Invasive breast carcinoma - IARC

Fig. 1.83 Atypical ductal hyperplasia. Several
rounded calcifications, possibly including 1-2 “tea
cup” shaped calcifications are seen. Usually such
calcifications indicate benign changes. However,
the calcifications appear to follow two ducts.
Furthermore, a faint group of very fine microcalcifications
can barely be perceived.
not an early event in malignant transformation
or that they are largely restricted
to high grade DCIS. Increased levels of
cyclin D1 expression were re c e n t l y
described in 27-57% of ADH {1172,
3264}. Nuclear accumulation of the TP53
protein is absent in ADH and low grade
DCIS {1567}. Nearly 90% of ADH are
negative for high molecular weight cytokeratins
1/5/10/14 (clones CK34BetaE12
and D5/16 B4), an important feature in
separating ADH from UDH {1963,2126}.
Genetic alterations
Fifty percent of ADH cases share their
LOH patterns with invasive carcinomas
from the same breast, strongly supporting
a precursor relationship between
these lesions {1567}. LOH has been
identified frequently on chro m o s o m e s
16q, 17p, and 11q13 {1567,1570}. T P 5 3
mutations are restricted to affected members
of Li-Fraumeni families.
Fig. 1.84 Atypical ductal hyperplasia. A terminal
duct-lobular unit with dilated ductules that are
partly filled with a CK5/6 negative ductal proliferation
which on H&E had the characteristics of a low
grade DCIS. Note on the left side some cytokeratin
positive ductules.
Ductal carcinoma in situ (DCIS)
Definition
A neoplastic intraductal lesion characterized
by increased epithelial pro l i f e r a t i o n ,
subtle to marked cellular atypia and an
i n h e rent but not necessarily obligate tendency
for pro g ression to invasive bre a s t
c a n c e r.
ICD-O code 8500/2
Synonyms
Intraductal carcinoma, ductal intraepithelial
neoplasia (DIN 1C to DIN 3).
Risk of progression
DCIS is considered a precursor lesion
(obligate or non-obligate), with a relative
risk (RR) of 8-11 for the development
of invasive breast cancer {732,885}.
However, there is evidence that conservative
treatment (complete local eradication)
is usually curative (see below).
Epidemiology
A striking increase in the detection of
DCIS has been noted with the intro d u c-
tion of widespread screening mammography
and increasing awareness of bre a s t
cancer in the general population since
1983. The average annual increase in the
incidence rate of DCIS in the decade of
1973 to 1983 was 3.9% compared to
17.5% annually in the decade between
1983 to 1992, increasing from 2.4 per
100,000 women in 1973 to 15.8 per
100,000 in 1992 for women of all races,
an overall increase of 557% {794}. In the
US, data from the National Cancer
I n s t i t u t e ’s Surveillance, Epidemiology and
End Results (SEER) program noted that
the pro p o rtion of breast carcinomas diagnosed
as DCIS increased from 2.8% in
1973 to 14.4% in 1995 {794}. While close
to 90% of pre-mammography DCIS were
of the high grade comedo type, nearly
60% of mammographically detected
lesions are non-comedo and this perc e n-
tage is incre a s i n g .
I n t e re s t i n g l y, despite the more limited
surgical excisions, mortality from "DCIS"
has declined. Of women with DCIS
diagnosed between 1978 and 1983
( p re-mammographic era), 3.4% died
of breast cancer at 10 years, despite
having been treated by mastectomy in
the vast majority of cases. On the other
hand, only 1.9% of women diagnosed
with DCIS between 1984 and 1989 died
of breast cancer at 10 years, despite the
i n c reasing trend toward lumpectomy
{794}. Judging from the 10-year follow-
A
Fig. 1.85 Atypical ductal hyperplasia. A Two adjacent ducts showing partial cribriform involvement in a background of flat epithelial atypia. B Partial involvement
of a duct by a cribriform proliferation of uniform, rounded cells in the setting of a flat epithelial atypia. Microcalcification is also present.
B
Intraductal proliferative lesions
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