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Ductal Carcinoma
In Situ
SYED A. HODA
C h a p t e r
11
Historical Background
Ductal carcinoma
in situ
(DCIS), a term that is synonymous
with intraductal carcinoma, was defined pathologically early
in the 20th century largely by surgeons interested in the
microscopic study of tumors they encountered clinically.
In situ
, Latin for “in its place,” was first used as a term for
noninvasive malignancy by Broders in 1932.
1
Among the
first studies of DCIS were those of Warren,
2
a surgeon prac-
ticing in Boston. Warren’s
2
investigation of “abnormal invo-
lution” or cystic disease led him to conclude that carcinoma
might develop by transition from hyperplastic duct lesions:
“It is precisely under these conditions that we most fre-
quently find the combination of abnormal involution and
carcinoma. The transition stage is observed when the
epithelium no longer confines itself to the cyst cavity, but
breaks through the limiting membrane and infiltrates the
adjacent structures.”
Fundamental pathologic and clinical studies of prolifera-
tive ductal lesions of the breast were performed during the
early decades of the 20th century by two other surgeons, Sir
G. Lenthal Cheatle of King’s College Hospital, London, and
Joseph Colt Bloodgood (a disciple of Halsted, of the epony-
mous mastectomy fame) of Johns Hopkins University Hos-
pital, Baltimore, Maryland. The extent to which Bloodgood
and Cheatle influenced each other is difficult to ascertain
from their published articles that rarely contained references
to work other than their own. Contemporaries separated by
the Atlantic Ocean, which was figuratively much wider at the
time, they seem to have pursued independent routes in their
efforts to more clearly distinguish between benign and ma-
lignant lesions of the breast.
Cheatle drew heavily upon his own detailed studies
of whole-organ sections of the breast to examine the re-
lationships of various lesions to carcinoma as part of a
systematic exploration of pathologic processes in the breast.
Bloodgood’s approach was case oriented, dealing largely
with an analysis of patients under his personal care at Johns
Hopkins University over several decades. Because of his
concern with diagnostic and therapeutic problems prevail-
ing in the operating room at the time, much of Bloodgood’s
attention was directed to biopsy specimens. He was, there-
fore, able to relate the morphology of many lesions to clini-
cal follow-up, sometimes of the unresected breast.
Early descriptions of DCIS outlined the major structural
patterns of the disease that are recognized today. Micro-
papillary DCIS was illustrated by Cheatle
3
in 1920 and by
Bloodgood
4
in 1921, but this term was not used by either au-
thor. Bloodgood
5
also drew attention to the problem of dis-
tinguishing between “borderline” hyperplastic lesions and
DCIS. Cheatle referred to the micropapillary proliferation
as
laciform
and noted the “cartwheel” appearance of car-
cinoma in a nearby duct. Today, many would describe the
“cartwheel” focus as
cribriform
. Muir
6
attributed the term
cribriform to Schultz-Brauns’
7
article on breast carcinoma
contained in Henke and Lubarsch’s 1935 Handbook.
The existence of “comedo” (a term that generally refers
to high-grade solid type of DCIS with central necrosis)
and cribriform patterns of DCIS is readily apparent in
Bloodgood’s
8
picture, which illustrated a tumor classified
as a comedocarcinoma. The accompanying description
provides an interesting historical vignette:
In 1893, forty-one years ago, I assisted Dr. Halstead in ex-
ploring a clinically benign tumor of the breast. The patient
was sixty-seven years of age and had observed a small tumor
for about eleven months . . . . The moment we cut into and
pressed on it, there extruded from its surface many grayish-
white, granular cylinders, which I called at that time com-
edos. From the gross appearance the tumor was diagnosed
as malignant, and the radical operation was performed. The
nodes were not involved . . . [and] the patient lived nineteen
years after operation, dying at age eighty-six.
8
Bloodgood recognized two types of “comedoadenocar-
cinoma,” which he referred to as “pure comedoadenocar-
cinoma and comedoadenocarcinoma with areas of fully
developed cancer of the breast,” the former being entirely
intraductal and the latter partly invasive. He observed that
large tumors with gross comedo features were more likely
to be in the invasive category. Follow-up revealed that 30%
of node-negative patients with invasive comedoadenocarci-
noma developed metastases and died of the disease.
Bloodgood’s
8
1934 paper described a patient who had a
remarkable clinical course. One-year following treatment
by excision alone in 1896, the patient developed recurrent
carcinoma at the site of prior surgery. A radical mastec-
tomy was then performed. The lymph nodes were negative,
and the patient lived more than 15 years without additional
recurrence. Because of the apparent curability of the “pure
