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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: [email protected]
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: [email protected]).
Copyright r 2014 by Lippinco
tt Williams & Wilkins
ORIGINAL ARTICLE
Am J Surg Pathol� Volume 39, Number 1, Ja
nuary 2015
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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