aneuploid stem line is identified. (Bottom) Histogram of DNA distribution by image analysis of a cytospin preparation derived from a 50.Km section from the areas of the 1988 paraffin block containing only squamous cell carcinoma. The inset (arrow) is a histogram of DNA distribution of 40 lymphocytes (control population) from the same paraffin block. As in the top panel, the cell count is shown on the x axis and the DNA mass on the y axis. Again, no aneuploid stem line is seen.
1049
HUMAN PATHOLOGY
Volume 22, No. 10 (October
ADDENDUM
squamous carcinoma may be a collision tumor and that the squamous component may have developed from squamous metaplasia following radiation or hormonal therapy. Moyana’ and Lager et al’ propose that the adenosquamous carcinoma of the prostate is derived from resident pluripotent stem cells capable of multidirectional differentiation. This report supports the existence of a pluripotent stem cell that, following appropriate stimuli (such as irradiation or estrogen therapy), alters its line of differentiation. The altered differentiation may account for the lack of expression of “normal” prostatic antigens (PAP and PSA) in the metaplastic and malignant squamous cells. The squamous component in this case, although appearing well differentiated by light microscopy, shows no specific ultrastructural features of either an adenocarcinoma or a squamous cell carcinoma. As an aneuploid peak was not identified in either malignant component by flow cytometry or image analysis, the presence of two separate tumors differentiating from a pluripotent stem cell is neither supported nor overruled.
Since this paper was accepted for publication, Wernert et al7 have described two cases of prostatic adenocarcinoma with a malignant squamous component occurring after estrogen treatment. They suggest that the basal cells of the prostatic gland, in which they have identified nuclear estrogen receptors, undergo squamous metaplasia in response to estrogen treatment, and suggest that this may be a precursor of the malignant squamous component. The authors thank Saundra Dalton for typing Acknowkdgmen~ the manuscript, and the Audio-Visual Department, Royal College of Surgeons in Ireland, for photographic assistance.
REFERENCES 1. Green LF, Mulcahy JJ, Warren MM, et al: Primary transitional cell carcinoma of the prostate. J Ural 110:235-237. 1973 2. Saito R. Davis BK, Ollapally EP: Adenosquamous carcinoma of the prostate. HUM PATHOI. 15:87-89, 1984 3. Lager DJ, Goeken JA. Kemp JD, et al: Squamous metaplasia (>f the prostate-An immunohistochemical study. Am J Clin Pathol 90:597-601. 1988 4. Bainborough AR: Squamous metaplasia uf prostate following oestrogell therapy. J Ural 68:329-336. 1952 5. Bennett RS. Edgerton EO: Mixed prostatic carcinoma. J L’rol I l&561563, 1973 6. Moyana TN: Adenosquamous carcinoma of the prostate. Am J Surg Pathol 11:403-407. 1987 7. Wernert N, Goebbels R, Bonkhoff H, et al: Squamous cell carcirloma of the prostate. Histopathology 17:339-344, 1990
CONCLUSION In conclusion, despite the common occurrence of mixed types of carcinomas in other sites such as the lung, adenosquamous carcinoma of the prostate is exceedingly rare with, including this report, only four documented cases in the world literature. Estrogen therapy, being administered in three cases, may be implicated in the development of these unusual mixed tumors.
GRANULOMATOUS AORTIC IN TAKAYASU AORTITIS LYNDA
RUSHING,
MD,
FREDERICK
From the Departments
VALVULITIS
of Pathology
ASSOCIATED
MD, PHD,
J. SCHOEN,
and Vascular
ALAN
Medicine,
Brigham and Women’s Hospital, Boston, MA; and the Department
of Pathology, Mayo Clinic Foundation, oublication December 10. 1990. *Present address: Cardiovascular
nesota, Minneapolis, MN.
Rochester,
MN. Accepted
for
Division, University of Min-
1991)
WITH
HIRSCH,*
AORTIC
MD,
INSUFFICIENCY
AND J. T. LIE,
MD
We report an unusual CUSPof Takayasu aortitis associated with a giant cell granulomatous ualvulitis presenting with aortic ins@ciency. Although nonspecific valuular abnormalities have been reported with Takayasu aortitis, this case is the first to describe inuolvemxnt of the aortir valve by the disease. HLL~PATHOI. 22: 10501053. Copyright 0 1991 by W. B. Saunders Company
Key words: aortitis,
valvulitis, Takayasu aortitis. Address correspondence and reprint requests to Frederick J. Schoen, MD, PhD, Department of Pathology, Brigham and Women’s
Hospital, 75 Francis St, Boston, MA 02115. Copyright 0 1991 by W.B. Saunders Company 0046-8177/91/2210-0015$5,00/O
Takayasu aortitis is an inflammatory vascular disease of uncertain etiology. Classically. this disorder affects young women, usually of Asian descent, diminished pulses, hypertension.
1050
who present with absent or or claudication.’ Other, less
Volume 22, No. 10 (October
10. Cottrill CM, Davis D, McMillen M. et al: Anomalous left coronaq’ artery from the pulmonary artery: Sigt%carlce of associated intracardiac defects. J Am Coil Cardioi 6:237-242, 1985 11. Esterly JR. Oppenheimer EH: Some aspects of cardiac pathology in infancy and childhood. I. Neonatal myocardial necrosis. Bull Hopkins Hospital 119:191-199, 1966 12. Donnelly WH. Bucclarelli RL, Nelson KM: Ischemir papillatry muscle necrosis in stressed newborn infattts. J Pediatr 96:295-300. 1980
ADENOSQUAMOUS
CARCINOMA
DEIRDKE M. DEVANEY. MRCPK~H,
OF THE PROSTATE:
A 70-year-old man presented with obstructive urinary symptoms in March 1980. A transurethral prostatectomy was performed and 70 g of tissue was removed. Histologic examination of the tissue revealed a prostatic adenocarcinoma (Gleason grade 3) (Fig 1). The patient had stage B disease and was treated with stilbestrol. 1 mg daily for 9 years. In March 1988, a repeat transurethral resection of the prostate was performed due to recurrence of symptoms. Biopsy specimens showed adenocarcinoma and focal squamous metaplasia of prostatic ducts (Fig 2). Serum prostatic acid phosphatase was normal and diagnostic imaging was negative for skeletal or visceral metastases. Stilbestrol therapy was continued. The patient underwent another biopsy in September 1988 for persistent obstructive urinary symptoms; specimens showed adenosquamous carcinoma (Fig 3). Stilbestrol therapy was discontinued in February 1989 following another resection, which demonstrated persistence of adenosquamous carcinoma. AND
13. Anderson KA. Burtwk JA. Fenton LJ. et al: Idiopathic arterial calcihc:ttion ,,f itlfanry in rlewbom siblings with unusual light and electron microscopic martifestations. Arch Pathol Lab Med 109:X38-840. 1985 14. Emmanouilide~ CC. Moss A,J, Duffie ER, et al: Pulmonary arterial pressure charlges irr human newborn infants from birth to 3 days of age. J Pediatr 55:327-333. 1964 1.5.Levm DC, Fellows KE, Abl-ams I-1L: Hemodynamically significant primary ;mo!nalies 01.the ~OII~IIV at-tet-iea. Circulation 58:25-34. 1978
A CASE REPORT
ANTHONY DORMAN, MB, ANI)Mary IXADEK, MD
Mixed ty!es of carcinoma of the jnostote are rure. The majority of those described (22 cases) are examples of mixed adenocarcinoma and transitional cell carcinoma. Much more unusual is the mixed adenosquamous carcinoma, of which only three cases have been described. This report presents an additional case of the rare actenosquamous carcinoma of the prostate. It discusses the cliGc@athologic features and the possible histogenesis of this tumor and suggests a role for stilbestrol in its development. HUM P.STMX 22:10461050. Copyright 0 1991 by W.H. Saunders Contpay
MATERIALS
1991)
METHODS
Pathology Light microscopy. Routinely processed paraffin blocks and hematoxylin-eosin-stained sections were available for study. The tissue specimen from 1980 showed a prostatic adenocarcinema (Gleason grade 3) with no evidence of squamous dif-
ferentiation (Fig 1). The March 1988 biopsy specimen also showed adenocarcinoma (Gleason grade 4); however, in addition, squamous metaplasia of prostatic ducts was also seen (Fig 2). In the biopsy material from September 1988 and February 1989 there was histologic evidence of an adenosquamous carcinoma (Fig 3). Both components were distinct and separate and. although closely juxtaposed, there was no obvious transition. The bulk of tumor now consisted of well-differentiated squamous carcinoma and the glandular component showed poorly differentiated adenocarcinoma (Gleason grade 4).
Immunohistochemisty The adenocarcinomatous component was positive for prostatic specific antigen (PSA; Dakopatts), prostatic acid phosphatase (PAP; Dakopatts). and the cytokeratin markers AEl/AE3 (Hybritech), and was negative for epithelial membrane antigen (EMA; Dakopatts). The malignant squamous component was positive for EMA and AEl/AEJ but negative for PSA and PAP. Squamous metaplasia showed only cytokeratin (AEl/AE3) positivity.
Electron Microscopy For ultrastructural studies, selected tissue specimens from 1989 were recovered from a paraffin wax block and sections were examined in a Jeol 1200EX transmission electron microscope. Ultrastructurally, the malignant squamous component lacked tight junctions, desmosomes, and tonofibrils and showed microvilli lining the intercellular spaces. Mucus granules were not seen.
DNA Analysis Selected areas of adenocarcinoma and squamous cell carcinoma were extracted from 1980 and 1989 blocks, respectively. Five-micrometer sections were cut and stained with Feulgen and were examined by an image analyzer (Cell Analysis System CAS 100, Becton Dickinson). Cytospin preparations of 50-Km sections were examined by image analysis (Fig 4) and by an EPICS Profile Flow Cytometer (Coulter). Diploid peaks were seen in the adenocarcinomatous component (Fig 4, top) and the malignant squamous component (Fig 4. bottom) by both methods of DNA analysis. No aneuploid stem lines were identified.
From the Departrrtent of Histopathology, Beaumont Hospital, Dublin. Ireland. and The Royal College of Surgeons in Ireland, Dublin, Ireland. Accepted for publication December 4. 1990. Key wordr: adenosquamous carcinoma, prostate, squamous metaplasia, stilbestml. Address correspondence and reprint requests to Mary Leader, MD, Department of Pathology, Beaumont Hospital, Dublin 9. Republic of Ireland. Copyright 0 1991 by W.B. Saunders Company 0046-8177/91/2210-0014$5.00/O
1046
CASE STUDIES
FIGURE
1.
Infiltrating adenocarcinoma
of the prostate from the 1980 biopsy. (Hematoxylin-eosin
I)ISCIiSSIOI\I
Adenoscluamous carcinoma of the prostate is a rare neoplasm. A review of the literature revealed three well-documented cases.‘.” Bainhorough,” in a 1952 review of scluarnous melaplasia of the prostate following estrogen therapy, referred to a single case showing a transition from adenocarcinoma to sclu;~mous cell carcinoma, but further details are scanty. In the three well-documented cases,‘.” a tissue di&osis of adellocarc11IioIiia was Inade initially and treatment included Tither radiotllerapy OI- estrogen therapy. or both (Table 1). Estrogrn was given in cx)mhination with radiotherapy for 9 to 4 years in two of the three reported cases.‘, In our case. estrogen was administered for 9 vears. In all foiir cases. adeIIc,sqI;a*Ilous carcinoma of the pros-
stain; magnification
= 348.)
tale appeared aftei- a variable nuIIIt~~r OF \carh (-4 IO !I vc3rs). SquaInous metaplasia was seen 011ly in the crihc pi-esenied. All four cases wcrc siIIIilaI- in presentation IO conventional prostatic aderlo~ar~inorna in term5 of agv group attected. clinical presentation, and mode of spread of Iun101. Two of the previousI\ reported patients died after 1 years; the third patient was alive and well at a .5-nlonth follo~up. In our crIse. the patient was alive at 9 months follow-up. Serum prostatic acid phosphatase was normal in two casts and elrvatrtl in IWO cases. The histogenesis of this uriusual tuniot‘ is still a matter of speculation. Saito et al’ have suggested that the imniunoreactivity of both the glandular and squamous c~oinpon~nts foI prostatic acid phosphatase provides e\ it1enc.e that the quamous elements were derivrd from the ;IdeIIo(.al.(.itIOIrl.I. HoweveI.. Bennett and hdgerron” hvl)ottIc=+i/rd Ih;II the aderIc)-
1047
Volume 22, No. 10 (October 1991)
HUMAN PATHOLOGY
FIGURE 2.
TABLE 1.
Squamous metaplasia of prostatic ducts from the 1988 biopsy
Cases of Adenosquamous
C;IW No. 2: Bennett and Edgerton
Case No. 1 : Sail0 et al’ Original tissue Age at original diagnosis (yr) Radiotherapy Estrogen therapy Ckmotherapy Time between diagnosis of conventional adenocal-cinema to ASCP Clinical symptoms Stage of disease of AXP at presentation Srrmm prostatir acid phosphatasc Response to estrogen therap! Dmation of follow-up period aftcl diagnosis of .ASCP Abhreviarion:
AXE’. adenosquamous
Adenocarcinoma 66 + _ 4 yt Urinary frequency dysuria C: Nor~mal No estrogens 5 mo, died
carcinoma
Carcinoma of the Prostate
and
given
Case No. 3: Present
Adenocarcintrma 58 + 4 yr-
I\demr-ar2r:::li 77 + 2 yt _
!I Vf _
-4 yt
10 yr
8 yr
Bone pain
Obstructive prostatism and hone pain D”
Obstructive
Raised Inadequately 5 mo. alive
Normal Poor I) mu, alive
DL’ Raised Poet Diagnosis autopsy
of the prostate.
1048
made at
Case
Adenocarcinoma 70 _
administered
I3
prostatism
CASE STUDIES
FIGURE 3. (Left) Infiltrating squamous cell carcinoma biopsy. (Hernatoxylin-eosin stain; magnification ~312.)
from the 1988 biopsy. (Right) infiltrating adenocarcinoma
from the 1988
FIGURE 4. (Top) Histogram of DNA distribution by image analysis of a cytospin preparation derived from a 50-pm section from the areas of a paraffin block containing c’nly the 1980 adenocarcinoma. The inset (arrow) is a histogram of DNA distribution of 40 lymphocytes (control population) from the same paraffin block. Cell count is shown on the x axIs and DNA mass on the y axis of each histogram. No aneuploid stem line is identified. (Bottom) Histogram of DNA distribution by image analysis of a cytospin preparation derived from a 50.Km section from the areas of the 1988 paraffin block containing only squamous cell carcinoma. The inset (arrow) is a histogram of DNA distribution of 40 lymphocytes (control population) from the same paraffin block. As in the top panel, the cell count is shown on the x axis and the DNA mass on the y axis. Again, no aneuploid stem line is seen.
1049
HUMAN PATHOLOGY
Volume 22, No. 10 (October
ADDENDUM
squamous carcinoma may be a collision tumor and that the squamous component may have developed from squamous metaplasia following radiation or hormonal therapy. Moyana’ and Lager et al’ propose that the adenosquamous carcinoma of the prostate is derived from resident pluripotent stem cells capable of multidirectional differentiation. This report supports the existence of a pluripotent stem cell that, following appropriate stimuli (such as irradiation or estrogen therapy), alters its line of differentiation. The altered differentiation may account for the lack of expression of “normal” prostatic antigens (PAP and PSA) in the metaplastic and malignant squamous cells. The squamous component in this case, although appearing well differentiated by light microscopy, shows no specific ultrastructural features of either an adenocarcinoma or a squamous cell carcinoma. As an aneuploid peak was not identified in either malignant component by flow cytometry or image analysis, the presence of two separate tumors differentiating from a pluripotent stem cell is neither supported nor overruled.
Since this paper was accepted for publication, Wernert et al7 have described two cases of prostatic adenocarcinoma with a malignant squamous component occurring after estrogen treatment. They suggest that the basal cells of the prostatic gland, in which they have identified nuclear estrogen receptors, undergo squamous metaplasia in response to estrogen treatment, and suggest that this may be a precursor of the malignant squamous component. The authors thank Saundra Dalton for typing Acknowkdgmen~ the manuscript, and the Audio-Visual Department, Royal College of Surgeons in Ireland, for photographic assistance.
REFERENCES 1. Green LF, Mulcahy JJ, Warren MM, et al: Primary transitional cell carcinoma of the prostate. J Ural 110:235-237. 1973 2. Saito R. Davis BK, Ollapally EP: Adenosquamous carcinoma of the prostate. HUM PATHOI. 15:87-89, 1984 3. Lager DJ, Goeken JA. Kemp JD, et al: Squamous metaplasia (>f the prostate-An immunohistochemical study. Am J Clin Pathol 90:597-601. 1988 4. Bainborough AR: Squamous metaplasia uf prostate following oestrogell therapy. J Ural 68:329-336. 1952 5. Bennett RS. Edgerton EO: Mixed prostatic carcinoma. J L’rol I l&561563, 1973 6. Moyana TN: Adenosquamous carcinoma of the prostate. Am J Surg Pathol 11:403-407. 1987 7. Wernert N, Goebbels R, Bonkhoff H, et al: Squamous cell carcirloma of the prostate. Histopathology 17:339-344, 1990
CONCLUSION In conclusion, despite the common occurrence of mixed types of carcinomas in other sites such as the lung, adenosquamous carcinoma of the prostate is exceedingly rare with, including this report, only four documented cases in the world literature. Estrogen therapy, being administered in three cases, may be implicated in the development of these unusual mixed tumors.
GRANULOMATOUS AORTIC IN TAKAYASU AORTITIS LYNDA
RUSHING,
MD,
FREDERICK
From the Departments
VALVULITIS
of Pathology
ASSOCIATED
MD, PHD,
J. SCHOEN,
and Vascular
ALAN
Medicine,
Brigham and Women’s Hospital, Boston, MA; and the Department
of Pathology, Mayo Clinic Foundation, oublication December 10. 1990. *Present address: Cardiovascular
nesota, Minneapolis, MN.
Rochester,
MN. Accepted
for
Division, University of Min-
1991)
WITH
HIRSCH,*
AORTIC
MD,
INSUFFICIENCY
AND J. T. LIE,
MD
We report an unusual CUSPof Takayasu aortitis associated with a giant cell granulomatous ualvulitis presenting with aortic ins@ciency. Although nonspecific valuular abnormalities have been reported with Takayasu aortitis, this case is the first to describe inuolvemxnt of the aortir valve by the disease. HLL~PATHOI. 22: 10501053. Copyright 0 1991 by W. B. Saunders Company
Key words: aortitis,
valvulitis, Takayasu aortitis. Address correspondence and reprint requests to Frederick J. Schoen, MD, PhD, Department of Pathology, Brigham and Women’s
Hospital, 75 Francis St, Boston, MA 02115. Copyright 0 1991 by W.B. Saunders Company 0046-8177/91/2210-0015$5,00/O
Takayasu aortitis is an inflammatory vascular disease of uncertain etiology. Classically. this disorder affects young women, usually of Asian descent, diminished pulses, hypertension.
1050
who present with absent or or claudication.’ Other, less
