Colorectal adenocarcinoma primarily affects elderly
people; increases by the sixth decade and reaches its peak
incidence between 60 and 70 years; mean age for both
gender is about 62-63[
4,
8,
11-
13]. Its incidence under
50 years reaches up to 20% as much and unless there is
an underlying condition with predisposition to colorectal
carcinoma, it is exceptionally rare under 40 years[
13].
Correspondingly, this study revealed similar findings, almost
akin to the given data.
Although proximal tumors seem to be increased during
the last few decades, approximately 50% of all carcinomas
occur in the rectosigmoid area as noted in the
current study[4,11,14]. However, tumors in cecum and
ascending colon were fairly less than expected. Likewise,
the proportion of well-differentiated tumors was remarkably
higher (28%) than poorly differentiated tumors (10%) on the contrary to general observation in which
almost the same incidence for both grades (about 15% to
20%) is shared[12]. Indubitably, stage is the most important
determinant in predicting the prognosis; and notably
localized (i.e. stage A) tumors seem to have a tendency to
increase compared to the decline in tumors with advanced
stages[13,15]. Unfortunately, in our series there was no
stage A tumor and stage B1 tumors were relatively low.
Consequently, tumors with advanced stages (and probably
with poor prognosis) constituted the majority; more
than half were stage B2. Another controversial and interesting
finding was the absence of lymph node metastasis
in six poorly differentiated tumors, which may partially
be explained by inadequate lymph node excision due to
surgical procedure or specimen handling.
Hormonal basis of colon cancer has also been a matter
of consideration besides genetic predisposition and
potential role of steroid hormones in both carcinogenesis
and tumor progression has been indicated[16,17]. When
equivalent age groups are regarded colon cancer is relatively
less frequent in females[4,5]. Nullipara women has a greater risk than multipara suggesting the protective effect
of increasing parity and hormone replacement therapy
is supposed to reduce development of colon cancer[6-11,18]. Moreover, coexistence of colon cancer and breast
cancer is relatively high[2,3]. Expressions of ER and PR
have been shown in several extramammary malignant
neoplasms including esophagus, stomach, lung, pancreas
and gallbladder[3,16,19-26]. ER expression in malignant
cells of gastric mucosa was proposed to be an independent
negative prognostic factor[21]; tamoxifen therapy was
found to be associated with prolonged survival[19].
Comparable studies, either biochemically or immunohistochemically,
revealed that both normal and malignant
colonic mucosal cells may express ER and/or
PR[9,24,27-37]. By biochemical methods, ER exhibited
a wide range, varying about 20% to 54% and while PR
expression was about 42%[9,24,31,34-39]. In addition,
ER and PR levels in colonic cancers are usually lower
than in mammary cancers and thus it may be difficult to detect immunohistochemical expression in gastrointestinal
cancers with lower levels[31,36,40]. The absence
of nuclear staining for both receptors in the current study
may also be explained by low levels of receptors probably
causing immunohistochemically undetectable expression.
In the largest immunohistochemical study composed of
156 colon carcinomas, none was positive for ER, and
only one case was reactive for PR while surrounding nontumoral
mucosa was stained with both receptors[9]. On
the other hand, ER and PR reactions were consecutively
found 32% and 23% by Kaklamanos et al.[34]. There are
also some conflicting reports regarding ER and PR status[32,35,36]. In terms of immunohistochemical staining
pattern nuclear staining of more than 5% of tumor cells
are generally accepted positive while cytoplasmic reaction
is considered non-specific. However, some reports
proposed that cytoplasmic ER staining should be considered[9]. No nuclear reaction for ER or PR was observed
in this study; six cases demonstrated cytoplasmic ER. In
part, this may be attributed to low receptor levels as previously stated. It may also be associated with other causes
such as cell characteristics affected by tissue processing,
immunohistochemical method, and perhaps clonality of
antibodies[9,35].
The potential importance of estrogen and progesterone
receptors is emphasized by evidence of protection by
hormone replacement therapy in women and, by a suggestion
that the anti-estrogen tamoxifen may enhance the risk
of colorectal cancer[9,10]. Patients with ER expression
are suggested to have a better survival rate[9,39]. This
observation was supported by animal models and anti-estrogenic
therapy was experimentally proved to reduce the
incidence of colon cancer[41,42]. Nevertheless, patients
receiving tamoxifen therapy for breast cancer have a relative
risk for colorectal carcinoma[17]. Moreover, mechanisms
other than receptor status may contribute to positive
tamoxifen effect in colorectal cancers[22]. Therefore, as
well as their detection, significance of ER and PR receptors
is still controversial in terms of both management and
prognosis.
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