www.najms.org North American Journal of Medical Sciences 2011 May, Volume 3. No. 5.

Original Article OPEN ACCESS

E-Cadherin as a diagnostic biomarker in breast cancer

Rajeev Singhai1, Vinayak W Patil1, Sanjog R Jaiswal4, Shital D Patil1, Mukund B Tayade3 Amit V Patil2

Departments of Biochemistry1 and General Surgery3

Grant Medical College and Sir J. J. Group of Hospitals Mumbai, India.
2
Department of General Surgery, Government Medical College, Miraj, Maharashtra, India.
4
Department of General Surgery, Seth G. S. Medical College and K.E.M. Hospital, Parel, Mumbai, India.

Citation: Singhai R, Patil VW, Jaiswal SR, Patil SD, Tayade MB, Patil AV. E-Cadherin as diagnostic biomarker in breast
cancer. North Am J Med Sci 2011; 3: 227-233.
Doi: 10.4297/najms.2011.3227
Availability: www.najms.org
ISSN: 1947 – 2714

Abstract
Background: E-cadherin is expressed in most normal epithelial tissues. Selective loss of E-cadherin can cause
dedifferentiation and invasiveness in human carcinomas, leading E-cadherin to be classified as a tumor suppressor. Loss of
E-cadherin has been demonstrated in invasive lobular carcinoma of the breast, but the relationship between E-cadherin
expression and breast cancer histopathology and prognosis is less clear. Aim: Our objective was to assess loss of
E-cadherin as a diagnostic breast cancer biomarker and as an aid to the sub-classification of invasive breast cancer. We
also correlated the loss of expression of E-cadherin with various clinical and pathologic prognostic factors. Material and
Methods: Breast cancer specimens after modified radical mastectomy were obtained from women who underwent surgery
at Grant Medical College and Sir J.J Group of Hospitals, Mumbai, India between May 2007 and October 2010. We stained
276 breast cancers specimens with monoclonal antibodies to E-cadherin. The breast cancers were classified by
histopathological type. Results: A statistical correlation of E-cadherin loss with a positive diagnosis of invasive lobular
carcinoma was found, but there was no correlation with any prognostic tumor variables. A negative E-cadherin stain was a
sensitive and specific biomarker to confirm the diagnosis of invasive lobular carcinoma (specificity 97.7%; negative
predictive value 96.8%; sensitivity 88.1%; and positive predictive value 91.2%). Positive E-cadherin expression was also
associated with tubulolobular carcinomas. Conclusions: E-cadherin immunohistochemistry is helpful in classifying breast
cancer cases with indeterminate histopathologic features. E-cadherin loss is uncommon in non-lobular carcinomas but
shows no correlation to currently established prognostic variables.

Keywords: Breast cancer, E-Cadherin, prognostic cancer tissue biomarkers, invasive lobular carcinomas, invasive ductal
carcinoma, tubulolobular carcinoma, invasive carcinoma.

Correspondence to: Dr. Rajeev Singhai, C-505, Beach Classic CHS Ltd, Near Gorai Pumping Station, Chikoowadi,
Borivali (W), Mumbai-400092, India. Tel.: +919699856615, Email: [email protected]

esophagus, ovary, and stomach [6-8]. Mechanisms by

Introduction which E-cadherin protein expression is lost include
E-cadherin is a calcium-regulated adhesion molecule E-cadherin gene mutation and loss of the wild-type allele
expressed in most normal epithelial tissues [1]. The by loss of heterozygosity [9-11]. These data indicate that
E-cadherin gene is located on chromosome 16q22.1 [2]. E-cadherin is a classic tumor suppressor gene [9, 12].
E-cadherin is associated with gland formation,
stratification, and epithelial polarization [3]. E-cadherin Ductal and lobular carcinomas of the breast represent the
knockout mice are non-viable and have abnormal main infiltrating carcinomas, the latter being less frequent.
epithelial morphogenesis [4]. Selective loss of E-cadherin Traditionally, histopathologic features have been used to
can cause dedifferentiation and invasiveness in human classify mammary carcinomas. Although the established
carcinomas [4, 5]. In various cell lines, a reciprocal histopathologic criteria distinguish invasive lobular from
relationship has been shown between levels of E-cadherin invasive ductal carcinoma, diagnostic difficulty occurs
expression and invasiveness [5]. Reduced expression of because of overlapping histopathologic features,
E-cadherin has been observed in aggressive tumors of the
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particularly with invasive lobular carcinoma (ILC) and 10 pleomorphic ILC); 4 cases of tubulolobular
variants and pleomorphic ILC [13-17]. Proper carcinoma (TLC); and 9 cases of invasive carcinoma (IC),
histopathologic categorization of breast carcinomas has with uncertain classification between lobular and ductal
prognostic implications [18]. type. Data on patient demographics, tumor size, axillary
lymph node status, stage of disease, ER and PgR status,
The majority of ILCs have shown a complete loss of and HER-2/neu overexpression were abstracted from the
E-cadherin expression [17-22]. The loss of E-cadherin is histopathology reports.
from the outset, i.e., in the pre-invasive stage of lobular
carcinoma in situ (LCIS). E-cadherin loss explains the Immunohistochemistry
histopathologic appearance of LCIS including a diffuse Tissue samples were fixed in 10% neutral buffered
growth pattern of this non-gland-forming tumor with formalin for 12 - 24 hours. Tissue samples were processed
discohesive tumor cells [23]. in an auto processer and embedded in paraffin wax on an
embedding station. The tissue blocks were sectioned by
However, the practical application of E-cadherin microtome into 4 μM sections that were dried overnight at
expression in breast cancer as a prognostic and diagnostic 37°C. Prior to antibody staining, the slides were
cancer biomarker remains controversial. Reduced pre-treated with microwave irradiation to unmask binding
E-cadherin expression was an adverse prognostic epitopes. After blocking endogenous peroxide activity
biomarker in some studies [24-27]. Although most studies with a 3% solution of hydrogen peroxide in methanol for
show reduced expression of E-cadherin to be associated 30 minutes, slides were immersed in 200 mL of 10 mM
with high histopathologic grade [20, 21, 25, 27, 28], citric acid (pH 6.0) for 5 minutes at 100 Watt power in a
correlation with nodal metastasis [29] and loss of estrogen microwave oven, followed by 4 cycles of 5 minute each on
receptor (ER) and progesterone receptor (PgR) [27, 28] 50 Watt power. After topping up the buffer with distilled
have been shown in only some studies. With the exception water, these steps were repeated. The slides were then left
of histopathologic grade, the relationship between to stand for 10 minutes in buffer at room temperature
E-cadherin expression in regard to different prognostic before being washed thoroughly in tap water.
markers and survival differs between studies [24, 30].
After three washes in tris-buffered saline (TBS), the slides
We evaluated E-cadherin expression as an aid to were incubated with a 1:50 dilution of mouse
sub-classification of invasive breast cancer. In addition, anti-E-cadherin monoclonal primary antibody (Clone:
we correlated the loss of expression of E-cadherin with NCH-38; M3612; DakoCytomation, Denmark) in TBS for
various clinical and pathologic prognostic factors. While 1 hour at room temperature. After three more washes in
correlating the prognostic criteria with E-cadherin loss, we TBS, the secondary antibody, biotinylated goat antibody
considered the inherent loss of E-cadherin in all lobular (LINK) to mouse/rabbit immunoglobulin (K0355;
breast carcinomas, irrespective of their histopathologic DakoCytomation, Denmark) at a dilution of 1:100 in TBS
grade, and the expression of other prognostic tumor was applied for 1 hour at room temperature. After an
variables that previous studies have not considered. additional three washes, a streptavidin-biotin-horseradish
peroxidase (HRP) complex (Enzyme Label) (K0355;
DakoCytomation, Denmark) was formed. After an
Materials and Methods additional three washes, the staining was visualized by
Human breast tumor tissue collection and histopathology adding diaminobenzidine (DAB) (K3467;
We collected 276 breast cancer specimens from women DakoCytomation, Denmark) for 5 minutes at room
undergoing modified radical mastectomy for operable temperature. The slides were washed well in tap water and
primary breast cancer between May 2007 and July 2010. counterstained with Harris’s hematoxylin for 10 seconds to
All breast cancer tissues were collected from surgeries 1 minute and then dehydrated, cleared, and mounted in
performed at Grant Medical College and Sir J.J Group of Distrene Plasticiser Xylene (DPX). Positive and negative
Hospitals, Mumbai, India. controls were performed with each batch of slides.
Surgical specimens from the same patient were stained on
Histopathology was based on hematoxylin and eosin the same run.
(H&E) stained slides. The pathology specimens were
reviewed independently by histopathologists to grade and The entire stained slide was evaluated for immunostaining
sub-classify the tumors based on established criteria [13, by light microscopy. Image collection and
14] without knowledge of immunohistochemical results. microphotographs were taken with an AxioImager M1
Discrepancies in diagnoses were resolved by consensus Microscope with AxioVision software (Carl Zeiss
with simultaneous viewing. All invasive carcinomas were Microscopy, Germany). The slides were first observed
graded using the Nottingham grading system of Elston and under a 10X objective to confirm that the cells were still
Ellis [31]. attached to the slide. Final evaluation was performed
under 400X objective magnification. All images were
After final histopathologic review, 276 breast cancer cases taken under 400X objective magnification without oil
were further studied, including 204 cases of invasive immersion lens. All images were processed with
ductal carcinoma (IDC) and ductal special types (tubular, AxioVision software.
mucinous); 59 cases of ILC and variants (49 conventional
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Table 1 Patient age, tumor histopathologic grade, and E-cadherin expression in breast cancer in 276 total cases
Histologic Type Age (years) Nottingham Grade E-Cadherin Score
Number (%) Mean ± SD Number (%) Number (%)
I II III 3+ 2+ 1+ 0
IDC 204 (73.9) 58.4 ± 15.0 29 (14.2) 83 (40.7) 92 (45.1) 199 (97.5) 4 (2.0) 0 (0.0) 1 (0.5)
IC 9 (3.3) 65.1 ± 13.5 0 (0) 8 (89) 1(11) 4 (44) 1 (11) 0 (0) 4 (44)
ILC 49 (17.8) 64.4 ± 13.0 46 (94) 3 (6) 0 (0) 2 (4) 3 (6) 0 (0) 44 (90)
PILC 10 (3.6) 58.2 ± 16.3 0 (0) 6 (60) 4 (40) 2 (20) 0 (0) 1 (10) 7 (70)
TLC 4 (1.4) 61.0 ± 9.1 2 (50) 2 (50) 0 (0) — — — —
Tubular — — — — 0 (0) 4 (80) — —
Lobular — — — — — — 2 (50) 2 (50)
IC: Invasive Carcinoma, IDC: Invasive Ductal Carcinoma, ILC: Invasive Lobular Carcinoma, PILC: Pleomorphic Invasive Lobular
Carcinoma, TLC: Tubulolobular Carcinoma.

Table 2 Analysis of prognostic cancer biomarkers with loss of E-cadherin expression*

All Cancers Non Lobular Carcinomas
Variable No. (%) EC+ EC– P Value No. (%) EC+ EC– P Value
Size 0.317 0.994
T1 153 (56.5) 126 (82.4) 27 (17.6) 126 (58.8) 124 (98.4) 2 (1.6)
T2 92 (33.9) 70 (76) 22 (24) 67 (31.3) 65 (97) 2 (3)
T3 13 (4.8) 8 (62) 5 (38) 9 (4.2) 8 (89) 1 (11)
T4 13 (4.8) 12 (92) 1 (8) 12 (5.6) 12 (100) 0 (0)
Grade <0.001 0.114
I 61 (22.1) 34 (56) 27 (44) 31 (14.3) 31 (100) 0 (0)
II 115 (41.7) 91 (79.1) 24 (20.9) 93 (42.9) 89 (96) 4 (4)
III 100 (36.2) 94 (94.0) 6 (6.0) 93 (42.9) 92 (99) 1 (1)
Node 0.167 0.798
N0 122 (59.8) 100 (82.0) 22 (18.0) 99 (62.7) 96 (97) 3 (3)
N1 78 (38.2) 56 (72) 22 (28) 56 (35.4) 54 (96) 2 (4)
N2 3 (1.5) 2 (67) 1 (33) 2 (1.3) 2 (100) 0 (0)
N3 1 (0.5) 0 (0) — 1 (0.6) 1 (100) 0 (0)
ER <0.001 0.783
Positive 208 (75.4) 154 (74.0) 54 (26.0) 153 (70.5) 149 (97.4) 4 (2.6)
Negative 68 (24.6) 65 (96) 3 (4) 64 (29.5) 63 (98) 1 (2)
PgR 0.127 0.598
Positive 187 (67.8) 144 (77.0) 43 (23.0) 141 (65.0) 139 (98.6) 2 (1.4)
Negative 89 (32.2) 75 (84) 14 (16) 76 (35.0) 73 (96) 3 (4)
HER-2/neu 0.765 0.635
Positive 47 (23.5) 41 (87) 6 (13) 43 (25.4) 41 (95) 2 (5)
Negative 153 (76.5) 130 (85.0) 23 (15.0) 126 (74.6) 125 (99.2) 1 (0.5)

EC: E-cadherin, ER: Estrogen Receptor, PgR: Progesterone Receptor, +: positive, –: negative. *: Data are given as number (percentage).
The numbers of cases for size, grade, node, ER, PgR, and HER-2/neu for all carcinomas are 271, 276, 204, 276, 276, and 200,
respectively, and for non lobular carcinomas, 214, 217, 158, 217, 217, and 169, respectively.

E-cadherin scoring used a 4-point scale adapted from [32]: correlation coefficient. Associations with ER and PgR
negative = 0; weak and heterogeneous = 1+; mild or weak were assessed with the Cochran-Armitage trend tests,
and homogeneous = 2+; moderate or strong and Kruskal-Wallis test, Wilcoxon rank sum test or the χ2 test,
heterogeneous = 3+; intense or strong and homogeneous = and confidence intervals. A 2-sided P value less than .05
4+. The intensity of staining was scored from 0 – 3, where was considered statistically significant.
0 = complete absence or negative; 1 = < 10% bright
membrane expression; 2 = >10% but ≤ 50% membrane
expression; and 3 = > 50% membrane expression.
Results
Patient demographics, histopathologic tumor subtypes, and
Statistical Analysis tumor grade along with E-cadherin immunoreactivity are
Statistical analyses were performed using SPSS-16 summarized in Table 1.
procedures (SPSS-16 Analytical Software Inc, Chicago,
IL). Immunohistochemical staining scores were correlated E-cadherin expression was seen in all but 1 case of IDC
with the histopathologic type, grade, nodal status, tumor and special ductal types (203/204, 99.5%). As shown in
size, hormone receptor status (ER and PgR), and Figure 1, E-cadherin expression was present in 100% of
HER-2/neu expression. The association between tumor cells in all positive cases, and the staining was 3+ in
E-cadherin and tumor type was assessed with the χ2 test. the majority (199 specimens) and 2+ in only 4 cases. The
Association with grade, nodal status, stage and HER-2/neu special types included 1 case of adenosquamous
overexpression were assessed with the Spearman rank carcinoma, 3 cases of mucinous carcinoma, and 3 cases of

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tubular carcinoma. Associated ductal carcinomas in situ E-cadherin, as shown in Figure 2; 5 (10%) of typical
(DCIS) was positive in 89 cases with 3+ E-cadherin histopathological ILC specimens showed complete
immunoreactivity. membrane staining in 100% of tumor cells. Three of these
E-cadherin-positive cases were well-differentiated nuclear
grade I and II; 2 were moderately differentiated nuclear
grade II according to the Nottingham grading system. Two
cases of ILC had mixed alveolar and solid patterns, both of
which were E-cadherin-negative. Twenty-five
E-cadherin-negative conventional ILC cases also had
E-cadherin-negative LCIS in the same slide. Two cases of
E-cadherin-positive ILC had associated
E-cadherin-positive LCIS, and 1 case had
Fig. 1 Invasive ductal carcinoma: (A) H & E, (B) E-cadherin
E-cadherin-positive DCIS.
positive immunoreactivity. Magnification = 400X.

Fig. 2 Invasive lobular carcinoma: (A) H & E, (B) no E-cadherin Fig. 5 Invasive carcinoma with lobular or ductal uncertainty: (A)
immunoreactivity. Benign duct serves as a positive internal H & E, (B) E-cadherin positive immunoreactivity. Magnification
control. Magnification = 400X. = 400X.

Fig. 3 Invasive lobular carcinoma: (A) H & E, (B) E-cadherin Fig. 6 Invasive carcinoma with lobular or ductal uncertainty: (A)
positive immunoreactivity. Magnification = 400X. H & E, (B) E-cadherin negative immunoreactivity. Magnification
= 400X.

Pleomorphic ILC was characterized by histopathology by

a growth pattern similar to classic ILC with greater
cytologic atypia, pleomorphism, and discohesion. Of 10
cases of pleomorphic ILC, 8 (80%) showed loss of
E-cadherin membrane staining in invasive and
corresponding in-situ components, as shown in Figure 3.
Two cases (20%) showed 3+ positive staining in 100% of
tumor cells. One E-cadherin-positive pleomorphic ILC had
E-cadherin positive LCIS.

The histopathology of TLC cases contained areas of

classic ILC along with focal but distinct tubule formation.
All cases of TLC exhibited a difference in E-cadherin
expression between the tubules and the cords, with classic
Fig. 4 Tubulolobular carcinoma with lobular component: (A) H single-file pattern of ILC, as shown in Table 1. The
& E, (B) E-cadherin negative immunoreactivity, Tubular tubules showed 2+ positive membranes staining, whereas
component: (C) H & E, (D) E-cadherin positive the single-file invasive cords showed loss of E-cadherin,
immunoreactivity. Magnification = 400X. as shown in Figure 4. One case also had
E-cadherin-positive DCIS, whereas E-cadherin-negative
Classic ILC was characterized by histopathology by LCIS was present in 2 other cases.
strands of discohesive small to medium-sized tumor cells
with mild to moderate cytologic atypia dispersed in a Nine cases were designated as invasive carcinomas
fibrous stroma. Of 49 ILC specimens with the classic because of overlapping histopathologic features uncertain
histopathologic pattern, 44 (90%) showed complete loss of
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for IDC or ILC. Of 9 cases, 5 (56%) showed positive cancer described by Foote and Stewart [34] and Wheeler
E-cadherin staining in all tumor cells, as shown in Figure 5, and Enterline [35] paved the way for identification of this
whereas the remaining 4 cases (44%) were negative for tumor by histopathologist when the classic features are
E-cadherin staining, as shown in Figure 6. present.

Comparison of E-cadherin staining in IDC, ILC, and ILC Identification of solid, alveolar, tubulolobular, and
variants revealed a highly significant difference between pleomorphic variants [15, 17, 36-38] of ILC has added
the groups (P<.001; Kruskal-Wallis test). Overall, new dilemmas to the existing problem of distinguishing
negative staining of E-cadherin in ILC was specific for the IDC of no special type with cord-like or trabecular
diagnosis of ILC (specificity, 97.7%; negative predictive patterns from ILC and its variants. Selective E-cadherin
value, 96.8%; 95% confidence interval, 94.7-99.3). loss, now well recognized [17, 19, 22], validates ILC as a
However, positive staining did not exclude the diagnosis distinct entity and explains its histopathologic appearance
of ILC (sensitivity, 88.1%; positive predictive value, [22] and distinctive growth patterns in metastases [23].
91.2%; 95% confidence interval, 77.1-95.1). Although E-cadherin is emerging as an excellent
biomarker to type breast cancers [17, 19, 22], the
All invasive carcinoma associations between E-cadherin conflicting reports of E-cadherin loss as predictor of
expression and tumor characteristics were assessed with increased invasiveness, metastatic potential, and poor
the Wilcoxon rank sum test or the χ2 test. Various tumor survival [24, 29] raise questions about its reliability for
variables (tumor size, nodal status, PgR status, and typing. Loss of E-cadherin alone cannot be a predictor of
HER-2/neu status) did not reveal significant associations metastatic potential and negative outcome as E-cadherin is
with loss of E-cadherin expression, as shown in Table 2. lost even in the pre-invasive stages of LCIS and atypical
lobular hyperplasia. Furthermore, ILC is a slow-growing
However, loss of E-cadherin was significantly associated tumor that has been shown to have better survival than
with tumor grade and ER status. The analysis was repeated ductal carcinoma of no special type [13, 18].
after excluding all ILCs, on the basis that previous data
have shown that ILCs are E-cadherin-negative irrespective As demonstrated in our study and in previous studies [23,
of their grade, nodal status, size, or hormonal status. 28], E-cadherin can help in the diagnosis of ILC. As in our
Complete loss of E-cadherin was seen in too few cases of study, complete E-cadherin loss has been reported in 86%
IDC and special types to be of prognostic or predictive to 100% of ILCs [19, 22], with most large studies
value, as shown in Table 2. reporting E-cadherin positivity in a small number of ILCs.
All of these studies also show good membrane positivity
for E-cadherin in all IDCs, including special types, even at
Discussion the advancing front. Almost all of our cases of invasive
E-cadherin is a cell adhesion molecule that is expressed in and in situ breast cancers were strongly
normal breast tissue and is useful as a phenotypic marker E-cadherin-positive (3+) or E-cadherin-negative (0). The
in breast cancer, with absence of its expression frequently exceptions were the few cases of TLC that showed 2+
observed in lobular type tumors. Reduced or impaired staining in the tubules only and a very few high-grade
E-cadherin expression is associated with a reduced cellular IDCs with apparent reduced expression of
disease-free interval and overall survival and with other E-cadherin. Acs et al [19] also report similar ―all or none‖
indicators of poor prognosis including a larger tumor size, E-cadherin expression in the majority of their cases,
higher histological grade, and development of distant including cases that were thought to have mixed or
metastasis and ER receptor negative tumors. indeterminate patterns.
E-cadherin immunostaining can be used in finding patients Berx et al [9] and Acs et al [19] observed variation in
with favorable outcomes among node-positive patients. E-cadherin intensity in IDCs and in some cases of
The loss of E-cadherin expression is a very early change in ―ductolobular‖ carcinomas. TLC, first described by Fisher
lobular breast carcinogenesis and the normal protein plays et al [39] as a rare variant of ILC, consists of a
a tumor-suppressive and invasion-suppressive role. predominant ILC component with a diffuse infiltrative
E-cadherin staining can help differentiate between lobular pattern and a component of variably defined small tubules
carcinoma in situ (LCIS)/lobular carcinoma and ductal [39]. All 4 of our TLCs fit this profile and had distinctive
carcinoma in-situ (DCIS)/infiltrating duct carcinoma biphasic E-cadherin expression in 3 cases with no
denoting the presence of DCIS or infiltrating duct immunoreactivity in the ILC component and moderately
carcinoma. positive immunoreactivity in the tubules.
Foote and Stewart [33] used the term lobular carcinoma in Diagnostic difficulty occurs in some cases because IDC
situ for a special type of non-invasive carcinoma of the may show a dispersed growth pattern, including
breast associated with a monotonous intralobular infiltration around benign ducts in a targeted manner
proliferation of cells. The concurrent invasive carcinoma similar to ILC [19]. Such cases were diffusely
with absence of tubule formation and single-file growth E-cadherin-positive in our study. Several authors have
pattern was established as ILC [33, 34]. The distinctive studied E-cadherin expression in ductolobular carcinomas
histopathologic features of this special type of breast
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or carcinoma of indeterminate type with similar results. Of

our 9 cases initially regarded as IC of uncertain type, 5
Conclusion
E-cadherin-positive cases seemed to be IDC with a Loss of E-cadherin is a sensitive and relatively specific
dispersed growth pattern, whereas the 4 biomarker to confirm a diagnosis of ILC and its variants.
E-cadherin-negative tumors had morphologic features A positive stain may not completely exclude the diagnosis
consistent with ILC. Thus, all of these cases could be ILC because E-cadherin expression may be retained in a
classified further based on immunohistochemical minority of cases with characteristic ILC morphologic
expression of E-cadherin. features. E-cadherin positivity clearly favors ductal
differentiation in ambiguous cases.
A category of mixed ductal lobular lesions is absent in our
study because we were able to classify most lesions as Biphasic immunostaining confirms that TLC is a rare and
ductal or lobular based on cytoarchitectural features. Most distinct variant of ILC. Partial loss of E-cadherin in a
studies have observed retained E-cadherin expression in minority of poorly differentiated IDCs is not of diagnostic
almost all IDCs but noted reduced expression, mainly significance. E-cadherin loss is rare in invasive
associated with poor differentiation and high tumor grade non-lobular carcinomas and does not correlate with
[21, 22, 25, 27, 28]. established prognostic variables when ILC is excluded.

Various studies have observed a correlation between Acknowledgement

reduced E-cadherin expression and lymph node status [28, Thanks to all members of histopathology section from
29] and ER and PgR status [27, 28]. Others have found no Grant Medical College and Sir J.J Group of Hospitals,
relationship to nodal or receptor status. To date, studies Mumbai, India, to provide surgical specimens tissue
correlating E-cadherin expression with outcome are few. samples. We would like to thank Dr. Belinda Peace for
Some suggest that reduced E-cadherin expression may professional editing assistance.
adversely affect overall and/or disease-free survival [24,
27] .
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