| Cervical
cancer is preceded by a group of precancerous lessions, termed CIN
which represent a continuum from mild dysplasia to carcinoma-in-situ
(CIN3). Studies of the natural history of cervical premalignant lesions,
show that if left untreated, cervical precancers of all grades can
spontaneously regress, persist or in minority of cases, progress to
the invasive stage.
Dr Hamidi's
study looked at clonality which is divided into two forms, polyclonal
where the cells in a group are genetically distinct and monoclonal
where the cells are genetic clones.
About one third
of CIN1 and 2 abnormalities progress to CIN3 or invasive disease.
This study demonstrated that monoclonality is the hallmark of cancer.
In her study Dr Hamidi looked at 21 cervical biopsies (18 SCC and
3 CIN3) and 23 cervical smears (4 invasive, 5 CIN3, 11 CIN2 and
3 CIN1). Sections cut from the biopsies were stained with haematoxylin
so that abnormal cells could be identified and removed. The cervical
smears were marked with a diamond pen to identify the areas with
abnormal cells before removing the cover slip, microbiopsies were
easier to identify than single cells. The cells were transferred
by using a glass pipette and analysed using polymerase chain reaction
(PCR).
The aim of this
study was to show that clonality can be used to predict the clinical
behaviour of CIN lesions.
|
Cervical
Smears
|
Number
of Cases
|
Monoclonal
|
Polyclonal
|
|
CIN
1
|
3
|
-
|
3
|
|
CIN
2
|
11
|
7
|
4
|
|
CIN
3
|
5
|
5
|
-
|
|
SCC
|
4
|
4
|
-
|
The above table
shows that Monoclonality correlates with aggressive CIN lesions.
Of the 18 biopsies showing SCC all were monoclonal and were positive
for HPV(esp type 16). There is also a correlation between clonality
and recurrent disease after treatment.
Dr. Hamidi believed that clonality analysis could be a valuable
tool in predicting the clinical behaviour of CIN and is trying to
find prognostic markers for this purpose.
|