Textbook Breast Pathology 2Nd Edition David J Dabbs Ebook All Chapter PDF
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BREAST
PATHOLOGY
Second Edition
DAVID J. DABBS, MD
Professor of Pathology and Chief of Pathology
Department of Pathology
Magee-Womens Hospital of UPMC
Pittsburgh, Pennsylvania
iii
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
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(other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical treat-
ment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluat-
ing and using any information, methods, compounds, or experiments described herein. In using such
information or methods they should be mindful of their own safety and the safety of others, including
parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manufacturer of each
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To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
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Printed in Canada.
v
vi Contributors
R. S. Saad, MD, PhD, FRCPC Gary M. Tse, MBBS, FRCPC, DAB, FRCPath
Director, Cytology Section Senior Medical Officer
Windsor Regional Hospital Department of Anatomical and Cellular Pathology
Toronto, Ontario, Canada Prince of Wales Hospital
Metastatic Tumors in the Breast The Chinese University of Hong Kong
Shatin, Hong Kong
Radial Scar
viii Contributors
ix
x Introduction
test results among different platforms than the variation (American Association for Cancer Research, April 2016).
that occurs with the grading of tumors by pathologists.6 The trial, sponsored in Europe by Agendia (Amsterdam,
Needless to say, treatments that are based on these tests The Netherlands), accrued more than 6000 patients
vary even more than they have before because there is and compared their genomic classifier score of MP with
little evidence for such clinical decisions. The longer a Adjuvant! Online (AO) to discern if the MP test offered
breast cancer molecular test is available, the more claims clinical utility beyond AO. The AO and MP tests were
the companies can make about the prowess of the test, concordant in about two thirds of patients, whereas one
especially for the older LDT generation of tests. There is third was discordant. For the discordant group, patients
one thing for certain regarding all these molecular breast were randomized to chemotherapy or no therapy. The
cancer tests regardless of vendor: those who have ben- results demonstrated that patients who had a low-risk
efited the most are the stockholders of the companies. AO assessment alone in the randomized group did not
These tests, introduced in 2004 as a first-generation benefit from chemotherapy. Overall, this resulted in a
testing platform and as a laboratory developed test, have 14% reduction in chemotherapy for the high-risk MP
had a significant impact on how patients are treated. group. These results present clinicians with a profound
However, 12 years after their introduction, there are no paradigm shift in the potential better use of the MP test
data that demonstrate exactly how patients benefit from with AO and should prompt clinicians to rethink the use
the use of these tests (see Chapter 10). In our review of of genomic classifiers in general.
the role of molecular testing for breast carcinoma for It is predicted that this group of prognostic/pre-
prognostic and predictive interpretation, we concluded dictive tests will melt away in the near future to give
that, in fact, these tests offer very little compared with way to specific actionable genomic aberrations, most
traditional pathologic data generated by a pathologist.7 likely documented through massively parallel sequenc-
These tests have proliferated into various branded ven- ing (next-generation sequencing). MATCH (Molecular
dors, and they are all based on populations of patients, Analysis and Therapy Choice) and UMBRELLA trials
sometimes heterogeneous, sometimes homogeneous, are currently under way by the National Cancer Insti-
some of which are laboratory developed tests, and tute (NCI) to determine actionable mutations for breast
some of which have been cleared by the Food and Drug cancer patients.
Administration (FDA). These in vitro diagnostic multi- The second edition of this multi-authored breast
index analyte assays have a high impact and are a high pathology textbook is meant to inform readers of the
risk for patients and, at a minimum, command clear- latest developments in diagnosis and practice in the field
ance by the FDA, an independent consumer-oriented of breast pathology. Some topics are more amenable to
agency whose intention is to maximize patient safety updates, depending on the pace of topic information.
(see Chapter 10). The topics brought to your attention here “up front”
Only recently have the prospective, randomized reflect some of the hottest topics of recent times.
MINDACT (Microarray in Node Negative Disease May My special thanks to every contributing author, as
Avoid Chemotherapy) trial data been released regard- we dedicate this volume to the patients that we serve.
ing the clinical utility of the MammaPrint (MP) test
David J. Dabbs, MD
1
Normal Breast 1 Menopause 18
Embryology 1 Male Breast 18
Gross Anatomy 1
Structure and Histology 3 Developmental Disorders 18
Ultrastructure 11 Amastia 19
Arterial Supply 13 Hypoplasia 19
Venous Drainage 14 Polymastia 19
Lymphatic System and Regional Lymph Nodes 14 Supernumerary Nipple 19
Nerve Supply 15 Aberrant Breast Tissue 19
Hormone Regulation 15 Macromastia 20
Thelarche 16 Other Disorders of the Breast 20
Pregnancy, Lactation, and Milk 16
Summary 20
1
2 Normal Breast and Developmental Disorders
A B
FIG. 1.4 Vertical section through the nipple. A, A collecting duct is shown approaching the surface of the
nipple (area in box is magnified in B). B, Squamous epithelium of the orifice undergoes gradual transition to
the columnar epithelium of the collecting duct. A and B, Hematoxylin and eosin stain.
A B
FIG. 1.5 Terminal duct lobular unit. A, The lobule is composed of multiple acini. Acini are on the right (area
in box is magnified in B). B, The terminal duct on the left is seen exiting the lobule. Note inner epithelial layer
(with denser cytoplasm) and outer myoepithelial layer (with clearer cytoplasm). A and B, Hematoxylin and
eosin stain.
The portion of the ductal system immediately below populated by a mixed inflammatory cell infiltrate par-
the collecting duct is the lactiferous sinus in which milk ticularly in the secretory phase of the menstrual cycle.
accumulates during lactation. This sinus communicates The lobule undergoes a variety of morphologic changes
directly with segmental duct, which subdivides into sub- under various physiologic influences (Fig. 1.6).
segmental ducts, which in turn subdivide into terminal The fundamental glandular unit of the breast, and its
ducts. The latter structures drain the lobule. Each lobe most actively proliferating portion, is the terminal duct
contains 20 to 40 lobules. The lobule is composed of lobular unit (TDLU). This unit comprises the lobule and
groups of small glandular structures, the acini. The latter its paired terminal duct. During pregnancy and lacta-
are the terminal point of the ductal system. The serially tion, the epithelial cells of the terminal ducts and lobules
and dichotomously branching structure of the mammary undergo secretory changes, and most disease processes
gland, from the tubular-like collecting duct to the termi- of the breast arise from the TDLUs (including cyst for-
nal acini, leads to its classification as a compound tubu- mation, which may simply represent “unfolding” of the
loacinar (or tubulolobular) gland (Fig. 1.5). terminal ducts and lobular units). Indeed, the only com-
The lobule is inapparent to the naked eye on cut sec- mon lesion thought to be strictly of ductal origin may be
tions of breast tissue. However, with the aid of a mag- the solitary intraductal papilloma (Table 1.1).
nifying lens, the lobules resemble minute drops of dew, Except for the squamous epithelium–coated most
and the ducts may appear as linear streaks. The size of distal portion of the collecting ducts, low-columnar to
the “normal” lobule is extremely variable, as are the cuboidal epithelium lines almost the entire ductal sys-
number of acini in each lobule. Each lobule consists of tem of the breast, including the segmental ducts, sub-
10 to 100 (range, 8–200) acini. The intralobular stroma segmental ducts, terminal ducts, and acini. This lining
consists of loose connective tissue and may also be epithelium is supported on its basal surface by a layer
Normal Breast 5
B
A
C D
E F
FIG. 1.6 Mammary lobule at various physiological stages. A, Lobule in an adult female breast, inactive.
B, Lobule in early puberty; note the incipient development of the lobule. C, Lobule in the secretory phase
of the menstrual cycle; note secretions in the glands. D, Lobule after menopause, with intralobular fibrosis. E,
Lobule after menopause, with intralobular adipocytes. F, Lobule in the elderly; note glandular atrophy amid
largely fatty stroma. A to F, Hematoxylin and eosin stain.
of myoepithelial cells. The basement membrane (basal is primarily responsible for the mechanical release of
lamina) lies under the layer of myoepithelial cells. Exter- milk (the milk let-down phenomenon).19
nal to the basement membrane is connective tissue. The myoepithelial cell layer is generally regarded
Myoepithelial cells facilitate milk secretion via their as being spindle shaped with usually inapparent cyto-
contractile property, which is largely under the influence plasm. Indeed, in fine-needle aspiration cytology prepa-
of oxytocin. Receptors for the latter have been detected rations, myoepithelial cells appear to be entirely devoid
on the surface of myoepithelial cells,18 and this hormone of cytoplasm (ie, “naked”). The thin and compressed
6 Normal Breast and Developmental Disorders
A B
FIG. 1.8 Myoepithelial immunostain (calponin) in ductal carcinoma in situ (DCIS). A, DCIS of solid and
micropapillary types. Hematoxylin and eosin stain. B, Calponin immunostain demonstrates complete my-
oepithelial envelope around the neoplastic cells.
A B
C
FIG. 1.9 Triple stain highlights the myoepithelium and epithelium of mammary glands. The mammary
ductal-lobular system is lined by a dual cell population: an inner epithelial cell layer and an outer myoepi-
thelial cell layer. Red cytoplasmic immunostaining is seen in epithelial cells with cytokeratin. Brown cytoplas-
mic staining is observed in myoepithelial cells with myosin. Brown nuclear staining in myoepithelial cells is
with p63. Shown here is a duct and an inactive lobule (A), ductal carcinoma in situ (B), and microinvasive
carcinoma (C, center). Note absence of myoepithelium around the cells of the microinvasive carcinoma.
A to C, Triple immunostain: CK AE1/3 + myosin + p63.
8 Normal Breast and Developmental Disorders
A B
C D
E F
FIG. 1.10 Physiologically inactive mammary lobule: histochemical and immunohistochemical demon-
stration of structure. A, Normal lobule, hematoxylin and eosin stain. B, Reticulin stain decorates basement
membrane. C, Collagen 4 immunostain also displays basement membrane. D, Smooth muscle myosin im-
munoreactivity demonstrates myoepithelial cells. E, p63 immunostain shows nuclei of myoepithelial cells. F,
Cytokeratin AE1/AE3 immunostain demonstrates epithelial cells.
Normal Breast 9
A B
FIG. 1.13 Cystic papillary apocrine hyperplasia with prominent apocrine granules. A, The apocrine type
of metaplastic cells bear bright orange-red intracytoplasmic granules (area in box is magnified in B). A and
B, Hematoxylin and eosin stain.
10 Normal Breast and Developmental Disorders
A B
FIG. 1.14 Cystic apocrine metaplasia with oxalate crystals. A, The apocrine cysts contain barely visible
calcium oxalate crystals. B, The crystals can be better visualized under polarizing microscopy. A and B,
Hematoxylin and eosin stain.
A B
FIG. 1.15 Clear cell metaplasia. A and B, Acini in a lobule show cells with abundant clear cytoplasm and
bland nuclei. Note unaffected glands in the vicinity. A and B, Hematoxylin and eosin stain.
A B
FIG. 1.17 Mammary foam cells. These finely vacuolated histiocytic-type cells typically appear within
cysts, which may (A) or may only focally (B) be lined by epithelial cells. The derivation of foam cells (epithe-
lial or histiocytic) had been controversial in the past. A and B, Hematoxylin and eosin stain.
A B
FIG. 1.19 Multinucleated stromal giant cells in the breast. A, Stromal giant cells (of mesenchymal pheno-
type) are seen here in association with stromal fibrosis. B, Detail of multinucleated stromal giant cells. A and
B, Hematoxylin and eosin stain.
A B
FIG. 1.20 Stromal elastosis. A, Periductal stromal elastosis in a 78-year-old woman. Hematoxylin and eosin
stain. B, Elastic stain highlights elastic fibers in stroma.
A B
FIG. 1.21 Cellules claires (clear cells) in a nipple with Paget disease. Intraductal carcinoma in underlying
collecting duct extends into the epidermis of the nipple as Paget disease (box in A). Clear cells, simulating
signet-ring cells, are abundant (best seen in B). A and B, Hematoxylin and eosin stain.
Normal Breast 13
A B
FIG. 1.22 Toker cells in epidermis of nipple. A, These benign seemingly vacuolated cells are scattered
mainly around the basal layer and possess more abundant cytoplasm and are paler than adjacent
keratinocytes. Hematoxylin and eosin stain. B, Cytokeratin 7 immunostain highlights Toker cells and imparts
a dendritic appearance to these cells.
A B
FIG. 1.23 Paget disease of the nipple. A, The much larger and paler malignant cells are evident amid
the native squamous epithelium of the nipple. Hematoxylin and eosin stain. B, Cytokeratin-7 immunostain
highlights the presence of Paget cells. Human epidermal growth factor receptor 2 immunostain displays 3+
(on a scale of 0 to 3+) cytoplasmic membrane reactivity in Paget cells (inset).
pole of the cells depends on the physiologic state of the “internal thoracic artery” refer to the same arterial
organ. A seemingly continuous layer of myoepithelial vessel.49 Necrosis of breast tissue after coronary artery
cells lies under the epithelial cells. This layer is oriented bypass graft with segments of internal mammary artery
at right angles to the epithelial cells. Contractile actin is a rarer complication than one might expect, especially
filaments are seen in myoepithelial cells that appear because this artery is so commonly used for this pur-
more electron-dense and contain intracytoplasmic myo- pose.50 The lateral thoracic artery supplies the upper and
fibrils with dense bodies and pinocytotic vesicles. The outer portions of the breast. Numerous other arterial
myoepithelial cells are attached to the underlying base- vessels, including various intercostal (mainly the second
ment membrane (basal lamina) via hemidesmosomes. to fourth), lateral thoracic, subscapular, thoracoacro-
The epithelial cells appear to rest directly on the basal mial, and thoracodorsal arteries and branches thereof,
lamina wherever there is a gap between myoepithelial contribute to the arterial supply of the breast.51,52
cells.47,48 Arteries in the breast normally exhibit sclerotic
changes and intramural calcifications of the type seen
Arterial Supply in so-called Monckeberg medial calcific arterial sclerosis
(named after Johann Monckeberg, the German cardio-
The principal arterial supply to the breast is via the vascular pathologist). Such calcified deposits are largely
internal mammary artery, which caters to its central an aging phenomenon similar to that observed in other
and medial portion. Somewhat confusing to the unini- organs (Fig. 1.24). Up to 9% of breasts in postmeno-
tiated is the fact that “internal mammary artery” and pausal women exhibit arterial calcifications detectable
14 Normal Breast and Developmental Disorders
SC
III
II
I
IM
Hormone Regulation AR, androgen receptor; CK, cytokeratin; EMA, epithelial membrane anti-
gen; ER, estrogen receptor; GCDFP; gross cystic disease fluid protein; PgR,
progesterone receptor; SMM-HC, smooth muscle myosin heavy chain.
The breast is the target organ of a variety of hormones
that are responsible for its physical development as well
as the initiation and maintenance of lactation.66–70 of stromal edema and lobular proliferation. Strictly
Estrogen and progesterone production by the ovary speaking, the use of the term resting breast in the pre-
at puberty influences the initial growth of the breast. menopausal breast is inaccurate because the breast is
Despite its predominant role, estrogen is unable to work hardly ever quiescent during these years. During preg-
independently of other hormones. Cyclic hormonal nancy, the development of the breast is further stimu-
changes during each menstrual cycle alter the histology lated by the continuous production of estrogen and
of mammary glands (Table 1.3). The breasts become progesterone. In this period, breast growth is further
swollen and somewhat lumpy in the latter half of the influenced by prolactin, steroids, insulin, and growth
cycle. These changes are the physical manifestations hormone.
16 Normal Breast and Developmental Disorders
A B
C D
FIG. 1.28 Changes in contour of breast at various phases. Schematic drawing illustrates contour of the
breast in a typical adult (A), fuller contour in midpregnancy (B), rounded contour in lactation (C), and
droop contour in postmenopause (D).
FIG. 1.29 Breast in midpregnancy. Acinar cells have a hobnail ap- FIG. 1.30 Lactating breast. The acini are expanded with accumu-
pearance with vacuolated cytoplasm. Note absence of luminal secre- lation of secretions. Acinar epithelia appear finely vacuolated. Hema-
tions. Hematoxylin and eosin stain. toxylin and eosin stain.
18 Normal Breast and Developmental Disorders
Menopause the male breast, are embedded amid fibrous stroma and
adipose tissue. The ducts are lined by a single layer of
The female breast undergoes gradual regression start- low cuboidal epithelium that lies on an inconspicuous
ing at the end of the fourth decade of life. The histo- myoepithelial cell layer. Lobule formation is only rarely
logic changes of regression are much more evident in the encountered in male breasts.
terminal duct lobular unit. There is progressive lobular Slight physiologic enlargement occurs at puberty, and
atrophy. Ducts become variably ectatic (ie, dilated), and in elderly men, it is caused by an androgen-estrogenic
there is an increase in stromal fat deposition. The regres- imbalance. Gynecomastia at puberty is common and
sive process continues until menopause (which typically affects most boys.
occurs some 10 years later) and beyond.79 The morpho-
logic pattern in elderly women may ultimately resemble DEVELOPMENTAL DISORDERS
the male breast; however, most menopausal women
produce enough endogenous estrogen to maintain some A variety of developmental anomalies affect the breast.
remnants of lobules. Some of these abnormalities preclude functioning of the
breast (eg, amastia), others hamper its optimal func-
Male Breast tioning (eg, inverted nipple), and some pose a cosmetic
problem (eg, polythelia and asymmetry). A variety of
The adult male breast consists mainly of large ducts morphologic abnormalities, without any functional def-
without lobule formation. The ducts, which generally icit, may be considered to be deformities. These include
do not extend beyond the central subareolar portion of the so-called Snoopy-nose breast in which the breast
resembles the shape of a tuberous plant root (named
after the nose of Charlie Brown’s pet dog in the Peanuts
comic strip).
Some degree of physiologic breast asymmetry is the
rule rather than the exception. Asymmetry is common
during breast growth and may persist into adulthood
in approximately 5% of cases.80,81 The left breast is
usually larger than the right, and this finding may be
related to handedness. A number of conditions, includ-
ing developmental disorders, surgery, radiation, and
trauma, may produce asymmetry. In states of extreme
malnutrition or emaciation, the breasts may reduce in
size in an asymmetrical manner; however, abnormali-
ties of development account for most cases of obvious
breast asymmetry. Surgery of either of the asymmetri-
cal set of breasts should not be undertaken for cosmetic
reasons alone, until full development has been achieved,
because of the high likelihood of permanent breast dam-
FIG. 1.31 Involution of breast 1-month after cessation of lactation.
age.82 Differences in size or length of the extension of
Acini are dilated with accumulation of secretions. Hematoxylin and eo- breasts into the axilla are regarded as variations, and
sin stain. not as disorders, of development. True developmental
A B
FIG. 1.32 Focal lactational and pregnancy-like change in a nonpregnant and nonlactating woman. Se-
cretory changes are present in a lobule with acinar cells appearing variably vacuolated. A, Characteristic
laminated calcifications are present. B, Adjacent lobule is inactive. Hematoxylin and eosin stain.
Developmental Disorders 19
disorders of breast include those instances in which the undergoing corrective surgery for congenital heart
breast tissue is absent or hypoplastic or when accessory defects.92
breasts or nipples are present. Multiple additional types of injury or trauma, includ-
ing those related to dog bites,93 burns, and seat belts,
Amastia have resulted in restricted breast growth. A wide range
of nipple and breast abnormalities can be associated
Amastia is an extremely rare condition in which the with Becker hairy pigmented nevus.94
normal growth of the breast and nipple does not occur That trauma to the breast before thelarche resulted in
because of the complete failure of mammary line devel- failure of the breast to develop was apparently known to
opment at around 6 weeks in utero.83 This disorder has the fictional Amazonians (from a maz, meaning “with-
been known literally since biblical times, and its first out breast”). This nation was composed of independent
recorded reference is in the Song of Solomon: “We have women who had trauma inflicted to the right breast at a
a little sister, and she hath no breasts” (VIII:8). tender age to retard its development to gain competitive
Amastia is the complete failure of the breast to advantage in combat, mainly in archery.
develop. This is an exceedingly uncommon abnormality
and may be accompanied by a variety of developmental Polymastia
defects including those of shoulder and chest. Amas-
tia has also been reported in association with skeletal The milk line (see earlier) usually undergoes regression
(mainly of the ulnar rays of the hand) and renal defects in fetal life. Persistence of portions of accessory mam-
and is known to occur in siblings.84,85 mary glandular tissue along the milk line (polymastia)
Ulnar mammary syndrome (UMS) is a rare pleiotro- is encountered in up to 3% of adult women (and exists
pic autosomal disorder characterized by the classic com- in more than one location in about one third of these
bination of ulnar defects, mammary and apocrine gland cases). Polymastia is most commonly identified in the
hypoplasia, and genital abnormalities. Having mapped axilla. Other common locations include the inframam-
the UMS locus in one kindred to 12q23-24.1, Bamishad mary fold and the vulva.95 There appears to be a left-
and associates86 identified TBX3 as the causal gene for sided preponderance.
UMS. TBX3 is a member of the T-box gene family. The The entire spectrum of breast diseases from fibro-
products of the latter are transcription factors that have cystic changes to carcinoma can occur in the accessory
been shown to be crucial in the embryological develop- breast tissue in these locations.96,97 The most common
ment of various organs including the pituitary gland and presentation of polymastia is an axillary lump with pre-
the heart. menstrual pain or tenderness. Occasionally, bulky poly-
Poland sequence, a usually sporadic and unilateral mastia can cause a cosmetic problem. Polymastia, when
condition, represents the major differential diagnosis associated with a nipple, may function during preg-
of isolated amastia. The two conditions can be clini- nancy.98 Accessory breasts are reportedly more common
cally confused unless the absence of the pectoralis major in people of Asian ancestry and were noted to occur in
muscle is identified through ultrasound examination. 5.2% of Japanese women more than a century ago.99
Athelia tends to occur unilaterally as part of the Poland
sequence and bilaterally in certain types of ectoder- Supernumerary Nipple
mal dysplasias. Isolated absence of the breast could be
related to a vascular disruption sequence as suggested Supernumerary or accessory nipple (polythelia) is the
by Bianca and coworkers.87 most common mammary anomaly to be identified in
either sex. It occurs along the milk line and has been
Hypoplasia found in up to 2.4% of neonates.100,101
Because of deeper pigmentation, accessory nipples are
Hypoplasia refers to a major difference in breast size not always recognized for what they are and are com-
relative to the other, beyond the slight asymmetry that monly mistaken for nevi, acrochordon, or cutaneous
occurs normally. Hypoplasia of breast can be unilateral fibroma. Accessory nipples are most commonly encoun-
or bilateral, and it can occur as a congenital defect or it tered below the breast on the left chest and may occa-
may88 be associated with carcinoma.89 sionally enlarge during pregnancy or lactation. Multiple
Congenital mammary hypoplasia is associated with nipples have been reported to occur within one are-
hypoplasia of the ipsilateral pectoral muscle in 90% of ola.102 Histologically, the supernumerary nipples may
cases. Acquired mammary hypoplasia has been com- show any or all of the features typically observed in the
monly encountered in patients who had been irradiated area of nipple, including epidermal thickening, pilose-
in the mammary region before puberty for cutaneous baceous units, smooth muscle, and mammary ducts.103
hemangiomas (and also in those, in the distant past,
for secretion of witch’s milk). In general, the degree of Aberrant Breast Tissue
mammary hypoplasia correlates with the dose of radia-
tion.90,91 Surgical excision of the developing mammary The presence of mammary glandular parenchyma
gland should be performed only in cases in which a beyond the usual anatomical extent of the breast or
neoplasm is highly suspected. In this regard, appro- of the milk line is referred to as aberrant breast tissue.
priate caution should be exercised to avoid the breast Neither nipple nor areola is formed in the aberrant tis-
area in surgical incisions on the chest of female children sue, and the tissue remains clinically inapparent unless
20 Normal Breast and Developmental Disorders
it becomes the site of a physiologic (hypertrophic and/ may be attributed to lack of suckling, obesity, or hor-
or hyperplastic) or pathologic process. The mammary monal problems (including increased progesterone lev-
glands in aberrant breast tissue are histologically indis- els attributable to retained placenta). Galactorrhea is
tinguishable from those in the native breast and may generally defined as inappropriate secretion of milk in
undergo changes similar to those encountered in the the absence of pregnancy or nursing for a period of 6
orthotopic organ, including almost all physiologic and months (pituitary prolactinoma is the “usual suspect”
pathologic changes. The extremely rare occurrence of in such cases).
aberrant breast glandular tissue within axillary lymph Occasional reports of seemingly inexplicable mam-
nodes could be mistaken for metastatic carcinoma.104 mary abnormalities such as presence of aberrant breast
tissue in the posterior thigh of a male (mammae errati-
Macromastia cae) have been reported.109
5
“The use of natural cement was introduced
by Mr. Parker, who first discovered the properties
of the cement-stone in the Isle of Sheppy, and
took out a patent for the sale of it in 1796, under
the name of ‘Roman Cement.’”—Edward
Dobson, Rudiments of the Art of Building
(London: John Weale, 1854).
Transient Cornerstone
On 17 June 1825, the cornerstone of the monument was laid
with impressive ceremonies. As the colorful procession marched up
Bunker Hill to the stirring rendition of “Yankee Doodle” by the
drummer of Colonel William Prescott’s regiment, who, 50 years
before, had been in the battle, the rear of the procession was just
starting from distant Boston Common. The little Boston of over a
century ago was crowded with visitors who had come from places as
remote as South Carolina by stagecoach, sailing vessel, or on foot,
to hear the great speech of Daniel Webster, President of the Bunker
Hill Monument Association, and America’s first orator of the day.
Years earlier, Chaplain Joseph Thaxter had paid the last offices to
dying soldiers in the battle; now, he invoked God’s blessing on the
young American republic, as 40 veterans of the battle sat in a place
of honor.
The most important visitor, of course, was General Lafayette,
who, as a good Mason, spread the mortar on the stone when it was
laid by Most Worshipful Grand Master of the Grand Lodge of
Massachusetts, John Abbot. As the battle’s only monument up to
this date had been erected by the Masons, it was considered
appropriate that the permanent monument should have its
cornerstone laid with the Masonic ceremony. A little later, this
procedure was sharply criticized during the Antimasonic period,
6
which occurred before the monument was finished.
6
Joseph Warren, the outstanding hero of the
battle, was Grand Master of Freemasons for
North America.
7
Annual Report of the Smithsonian Institution,
1889.
8
For more data on the Granite Railway and
Gridley Bryant, see: Charles B. Stuart, Civil and
Military Engineers of America (New York: D. Van
Nostrand Company, Inc., 1871); and The First
Railroad in America (Boston: Privately printed for
Granite Railway Company, 1926).
9
George E. Ellis, History of the Battle of
Bunker’s (Breed’s) Hill (Boston: Lockwood,
Brooks and Company, 1875).
Hoc nomen est in æternum, et hoc
memoriale in generationem et generationem.
© R. Ruzicka 1915