TM

Volume 18 No.2Fall 20151-888-92-PHENO www.phenopath.com

PhenoPath’s highly trained and knowledgeable team is the key to our quality cytogenetics service. They continually evaluate PhenoPath’s assay performance and meet regularly with PhenoPath scientists and pathologists to ensure the highest quality service. If you would like more information about PhenoPath’s Cytogenetics service, please contact your sales representative or any of our pathologists (888.927.4366).

PhenoPath is proud to announce the one-year anniversary of our Cytogenetics Laboratory, providing reliable and reproducible karyotyping for our pathology and oncology clients nationwide. PhenoPath offers comprehensive chromosomal studies for all of the hematological malignancies, including acute leukemia, myeloproliferative neo-plasms (including chronic myeloid leukemia, CML), myelodysplastic syndromes (MDS), multiple myeloma, and lymphoma / chronic lymphop-roliferative disorders (including chronic lymphocytic leukemia/small lymphocytic lymphoma, CLL/SLL). PhenoPath also performs chromosomal studies on non-hematopoietic neoplasms. Testing can be performed on a variety of fresh specimens, listed below. To increase the sensitivity for detecting abnormalities, each specimen is uniquely cultured according to specimen type, clinical indication, and flow cytometric findings (if ap-plicable). The Cytogenetics Laboratory combines state-of-the-art cell preparation techniques with comprehensive interpretation of test results by experi-enced, board-certified cytogenetics experts. Karyotyping is aided by MetaSystems image analysis, which increases the ability to identify metaphases when the mitotic index is low. If indicated, FISH will be performed over standard Giemsa (G)-banded metaphase spreads to confirm karyotype results. Our laboratory, is accredited by the College of American Pathologists (CAP), has CLIA certification, and is licensed in the states of Wash-ington, Florida, California, Maryland, and Rhode Island.

Service Features• Specimens: heparin-anticoagulated peripheral blood or bone marrow aspirate; non-anticoagulated body fluid; bone marrow core biopsy

in RPMI/fetal bovine serum; finely minced lymph node, spleen or other tissue in RPMI/fetal bovine serum • Turnaround time for karyotyping to rule out hematopoietic neoplasms: 5 to 7 business days• Turnaround time for karyotyping to rule out non-hematopoietic neoplasms: 10 to 14 business days (due to more fastidious culture

requirements)• Culture success rates: > 95%• Minimum number of cells analyzed: 20 (if available)• Minimum target resolution: 350-400 bands (Giemsa banding)• Automated metaphase identification with MetaSystems scanning platform• Initial independent analysis by two cytogenetic technologists, plus an additional quality control step for each case• Final analysis and report verification by a board-certified cytogeneticist, with references to the literature as appropriate

Our Cytogenetics TeamDirector: Shawna Pyott, PhD Board certified in Cytogenetics by the American Board of Medical Genetics (ABMG), and a Fellow of the American College of Medical Genetics (FACMG)Cytogenetic technologists: Certified by the American Society of Clinical Pathologists (ASCP) Board of Certifica-tion (BOC) in cytogenetics (CG) or medical technology (MT); over 40 years of cumulative experienceTricia Makin, CG (ASCP)Ashlie Cindric, MT (ASCP)Ray ClemesKarishma Hendrickson, CG (ASCP) - per diemMelissa Chiu, CG (ASCP) Itu Mohapatra, CG (ASCP) (not pictured) - per diem

PhenoPath Cytogenetics - Here to serve your diagnostic needs

Shawna, Tricia, Ashlie, Ray, Karishma, Melissa

PD-L1PD-L1 (Programmed Death-Ligand 1), also known as CD274, is a 40 kDa type 1 transmembrane protein that has been speculated to play a major role in suppressing the immune system during particular events such as pregnancy, tissue allografts, autoimmune disease, and cancer. In the non-neoplastic setting, PD-L1 is expressed on activated T cells, B cells, dendritic cells and macrophages, in addition to some immune-privileged non-hematopoietic tissues such as retina and placenta. Binding of PD-L1 to its ligand PD-1, which is expressed by various immune cell types including T cells, transmits an inhibitory signal that attenuates T cell function, expansion, and survival.

More recently, it has been discovered that the neoplastic cells of many human tumors can express PD-L1, including breast, ovarian, gastric, pan-creatic, lung and renal cell carcinomas, and classical Hodgkin lymphoma (CHL). PD-L1 expression by tumor cells is thought to inhibit the local immune response to the tumor, at least in part by binding to T cell PD-1 and protecting the tumor from T-cell-mediated immunity.

Blockade of the PD-1/PD-L1 axis by humanized monoclonal antibodies against PD-1 and PD-L1 has emerged as a promising new cancer therapy. In recent clinical trials, anti-PD-1 therapy has been associated with significant clinical responses in patients with refractory non-hematopoietic tumors including melanoma, renal cell carcinoma, and non-small cell lung carcinoma (NSCLC), as well as CHL and diffuse large B cell lymphoma. As a result of these trials, the anti-PD-1 antibody nivolumab and pembrolizumab have received FDA approval for treating metastatic squamous NSCLC and metastatic melanoma, respectively.

PhenoPath scientists and pathologists are at the forefront in working with pharmaceutical companies looking for the features of the tumor which might predict response to these anti-PD-L1 agents, particularly the expres-sion of PD-L1 on the tumor cell population, as determined by immunohistochemistry. From these studies, we have optimized PD-1 and PD-L1 protocols, which have been analytically validated in our laboratory. While at the current time, no universally agreed-upon scoring system for PD-L1 exists, we are employing the same scoring system used in several of the clinical trials presented at the 2015 ASCO meeting, in which the percent of tumor cell positivity and the intensity are recorded.References: 1.Teixidó C, et al. Cancer Biol Med Jun;12(2):87-95, 2015, 2.Patel SP, Kurzrock R. Mol Cancer Ther 14(4):847-56, 2015, 3.Ansell SM, et al. NEJM 22;372(4):311-9, 2015, 4.Larkin J, et al. NEJM 2;373(1):23-34, 2015, 5.Brahmer JR, et al. NEJM 28;366(26):2455-65, 2012, 6.Pico de Coana Y, et al. TRMOME 1046:1-10, 2015, 7. Le DT, et al. NEJM 372:2509-20, 2015, 8.Taube, JM, et al. Clin Cancer Res 20:5064-74, 2014

STAT6In the past, markers such as CD34 have been employed in the immunohistochemical confirmation of the di-agnosis of solitary fibrous tumor (SFT) and the tumors formerly known as hemangiopericytoma (now known to be one and the same). However, CD34 is by no means a specific marker of SFT, and there do not appear to be any lineage-specific markers that define this tumor. The molecular alteration that characterizes solitary fibrous tumors is a fusion between NAB2 and STAT6, adjacent genes on chromosome 12q13. While there are several fusion variants, all result in formation of a NAB2-STAT6 chimeric protein that relocates to the nucleus. Nuclear STAT6 immunoreactivity has been reported as an excellent surrogate marker for the NAB2-STAT6 gene fusion, and STAT6 is a highly sensitive and specific immunohistochemical marker for SFT.References: 1.Cheah AL, et al. Pathology. 46(5):389-95, 2014, 2.Yoshida A, et al. AJSP 38(4):552-9, 2014, 3.Doyle LA, et al. Mod Pathol 27(3):390-5, 2014

HGALHGAL - also known as GCET2, GCAT2, and GCSAM – is a cytoplasmic protein expressed by benign and neoplastic follicle center (germinal center)-derived B cells. As part of a panel of IHC antibodies, HGAL is useful to distinguish follicle center-derived B cell non-Hodgkin lymphoma (see Figure 1) from other B cell proliferations, particularly marginal zone lymphomas. Note that one study of germinal center B cell markers (reference 1) reported that, in a series of 29 nodal and extranodal follicular lymphomas, HGAL was a more sensitive immunohistochemical marker of follicle center origin than CD10, bcl-6, or LMO2.

New IHC Markers In Hematologic Diseases

Figure 1

Figure 2 Figure 3

PD-L1

STAT6

MNDAAlthough the expression of MNDA was initially thought to be restricted to the myelomonocytic lineage, several studies (reference 2) have shown expression of this protein in normal and neoplastic B lymphocytes of mar-ginal zone derivation (see Figure 2, from normal spleen), but not in fol-licle center-derived B cells (see Figure 3, from normal tonsil). MNDA has been shown to be expressed in splenic marginal zone lymphomas, mantle cell lymphomas, nodal marginal zone lymphomas, and hairy cell leukemia. MNDA can be used as part of a panel of IHC antibodies to help distin-guish marginal zone B cell lymphoma (MZL) from follicle center-derived B cell lymphoma, particularly CD10-negative FL.References: 1.Younes SF, et al. AJCP 135:697-708, 2011, 2.G Kanellis, et al. Leuke-mia 23:1847-57, 2009

New IHC Markers in Solid Tumors

New Markers of Basal-Like Breast Cancer, Nestin and INPP4BBasal-like breast cancers constitute 10-15% of all breast cancers. These were first defined by the gene expression studies in the early 2000s, with out-come data showing these tumors to have the poorest prognosis amongst the various molecular subtypes. While the ‘triple-negative’ immunopheno-type (ER, PR and HER2 negative) is known to overlap strongly with this group of basal-like breast cancers, there have been several efforts to look for other positive or negative immunohistochemical markers which might bet-ter define the group. In a collaborative study published in 2004 (in which PhenoPath participated), a panel of four antibodies (ER, EGFR, HER2, and keratin 5) was found to be the optimal panel. But in a study from 2013,

some of the same authors updated this analysis, employing a wider panel of potential markers. The two markers which, in conjunction, displayed the highest specificity (96%) and sensitivity (83%) were nestin and INPP4B, with the latter a negative marker of basal-like tumors. Nestin is a major intermediate filament protein of embryonic central nervous system progenitor cells, and INPP4B encodes the inositol polyphosphate 4-phosatase type II, one of the enzymes involved in phosphatidylinositol signaling pathways. PhenoPath has validated the two markers in the context of breast cancers and recommends their use instead of the older panels. References: 1.Won JR, et al. Mod Pathol 26(11):1438-50, 2013, 2.Parry S, et al. J Clin Pathol 61(9):1045-50, 2008

Cathepsin KCathepsin K is a lysosomal cysteine protease which is a member of the peptidase C1 protein family. In the non-neoplastic setting, it is expressed predominantly in osteoclasts.

In malignant tumors, cathepsin K expression is quite restricted. Cathepsin K is expressed in alveolar soft part sarcoma, and among carcinomas, cathepsin K expression is highly specific for translocation renal cell carcinomas (RCCs), which include those tumors harboring translocations involving genes coding for TFE3 (Xp11 translo-cation RCCs) and TFEB [t(6;11) RCCs]. In mesenchymal neoplasms, cathepsin K expression is characteristic of granular cell tumors and melanoma.References: 1.Smith NE, et al. AJSP 38(5):604-14, 2014, 2.Rao Q, et al. AJSP 37(6):804-15, 2013, 3.Zheng G, et al. AJCP 139(2):151-9, 2013, 4.Martignoni G, et al. Mod Pathol 24(10):1313-9, 2011

Cathepsin K

INPP4BNestin

An international study to increase concordance in Ki67 scoringPolley MY, Leung SC, et al. Mod Pathol 28(6):778-86, 2015This is the most recent installment of an international concordance study involving 16 laboratories in eight countries (in which PhenoPath is participating) to determine optimal scoring methodologies for evaluation of Ki67-defined cell proliferation indices in breast cancer. Although it is widely recognized as an important biomarker in breast cancer, to date Ki67 has not had a standardized scoring method, which has limited its clinical use. In the present study, which required calibration to a common method using a web-based tool, based on tissue microarray samples of 18 breast cancers, an extremely high intra-class correlation of 0.94 was found. It was concluded that laboratories can achieve very high inter-laboratory reproducibility in Ki67 scoring of breast cancers. The next phase of the study will extend this approach to biopsies and whole sections rather than tissue microarrays, to account for staining variability, and link to outcomes.

GATA-3 expression in trophoblastic tissues: an immunohistochemical study of 445 cases, including diagnostic utilityBanet N, Gown AM, et al. AJSP 39(1):101-8, 2015GATA-3 is known mostly as a marker of breast and bladder carcinomas, in which it shows an extremely high sensitivity of >95%, but it is also a potential marker of trophoblastic tissues and tumors. In this col-laborative immunohistochemical study of 445 cases, pathologists from Johns Hopkins Medical Center and PhenoPath examined GATA-3 expression in placentas, hydatidiform moles, implantation sites, and cho-riocarcinomas. GATA-3 was found to be frequently expressed in normal and lesional trophoblastic tissues, and differentially expressed in intermediate trophoblast, cytotrophoblast, and syncytiotrophoblast, which varies according to time during pregnancy. Recognition of GATA-3 expression in trophoblastic tumors is important to avoid the diagnostic pitfalls of examination of tumors involving the GYN tract.

New Publications By PhenoPath Pathologists

An international study

to increaseconcorda

nce

in Ki67 scoring

Mei-Yin C Polley1, Samuel CY Leung

2, DongxiaGao

2, Mauro G Mastropasqua3,

Lila A Zabaglo4, John MS Bartlett

5, Lisa M McShane1, Rebecca

A Enos6, Sunil S

Badve7,

Anita L Bane8, Signe Borgquist

9, Susan Fineberg10, Ming-Gang

Lin11, Allen M Gown12,

Dorthe Grabau9, Carolina

Gutierrez13, Judith C Hugh1

4, TakuyaMoriya

15, YasuyoOhi16,

C Kent Osborne13, Frédériq

ue M Penault-Llorca

17, Tammy Piper18, Peggy L Porter

11,

Takashi Sakatani

19, RobertoSalgado

20, Jane Starczynski21, Anne-Vibek

e Lænkholm22,

GiuseppeViale

23, Mitch Dowsett24, Daniel F

Hayes25, Torsten

O Nielsen2

on behalf ofthe Internatio

nal Ki67in Breast Ca

ncer Working Group of the Breast

International Group

and North American Breast Cancer Grou

p (BIG-NABCG)

1Biometric ResearchBranch, D

ivision of CancerTreatment and Diagnosis

, National Cancer Insti

tute,

Bethesda,Maryland, U

SA;2Pathology

and Laboratory Medicine, U

niversityof British

Columbia, Vancouver,

British Columbia, Canada; 3Divis

ion of Pathology and Laborator

y Medicine, European Institute of Oncology,

Milan, Italy; 4Breakth

rough Breast Cancer Rese

arch Centre, The Institute of Cancer

Research,London, U

K;

5Transformative Pathology

, Ontario Institute for Cancer Researc

h, Toronto, Ontario, Ca

nada;6The Emmes

Corporation, Rockv

ille, Maryland, USA;

7Indiana UniversitySimon Cancer Ce

nter, Indianapolis,

Indiana,

USA;8Department of Pat

hology and Molecular Medicine, J

uravinskiHospital an

d Cancer Centre, McMaster

University,Hamilton, Ontario, Ca

nada;9Department of Cli

nical Sciences, Divi

sion of Oncology and

Pathology, Lund University,

Lund, Sweden;

10MontefioreMedical Ce

nter andthe Albert Ein

stein College of

Medicine, Bronx, New York, USA;

11Fred HutchinsonCancer Re

search Center, Seattle, Washington

, USA;

12PhenoPath Laborator

ies, Seattle, Washington

, USA;13Lester and

Sue Smith Breast Center and

Dan L.

Duncan Cancer Center, Bayl

or Collegeof Medicine, H

ouston, Texas, USA;

14Department of Laboratory

Medicine and Pathology, University

of Alberta, Alberta,

Canada;15Department of Pat

hology, Kawasaki

Medical School, Kur

ashiki City, Japan;

16Department of Pathology, H

akuaikaiSagara Hospital,

Matsubaracho, Kagos

hima, Japan;17Department of Pat

hology, Centre Jean Perrin and Université d'Auvergn

e,

Clermont-Ferrand, France

; 18Edinburgh Cancer Re

search Centre, Western General H

ospital, Edinburgh,

UK;

19Department of Pathology, Ji

chi Medical University,Shimotsuke, T

ochigi, Japan;

20Institut Jules Bordet,

Brussels,Belgium; 21Birmingham Heart of En

gland, National Health Service, B

irmingham, UK; 22Slagelse

Hospital, Slagelse, R

egion Sjælland, Denmark;

23Division of Pathology and Laborator

y Medicine, European

Institute of Oncology, and University

of Milan, Milan, Italy; 24Acade

mic Department of Biochemistry, Roy

al

Marsden Hospital, London, U

K and25Breast Oncology Program, University

of Michigan Comprehensive

Cancer Center, Ann

Arbor, Michigan, USA

Althoughan important b

iomarker in breast cancer, Ki6

7 lacks scoring standardization, w

hich has limited its

clinical use. Our previou

s study found variabilitywhen laborator

ies used their ownscoring methods on centrally

stained tissue microarrayslides. In

this current study, 16 laborator

ies from eight countries calibrated

to a specific

Ki67 scoring method and then scored 50 centrallyMIB-1 stained tissue microarray

cases. Simple instructio

ns

prescribed scoring pattern and staining threshold

s for determination of the percentag

e of stainedtumor cells. T

o

calibrate,laborator

ies scored 18 ‘training’and ‘test’ web-based

images. Software tracked object se

lection and

scoring.Success

for the calibration was prespecif

ied as Root Mean Square Error of scores compared with

referenceo0.6 and Maximum Absolute

Deviationfrom reference

o1.0 (log2-transformed data). Pre

specified

successcriteria for tissue

microarrayscoring required

intraclasscorrelatio

n significantly 40.70 but aiming for

observedintraclass

correlation ≥0.90. Lab

oratory performance showed non-significant but

promising trends of

Correspondence: Dr

TO Nielsen, MD/PhD FRCPC, P

athologyand Laborator

y Medicine, University

of British Columbia, Anatomical

Pathology, JP 1401, Van

couver Hospital and Health Sciences C

entre, 855W 12th Avenue, Va

ncouver, British Columbia V5Z 1M9, Canada

.

E-mail: torsten@mail.ubc.ca

Received14 October 20

14; revised 17 December 2014;

accepted18 December 2014;

publishedonline 20 February

2015

Modern Pathology (2015) 28

, 778–786

778

© 2015 USCAP, Inc All rights

reserved 0893-3952/15 $32.00

www.modernpathology.orgGATA-3

Expression in Trophob

lastic Tissues

An Immunohistochemical Stud

y of 445 Cases,

IncludingDiagnost

ic Utility

Natalie Banet, MD,* Allen M. Gown, M

D,w Ie-Ming Shih, MD, PhD,*zy Qing Kay Li, MD, PhD,8

RichardB.S. Rod

en, PhD,* Marisa R. Nucci, MD,z Liang Cheng, M

D,#

Christopher G. P

rzybycin,MD,** Niloofar N

asseri-Nik, MD,ww Lee-Shu-Fune Wu, MHS,zz

George J. Netto, MD,yy Brigitte M. Ronnet

t, MD,*z

and Russell Vang, MD*z

Abstract: Immunohisto

chemical expression of GATA-3 is seen

predominantly in non-neoplastic bladder

and breast epithelium

and their respective ca

rcinomas; however, data

on expression in

normal and lesionaltrophob

lastic tissues are limited. Im-

munohistochemical staining

for GATA-3 was assessedin a

range ofnormal/lesion

al trophoblastic ti

ssues and tumors in the

differential diagn

osis (n=445), inc

luding nonmolar products of

conceptions/seco

nd and third trimester placentas/ectopic

preg-

nancies,hydatidi

form moles, placental si

te nodules,normal/ex-

aggerated implantatio

n sites, choriocarcinomas, epithelio

id

trophoblastic tumors, placenta

l site trophoblastic tumors,

atypicalsmooth muscle tumors (includin

g leiomyosarcoma),

and cervicaland pulmonary squamous cell carcinom

as.

The extent of exp

ression (0 to 4+) and intensity(weak to strong)

were recorded. All cases w

ith developing trophob

last/non-neo-

plastic trophoblastic prolifera

tion and 81% of trophoblastic

neoplasms were positive.

Of all non-neoplas

tic trophoblast cell

types, expression

was observedin cytotrop

hoblastin 89% of

cases, syncytiotro

phoblastin 50%, intermediate trophob

last in

100%, and villous trophoblastic columns in 100%. Increas

ing

gestational age wa

s associated with a decrea

se in extent/intensity

of expression in non-neo

plastic cytotrophoblast

and syncytio-

trophoblast, whe

reas intermediate trophoblast maintained

dif-

fuse and strongexpressio

n from early to late gestation

(P<0.0001).Eighty-n

ine percentof normal/exagg

erated im-

plantation sites sho

wed 3+ or 4+ expression, where

as staining

in 55% of placental site

noduleswas 1+ or 2+. Stainin

g for

GATA-3 was present in 78% of chorio

carcinomas, 95%

of ep-

ithelioidtrophob

lastic tumors, and 71% of placental site

trophoblastic tumors. Although

the number of choriocarcino

-

mas and placental site trophob

lastic tumors that showeda

spectrumof expressio

n rangingfrom negative

to diffuse was

relativelyevenly distribut

ed, 81%of epithelio

id trophoblastic

tumors had 3+ or 4+ staining.None of the atypical

smooth

muscle tumors and3% of squam

ous cellcarcinom

as werepos-

itive, allof which exhibited

weak staining.We conclude

that

GATA-3 is frequently expresse

d in normal and lesional

trophoblastic tissues. I

t is also differentially expresse

d in inter-

mediate trophoblast and cytotrop

hoblast/syncytiotr

ophoblast,

which varies according to time during pregnan

cy. Thisstudy

expandsthe spect

rum of neoplasms known

to express GATA-3.

Thus, recognition

of expression in trophobl

astic tumors is im-

portant,because

it can present adiagnost

ic pitfall inthe assess-

ment of suspectedmetastatic

bladderor breast carcinom

as

involvingthe gynec

ologic tract. In the evalu

ation of diagnostically

problematic tumors for which trophobl

astic neoplasms are in the

differential diagno

sis, suchas leiomyosarcom

a and squamous cell

carcinoma, GATA-3 can be included

as part of an im-

munohistochemical pane

l particularly when other trophobl

astic

markers are either no

t available or yiel

d ambiguousresults.

Key Words: GATA-3, trophoblast, c

horiocarcinoma, leiom

yo-

sarcoma, squamous cell

carcinoma

(Am J Surg Pathol 2015;39:1

01–108)

From the *Department of Pathology

, Division of Gynecologic Pathol-

ogy; yyDepartment of Pathology, Division of Urologic Patholog

y;

Departments of zGynecology & Obstetrics

; yOncology,The Johns

Hopkins University

School of Medicine a

nd Hospital; 8Department

of Pathology, Th

e JohnsHopkins B

ayview Hospital; zzDepartment

of International Health, Bl

oomberg School of Public Health, Th

e

Johns Hopkins UniversitySchool

of Medicine,Baltimore, MD;

wPhenoPath Laborat

ories, Seattle, WA; zDepartment of Pa

thology,

Division of Women’s andPerinata

l Pathology, Brigh

am and Wom-

en’s Hospital,Boston,

MA; #Department of Pathology

and Labo-

ratoryMedicine,

IndianaUniversity

Schoolof Medicine,

Indianapolis, IN; **Robert J.

Tomsich Pathology and Laborat

ory

MedicineInstitute

, The Cleveland Clinic, Clevelan

d, OH; and

wwDepartment of Pathology,

South Miami Hospital, Baptist Health,

South Miami, FL.

Conflictsof Interest

and Source of Funding: The preparat

ion of the

cervicalsquamous cell

carcinoma tissue microarray

s was funded by

NIH grant P50 CA098252.

The following authors

have sourcesof

fundingto disclose:

N.B. (Genentech—pending)

; R.B.S.R. (National

CancerInstitute

—Grant P50 CA098252);M.R.N. (expert

testimony—Campbell, Campbell, Ference;grant—Liddy Shriver

Grant; lecture hon

oraria—Banff So

ciety of Pathology and MSKCC

Grand Rounds;royalties

—Lippincott, Williams, and Wilkins;

Elsevier;and Amirsys); an

d B.M.R. (consultant—Merck Inc.; lect

ure

honoraria—various;

royalties—Springer

Verlag ARP Press; travel/

accommodations/meeting expenses

unrelatedto activities

listed—

various).For the

remaining authorsnone were declared

.

Correspondence:

Russell Vang, MD, Department of Patholog

y, Divi-

sion of Gynecologic Patholog

y, The Johns Hopkins Hospital,401

North Broadway, Weinberg

Building, Room 2242, Ba

ltimore, MD

21231 (e-mail: rvang1@jhmi.edu).

Copyright r 2014 by Lippinco

tt Williams & Wilkins

ORIGINAL ARTICLE

Am J Surg Pathol� Volume 39, Number 1, Ja

nuary 2015

www.ajsp.com| 101

551 North 34th Street, Suite100Seattle, Washington, 98103P (206) 374-9000 F (206) 374-9009

PhenoPathDiagnoses you can count on®

FEATURED At PhenoPath ConferenceBrigitte M. Ronnett, MD The Johns Hopkins Hospital, Baltimore MD

Brigitte M. Ronnett, MD presented “Ovarian mucinous tumors: evolution, revolution, and adventures in masquer-ading” at the PhenoPath Conference at 7:00 pm on Thursday, September 17, 2015. Dr. Ronnett also gave a daytime lecture, “Hydatidiform moles: ancillary techniques to refine diagnosis” at noon the same day.

Dr. Ronnett is Professor of Pathology and Gynecology & Obstetrics at The Johns Hopkins Hospital, Baltimore, MD. She received her medical degree from the University of Chicago Pritzker School of Medicine and completed residency training in anatomic and clinical pathology at The Johns Hopkins Hospital, Baltimore, MD. She also completed a 1-year surgical pathology fellowship at Memorial Sloan-Kettering Cancer Center and a 1-year surgical pathology fellowship/chief residency at The Johns Hopkins Hospital. Dr. Ronnett then completed a 2-year subspe-cialty fellowship in gynecologic pathology at The Johns Hopkins Hospital, Baltimore, MD. She joined the faculty of the Department of Pathology at The Johns Hopkins Hospital in 1995 and achieved the rank of full Professor in 2007.

Her clinical efforts are focused on a large gynecologic pathology consultation practice at The Johns Hopkins Hospi-tal. Her research has focused on ovarian mucinous tumors (distinction of primary and metastatic mucinous tumors in the ovaries, and the origin of pseudomyxoma peritonei in women), uterine, cervical and endometrial pathology (HPV-related cervical lesions, ancillary techniques for distinction of endocervical and endometrial adenocarcino-mas and subtyping of endometrial adenocarcinomas), and hydatidiform moles (ancillary techniques for refined diagnosis).

PhenoPath, Thursday, September 17, 2015, 7:00 PM