Invasive breast carcinoma - IARC

Fig. 2.02 Serous adenocarcinoma. The sectioned
surface of the tumour shows two solid nodules
within a multiloculated cyst.
disease may spread through lymphatics
to either the inguinal or left supraclavicular
lymph nodes, which may be readily
palpable. It may advance into the pleural
cavity as a malignant effusion, usually on
the right side or bilateral, in which case
the lung bases exhibit dullness to percussion
and decreased breath sounds
and egophony to auscultation (stage IV).
Advanced intra-abdominal ovarian carcinomatosis
may also present with signs of
intestinal obstruction including nausea,
vomiting and abdominal pain.
Imaging
Due to its wide availability, ultrasound
(US) is the imaging method of choice to
assess an ovarian lesion and to determine
the presence of solid and cystic
elements. The distinction between benign,
borderline and malignant tumours
is generally not possible by US, either
alone or in combination with magnetic
resonance imaging (MRI) or computed
tomography (CT). None of these methods
has a clearly established role in preoperative
tumour staging. Surgical exploration
remains the standard approach
for staging {1116,1417,1522,1795,2898}.
Tumour spread and staging
About 70-75% of patients with ovarian
cancer have tumour spread beyond the
pelvis at the time of diagnosis {1770}.
Ovarian cancers spread mainly by local
extension, by intra-abdominal dissemination
and by lymphatic dissemination, but
rarely also through the blood stream. The
International Federation of Gynecology
and Obstetrics (FIGO) Committee on
Gynecologic Oncology is responsible for
the staging system that is used internationally
today {217}. The pTNM-system is
based on the postoperative pathological
staging for histological control and confirmation
of the disease. {51,2976}.
Histogenesis
The likely origin of ovarian surf a c e
e p i t h e l i a l - s t romal tumours is the
mesothelial surface lining of the ovaries
and/or invaginations of this lining into the
superficial ovarian cortex that form inclusion
cysts {838}.
Genetic susceptibility
Familial clustering
N u m e rous epidemiological investigations
of ovarian cancer have attempted to quantify
the risks associated with a positive
family history. Whereas ovarian cancer has
not been as extensively studied as bre a s t
c a n c e r, several studies point to familial
clustering. The relative risk of ovarian cancer
for first degree relatives varies fro m
1.94 to 25.5, the latter if both a mother and
sister are affected {1029,2557,2801}.
BRCA1/2
A number of specific genes have been
identified as playing a role. The most imp
o rtant of these, BRCA1 and BRCA2, are
discussed in chapter 8. In contrast to
b reast cancer in which only a minority of
the familial clustering could be explained
by known major susceptibility loci such
as BRCA1 and BRCA2, it is likely that the
majority of the familial risk of ovarian cancer
is explained by BRCA1 and to a lesser
extent BRCA2, MLH1 and MSH2.
Using statistical modelling and the re s u l t s
f rom BRCA1 and BRCA2 mutation testing
in 112 families with at least two cases of
ovarian cancer (allowing for insensitivity
of the mutation detection assay), BRCA1
and BRCA2 accounted for nearly all of
the non-chance familial aggregation {973}.
HNPCC
Ovarian cancer is a minor feature of the
h e re d i t a ry nonpolyposis colon cancer synd
rome caused by mutations in genes
associated with DNA base mismatch rep
a i r, the most frequent of which are M L H 1
and M S H 2.
A
Fig. 2.03 Serous adenocarcinoma. A The tumour is composed of closely packed papillae most of which lack fibrous cores lined by cells with atypical nuclei and
high nuclear to cytoplasmic ratios. B This poorly differentiated tumour shows relatively solid papillary aggregates without fibrovascular cores and scattered bizarre,
pleomorphic nuclei. Cherry red nucleoli are apparent in some nuclei.
B
118 Tumours of the ovary and peritoneum