Choroid Plexus Carcinoma

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TABLE OF CONTENTS

[CLINICAL = FEATURES] [NEUROIMAG= ING]=20 [GROSS=20 PATHOLOGY] [HISTOPATH= OLOGY/=20 DIAGNOSIS] [DIFFERENT= IAL=20 DIAGNOSIS] [IMMUNOHIS= TOCHEMISTRY]=20 [GENETICS<= /A>]=20 [TREATMENT= /PROGNOSIS]=20 [CONCLUSI= ON]=20 [REFERENC= ES]=20 [TABLE= S] [FIGU= RES]

=A9=20 Copyright by College of American Pathologists 2008=20

Archives of Pathology and Laboratory = Medicine:=20 Vol. 132, No. 8, pp. 1350=961354.

Choroid Plexus Carcinoma

Purva Gopal, MD; John R. Parker, MD; Robert Debski, MD; = Joseph C.=20 Parker, Jr, MD

From the Department of Pathology and Laboratory Medicine (Dr = Gopal)=20 and the Department of Pathology and Laboratory Medicine, Division = of=20 Neuropathology (Drs J. R. Parker and J. C. Parker, Jr), University = of=20 Louisville, Louisville, Ky; and the Department of Pathology and = Laboratory=20 Medicine, Kosair Children's Hospital, Louisville, Ky (Dr=20 Debski)

Accepted January 10, 2008

Choroid plexus carcinoma is an uncommon neoplasm = of the=20 central nervous system most commonly found in the pediatric = population. It=20 is associated with a dismal prognosis, especially if incompletely = resected.=20 Accurate histopathologic diagnosis is imperative, and this neoplasm = should=20 always be included in the differential diagnosis of a papillary=20 intraventricular tumor. Histopathologic features include blurring of = papillary architecture, layers of neoplastic choroid plexus = epithelial cells=20 with pleomorphic nuclei, increased nuclear-to-cytoplasmic ratio, = increased=20 mitotic activity, areas of necrosis, and brain invasion. Current = accepted=20 treatment is gross total surgical resection of the tumor as the = goal. Use of=20 adjuvant chemotherapy is controversial at this time; however, it is=20 considered in some cases.

3D"" Choroid plexus tumors are uncommon neoplasms = derived from=20 choroid plexus epithelium and characterized by papillary and = intraventricular=20 growth. Within this family of tumors, there are benign and malignant = variants,=20 typically classified as choroid plexus papilloma (CPP) and choroid = plexus=20 carcinoma (CPC), respectively. Choroid plexus tumors account for = approximately=20 0.4% to 0.6% of all brain tumors.¹=20 Within the pediatric population, however, these neoplasms are more = common,=20 representing approximately 1% to 4% of all childhood brain tumors, with = 10% to=20 20% occurring during the first year of life.¹=20 Although reported in adults, 80% of CPCs occur in the pediatric = population, and=20 20% to 40% of all choroid plexus tumors in children are CPCs.¹

3D"" Choroid plexus carcinoma is a highly aggressive = malignant=20 tumor (World Health Organization [WHO] grade III) which must be = distinguished=20 from CPP (WHO grade I). Distinction between these entities is imperative = but can=20 be challenging, and it is generally based on increased necrosis, mitotic = activity, and change in growth pattern.²=20 According to some authors,^3,⁴=20 histologic features may have no correlation with biologic behavior in = that both=20 CPPs and CPCs have been associated with metastatic disease.⁵=20 The =93atypical choroid plexus papilloma=94 has been described as a = tumor with a few=20 histologic features of malignancy, but diagnostic criteria for this=20 classification are vague.

3D"" Current treatment strategy consists of gross total = surgical=20 resection for both CPP and CPC, with controversial use of adjuvant = chemotherapy=20 and radiotherapy for patients with CPC.³=20 Complete resection is difficult due to the high risk of intraoperative=20 hemorrhage; however, review of the literature supports complete surgical = resection as the major prognostic factor for patients with CPC.⁴

CLINICAL FEATURES Return=20 to TOC

3D"" Choroid plexus carcinoma is an uncommon, = aggressive,=20 malignant, central nervous system neoplasm that typically occurs in = children and=20 presents with the signs and symptoms of cerebrospinal fluid obstruction. = Within=20 the pediatric population, the median age is approximately 26 to 32 = months.¹=20 Choroid plexus carcinomas are believed to arise from the choroid plexus=20 epithelium. In general, they occur as follows: 50% lateral ventricles, = 40%=20 fourth ventricle, 5% third ventricle, and 5% multiple ventricular = involvement.^1,⁶=20 Although infrequent, CPCs can occur in the cerebellopontine angle near = the=20 foramina of Lushka, and extremely rare cases may present as a = suprasellar and/or=20 intraparenchymal mass.⁶⁼⁹⁶⁸

3D"" Choroid plexus carcinoma has been associated with = obstruction=20 of the cerebrospinal fluid pathways and, potentially, overproduction of=20 cerebrospinal fluid, leading to hydrocephalus and increased intracranial = pressure.⁶=20 An infant may present with hydrocephalus manifesting with increased head = circumference, and signs and symptoms of increased intracranial = pressure,=20 including delayed development, bulging fontanelles, separated sutures,=20 strabismus, or vomiting. An older child or adult can present with = features of=20 increased intracranial pressure, including vomiting, headache, = neurologic=20 deficits, seizures, lethargy, visual, and/or behavioral changes.

NEUROIMAGING Return=20 to TOC

3D"" Studies generally include computed tomography and/ = or magnetic=20 resonance imaging. These radiographic studies typically demonstrate a = large,=20 hyperdense, contrast-enhancing, intraventricular mass (Figure=20 1 3D"" ). The tumor is usually associated with hydrocephalus and = may=20 contain focal calcification and hemorrhage. The vascular nature of the = neoplasm=20 can be appreciated with multiple flow voids.⁶=20 Choroid plexus carcinoma may have metastases along the cerebrospinal = fluid=20 pathways, so imaging the entire neuraxis is important.

GROSS PATHOLOGY Return=20 to TOC

3D"" Choroid plexus carcinomas typically have a friable = papillary=20 or =93cauliflower-like=94 appearance. Intraoperatively, CPCs may be = loosely or=20 densely adherent to the ventricular wall and minimally or widely invade = the=20 adjacent brain parenchyma. On sectioning, the tumors display solid areas = intermixed with necrotic and hemorrhagic foci. Unlike CPCs, CPPs are = usually=20 well delineated from the underlying brain parenchyma and lack = necrosis.^1,⁶

HISTOPATHOLOGY/ DIAGNOSIS Return=20 to TOC

3D"" Choroid plexus papilloma is characterized as a WHO = grade I=20 neoplasm, and it is histologically described as a benign tumor with a = papillary=20 configuration consisting of delicate fibrovascular cores lined by a = single layer=20 of cuboidal to columnar epithelium. The epithelial cytoplasm is abundant = and=20 eosinophilic, and the tumor nuclei are basal, monomorphic, and round to = oval.=20 The difference between CPP and normal choroid plexus resides in the = crowding and=20 elongation of cells in the papilloma. There is no invasion or necrosis, = and=20 mitotic activity should be rare. When a CPP has some limited malignant = features,=20 the diagnosis =93atypical choroid plexus papilloma=94 is appropriate; = however,=20 distinctive criteria for diagnosis are not established.¹=20 A 2006 study by Jeibmann et al⁹=20 examined a series of 164 choroid plexus tumors for the presence of = atypical=20 features and correlated these features with prognosis in an effort to = create=20 criteria for the diagnosis of atypical CPP. They showed that mitotic = activity is=20 the only feature that impacted the probability of recurrence in patients = diagnosed with CPP. The group proposed that a mitotic count greater than = or=20 equal to 2 per 10 high-power fields could define a choroid plexus tumor = as=20 atypical, and the same study suggested that if at least two of the = following=20 histologic features are seen, including increased cellularity, nuclear=20 pleomorphism, solid growth pattern, and/or necrosis, a diagnosis of = atypical CPP=20 would be warranted.⁹=20 Using these criteria, the study examined a series of 124 previously = diagnosed=20 CPPs, and 15% of these were atypical CPPs.⁹=20 Malignant evolution of a CPP which recurred as CPC has been reported in = two=20 patients,³=20 but documented transition from benign to malignant histology is = extremely=20 rare.¹⁰

3D"" In comparison with the papilloma, the diagnosis of = CPC is=20 rendered in the setting of increased cell density, increased mitotic = figures=20 (usually greater than 5 per 10 high-power fields), nuclear pleomorphism = (Figure=20 2 3D"" ), and necrosis (Figure=20 3 3D"" ). Diffuse invasion of the adjacent brain parenchyma is = often=20 present (Figure=20 4 3D"" ). While distinct papillary configuration is a hallmark = of=20 low-grade CPP, in CPC the papillary features are blurred or can be lost = in the=20 sheets of epithelial tumor cells, and this ill-defined growth pattern = can make=20 diagnosis challenging.^3,¹⁰=20 Proliferation indices, such as Ki-67/MIB-1 (Figure=20 5 3D"" ) can be useful in the diagnosis of CPC, with reported = mean nuclear=20 labeling rates of 1.9% for CPP and 13.8% in CPC. Choroid plexus = carcinoma is=20 classified as a WHO grade III tumor.¹

DIFFERENTIAL DIAGNOSIS Return=20 to TOC

3D"" An expansive differential diagnosis can be created = in the=20 clinical setting of an intraventricular papillary tumor. Within the = choroid=20 plexus, in addition to CPC and CPP, another consideration is villous = hypertrophy=20 of the choroid plexus, which is a benign proliferation causing = enlargement of=20 the choroid plexus in the lateral ventricles. Microscopically, these = lesions=20 have normal choroid plexus histology¹=20 and can also be distinguished from a neoplastic lesion using = proliferation=20 markers.¹¹=20 Ependymoma, particularly the papillary variant, is an additional = consideration;=20 however, characteristic cytologic and morphologic features on histologic = examination, especially in a well-differentiated ependymoma, should be = present.=20 These features include monomorphic cuboidal cells with a flattened = surface,⁶=20 micronucleoli, stippled chromatin, ependymal rosettes, and the presence = of=20 perivascular pseudorosettes consisting of tapered cell processes = oriented toward=20 a central blood vessel.¹²=20 Papillary meningioma, a rare high-grade (WHO grade III) variant of = meningioma,=20 can arise in the choroid plexus, especially in patients in the pediatric = age=20 group.^12,¹³=20 This tumor is described histologically as having a pseudopapillary or=20 perivascular pattern in part of the tumor, which makes this meningioma a = WHO=20 grade III neoplasm. In infants, some embryonal-type (primitive = neuroectodermal)=20 tumors can occur in the same area. Of these, specific attention should = be given=20 to atypical teratoid/rhabdoid tumor (AT/RT), due to its aggressive = nature.=20 Histologically, AT/RT usually has groups of rhabdoid cells with = eccentric,=20 pleomorphic nuclei, and abundant eosinophilic cytoplasm. These tumors = are high=20 grade, with increased mitoses and necrosis. Atypical teratoid/rhabdoid = tumor can=20 be somewhat challenging to distinguish from CPCs that are poorly = differentiated=20 with foci of epithelial differentiation. Immunohistochemical staining = can be=20 useful in distinguishing between the two tumors, and it will be = discussed in=20 further detail below. Finally, metastatic neoplasms to the choroid = plexus,=20 especially in the adult population, are possible. The reported incidence = of=20 solitary metastases to the choroid plexus with no evidence of tumor in = the brain=20 parenchyma is rare, accounting for 0.14% of all cerebral metastases, the = most=20 common in adults being renal cell carcinoma.^14,¹⁵

IMMUNOHISTOCHEMISTRY Return=20 to TOC

3D"" Choroid plexus carcinomas typically stain positive = for=20 cytokeratins, and display variable expression of vimentin, S100, = transthyretin,=20 and glial fibrillary acidic protein (GFAP) (Figure=20 6 3D"" ). Positivity for S100 and transthyretin is typically = less than=20 that seen in CPP. Choroid plexus carcinomas stain positive for GFAP in=20 approximately 20% of tumors, and they can express carcinoembryonic = antigen.^1,¹⁰=20 Choroid plexus carcinomas are typically negative for epithelial membrane = antigen.

3D"" The staining characteristics of CPC are somewhat = inconsistent=20 in that the commonly used markers lack specificity.^16=9618=20 Hasselblatt et al²=20 recently described a microarray-based approach to identify new = diagnostic=20 markers for CPC. Antibodies directed against stanniocalcin 1, a = glycoprotein=20 found in choroid plexus, and Kir 7.1, a choroid plexus apical epithelial = protein=20 thought to be involved in transepithelial potassium transport, were = found to be=20 specifically expressed in CPC and CPP, and could further assist in the = diagnosis=20 of these neoplasms.²

3D"" Furthermore, in 2006, Judkins et al¹⁹=20 developed an immunohistochemical stain using the BAF47 clone of INI1 = antigen.=20 INI1 is a tumor suppressor gene that can be deleted and/or = mutated in=20 AT/RT. The group compared INI1 staining in CPC and AT/RT and found that = most=20 CPCs (21/28) stained positively for INI1, whereas the majority of AT/RTs = did not=20 stain. This immunostain could potentially assist in distinguishing = between a=20 poorly differentiated CPC and an AT/RT with extensive epithelial = differentiation=20 (Table=20 3D"" ).

GENETICS Return=20 to TOC

3D"" Choroid plexus carcinoma has been described in = association=20 with Li-Fraumeni syndrome in families that carry TP53 germline = mutations.=20 The TP53 gene is located on chromosome 17p13.1 and encodes the = tumor=20 suppressor protein p53. A mutation of this gene causes loss of p53 = function and=20 prolongs the half-life of this protein. Appropriately, = immunohistochemical=20 staining for p53 can be increased in this setting.²⁰=20 According to a 2002 study by Carlotti et al,²¹=20 positive nuclear staining for p53 was found in 10 of 11 CPCs, whereas = only 1 of=20 12 CPPs stained positively. Also in 2002, 5 new families of pediatric = patients=20 with CPC were identified with TP53 mutations. This strengthens = the=20 previous belief that CPC could be used as an indicator of a germline = TP53=20 mutation, especially in the setting of a family history of cancer.²²=20 Somatic TP53 mutations and spontaneous germline mutations have = also been=20 identified in some CPCs.²³=20 The presence of this genetic defect is believed to have important = implications=20 in the prevention and treatment of cancers in affected families.²¹

3D"" Comparative genomic hybridization has demonstrated = the=20 following common chromosomal additions and deletions in CPCs: +12p, = +12q, and=20 +20p (60%); +1, +4q, and +20q (53%); +4p (47%); +8q and +14q (40%); +7q, = +9p,=20 and +21 (33%); −22q (73%); −5q (40%); and −5p and = −18q (33%).^22,²³=20 A study by Rickert et al²⁴=20 also examined the behavior of CPCs with certain chromosomal additions = and=20 deletions and concluded that tumors with a gain of 9p and loss of 10q = were=20 associated with significantly longer survival.

TREATMENT/PROGNOSIS Return=20 to TOC

3D"" Choroid plexus carcinomas usually grow rapidly and = have a=20 5-year survival rate of approximately 40%. Two thirds of these tumors=20 disseminate throughout the cerebrospinal fluid pathway, and malignant = cells may=20 be present in cerebrospinal fluid prior to resection. Systemic = metastases may be=20 seen in patients with longer survival.¹⁰=20 There is currently no established protocol for the treatment of CPC; = however,=20 complete resection of the tumor is the primary goal. Gross total = resection=20 allows for the best chance of survival and improves the overall = prognosis,^4,²⁵=20 but complete resection is achieved in only 40% to 50% of children with = CPC.^26,²⁷=20 The prognosis of CPC is grave if not totally resected. Complete = resection of=20 this neoplasm is associated with high morbidity due to such factors as = patient=20 age, widespread tumor dissemination, and tumor vascularity, which puts = patients=20 at increased risk for intraoperative hemorrhage. The use of neoadjuvant=20 chemotherapy to reduce tumor vascularity prior to surgery has been = reported²⁸;=20 however, this has not been accepted as a standard approach. Adjuvant=20 chemotherapy after surgery remains controversial.²⁹=20 Some studies have demonstrated a decrease in tumor recurrence with = adjuvant=20 chemotherapy, whereas others have not shown any benefit.³⁰=20 Although some studies have demonstrated the benefit of postsurgical = radiation=20 therapy, radiation is generally avoided in the pediatric population due = to=20 severe long-term sequelae. Radiation is considered in the treatment of = adult=20 patients with CPC.⁵

3D"" With incomplete resection of CPC, second surgery = may be=20 beneficial.⁴=20 One study of patients with CPC who had surgery was divided into = subgroups of=20 patients with completely resected tumors and incompletely resected = tumors.⁴=20 In those with incompletely resected tumors, 22.6% had a second surgery, = and=20 these patients had an increased 2-year survival of 69% compared with a = survival=20 of 30% for patients without second surgery.⁴

CONCLUSION Return=20 to TOC

3D"" Choroid plexus carcinoma is an uncommon tumor that = usually=20 occurs in the lateral and fourth ventricles. It is associated with a = poor=20 prognosis. While the median age of occurrence is 26 to 32 months, this = neoplasm=20 should be considered in the differential diagnoses of a papillary=20 intraventricular neoplasm, especially in children and less commonly in = adults.=20 Choroid plexus carcinoma is a WHO grade III tumor which is distinguished = histologically from CPP based on increased nuclear to cytoplasmic = ratios,=20 increased mitotic figures, nuclear pleomorphism, the presence of = necrosis, and=20 distortion or blurring of the papillary structure of CPP by sheets of = cells in=20 the malignant counterpart. Immunohistochemical stains, while not = entirely=20 specific, can be useful in the diagnosis of CPC. Molecular studies = including=20 microarray analysis of CPC have identified other markers that may be = useful in=20 its diagnosis. CPC has been associated with Li-Fraumeni syndrome, and = five=20 additional families with children with CPC and the TP53 mutation = were=20 recently identified, suggesting that the presence of CPC in a family = could be=20 used as an indicator of a germline TP53 mutation. The current = accepted=20 treatment for CPC is surgical excision with controversial use of = adjuvant=20 chemotherapy. Although difficult due to the excessive vascularity of the = tumor,=20 gross total resection is the surgical goal, since this is associated = with the=20 most favorable prognosis.

Acknowledgments

We would like to thank Barbara K. Pawely, MD, of the Department of = Radiology=20 at Kosair Children's Hospital for providing the neuroimaging = studies.

References Return=20 to TOC

1. Paulus W, Brandner = S.=20 Choroid plexus tumours. In: Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, = eds.=20 WHO Classification of Tumours of the Central Nervous System. = Lyon,=20 France: IARC Press; 2007:81=9685.

2. Hasselblatt M, Bohm C, = Tatenhorst L.=20 et al. Identification of novel diagnostic markers for choroid plexus = tumors, a=20 microarray-based approach. Am J Surg Pathol 2006;30:66=9674. =

3. Chow E, Reardon DA, Shah AB. = et al.=20 Pediatric choroid plexus neoplasms. Int J Radiat Oncol Biol Phys=20 1999;44:249=96254.

4. Wrede B,=20 Liu P, Ater J, Wolff JEA. Second surgery and the prognosis of choroid = plexus=20 carcinoma-results of a meta-analysis of individual cases. Anticancer = Res=20 2005;25:4429=964434.

5. Wolff=20 JEA, Sajedi M, Brant R, Coppes M, Egeler RM. Choroid plexus tumors. = Br J=20 Cancer 2002;87:1086=961091.

6. Rickert CH, Paulus W. Tumors = of the=20 choroid plexus. Microsc Res Tech 2001;52:104=96111.

7. Kimura M, Takayasu M, Suzuki = Y. et al.=20 Primary choroid plexus papilloma located in the suprasellar region: case = report.=20 Neurosurgery 1992;31:563=96566.

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13. Singh A, Vermani S, Sharma = S, Chand=20 K. Papillary meningioma: a rare but distinct variant of malignant = meningioma.=20 Diagn Pathol 2007;2:3

14. Al-Anazi A, Shannon P, = Guha A.=20 Solitary metastasis to the choroid plexus. J Neurosurg = 2000;92:506=20

15. Kohno M. = Solitary=20 metastasis to the choroid plexus of the lateral ventricle: report of = three cases=20 and a review of the literature. J Neurooncol 1996;27:47=9652. =

16. Coffin C, Wick M, Braun J. = et al.=20 Choroid plexus neoplasms: clinicopathologic and immunohistochemical = studies.=20 Am J Surg Pathol 1986;10:394=96404.

17. Paulus W, Brandner S. = Synaptophysin=20 in choroid plexus epithelial cells: no useful aid in differential = diagnosis=20 [letter]. J Neuropathol Exp Neurol 1999;58:1111=961112. =

18. Paulus W, Janisch W.=20 Clinicopathologic correlations in epithelial choroid plexus neoplasms: a = study=20 of 52 cases. Acta Neuropathol 1990;80:635=96641.

19. Judkins A, Burger P, = Hamilton R. et=20 al. INI1 expression distinguishes atypical teratoid/rhabdoid tumor from = choroid=20 plexus carcinoma. J Neuropathol Exp Neurol 2005;64:391=96397. =

20. Pollack IF, Finkelstein = SD, Woods J.=20 et al. Expression of p53 and prognosis in children with malignant = gliomas.=20 New Engl J Med 2002;346:420=96427.

21. Carlotti C, Salhia B, = Weitzman S. et=20 al. Evaluation of a proliferative index and cell cycle protein = expression in=20 choroid plexus tumors in children. Acta Neuropathol = 2002;103:1=9610.=20

22. Krutilkova V, = Trkova M,=20 Fleitz J. Identification of five new families strengthens the link = between=20 childhood choroid plexus carcinoma and germline TP53 mutations. Eur J = Cancer 2005;41:1597=961603.

23. Kamaly-Asi ID, Shams N, = Taylor MD.=20 Genetics of choroid plexus tumors. Neurosurg Focus 2006;20:1 =

24. Rickert C, Wiestler O, = Paulus W.=20 Chromosomal imbalances in choroid plexus tumors. Am J Pathol=20 2002;160:1105=961113.

25. Dickens D, Dothage J, = Heideman R,=20 Ballard E, Jubinsky P. Successful treatment of an unresectable choroid = plexus=20 carcinoma in a patient with Li-Fraumeni syndrome. J Pediatr Hematol = Oncol=20 2005;27:46=9649.

26. Packer R,=20 Perilongo G, Johnson D. et al. Choroid plexus carcinoma of childhood.=20 Cancer 1992;69:580=96585.

27. Pierga J, Kalifa C, = Terrier-Lacombe=20 MJ. et al. Carcinoma of the choroid plexus: a pediatric experience. = Med=20 Pediatr Oncol 1993;21:480=96487.

28. St. Clair S, Humphreys R, = Pillay P.=20 et al. Current management of choroid plexus carcinoma in children. = Pediatr=20 Neurosurg 1991;17:225=96233.

29. Berger C, Thiesse P, = Lelouch-Tubiana=20 A. et al. Choroid plexus carcinomas in childhood: clinical features and=20 prognostic factors. Neurosurgery 1998;42:470=96475.

30. Chow E, Jenkins JJ, Burger = PC. et=20 al. Malignant evolution of choroid plexus papilloma. Pediatr = Neurosurg=20 1999;31:127=96130.

Tables Return=20 to TOC

3D""=20 Immunohistochemical Staining of = Tumors in=20 Differential Diagnosis of Choroid Plexus Carcinoma=20 (CPC)*

Figures Return=20 to TOC

Click on thumbnail for full-sized = image.

3D""=20

3D"" Figure 1. 3D""=20 Magnetic resonance image demonstrating a large mass within = the right=20 lateral ventricle extending into the basal ganglia and laterally into = the right=20 temporoparietal region and occipital lobe in a 5-year-old boy with = choroid=20 plexus carcinoma.

3D"" Figure 2. 3D""=20 Choroid plexus carcinoma with nuclear pleomorphism and high = vascularity=20 (hematoxylin-eosin, original magnification =D7400).

3D"" Figure 3. 3D""=20 Choroid plexus carcinoma with areas of necrosis = (hematoxylin-eosin,=20 original magnification =D7100).

3D"" Figure 4. 3D""=20 Solid sheet of choroid plexus carcinoma invading adjacent = brain=20 parenchyma (hematoxylin-eosin, original magnification =D7100).

3D"" Figure 5. 3D""=20 Markedly increased MIB-1 nuclear labeling in choroid plexus = carcinoma=20 (original magnification =D7400).

3D"" Figure 6. 3D""=20 Positive cytokeratin (CAM 5.2) staining in choroid plexus = carcinoma=20 (original magnification =D7100)

The authors have no relevant financial interest in the = products or=20 companies described in this article.

Reprints: Joseph C. Parker, Jr, = MD,=20 Department of Pathology and Laboratory Medicine, University of = Louisville=20 Hospital, 530 S Jackson St, Room COF19, Louisville, KY 40202 (E-mail: jcpark01@gwise.louisville.e= du)

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