world cancer report - iarc

Fig. 5.58 A “Healthy Women” group in a Nigerian
village discusses the benefits of condom usage to
prevent sexually transmitted diseases.
Fig. 5.59 An invasive cancer of the cervix, seen by
unaided visual inspection.
ed with sexual behaviour, such as multiple
sexual partners and early age at initiation
of sexual activity, simply reflect the probability
of being infected with HPV. HPV DNA
has been detected in virtually all cervical
cancer specimens [4, 5]. The association
of HPV with cervical cancer is equally
strong for the two main histological types:
squamous cell carcinoma and adenocarcinoma.
Over 100 HPV types have been
identified and about 40 can infect the genital
tract (Table 5.2 B). Fifteen of these
have been classified as high-risk (HPV
16,18, 31, 33, 35, 39, 45, 51, 52, 56, 58,
59, 68, 73, and 82), three as probably
high-risk (HPV 26, 53, and 66) and twelve
as low-risk (HPV 6, 11, 40, 42, 43, 44, 54,
61, 70, 72, 81, and CP6108) [1, 4, 6].
However, since only a small fraction of
HPV-infected women will eventually develop
cervical cancer, there must be other
exogenous or endogenous factors which,
acting in conjunction with HPV, influence
the progression from cervical infection to
cervical cancer. The assessment of the
role of these co-factors requires that the
216 Human cancers by organ site
Phylogenetic
Classification Epidemiologic Classification
central and strong effect of HPV is taken
into account. A review of studies fulfilling
this requirement has revealed that high
parity, smoking and long-term use of oral
contraceptives are co-factors that increase
the risk of cervical cancer. The role of
additional co-factors such as, herpes simplex
virus type 2 (HSV-2), Chlamydia trachomatis
infection, HIV and other causes
of immunosuppression, certain nutritional
deficiencies and genetic susceptibility, is
being investigated.
Detection
Early changes in the cervix, specifically cervical
intraepithelial neoplasia, can be
detected years before invasive cancer
develops, and this is the basis for the effectiveness
of cytological screening in secondary
prevention. The diagnosis of cervical
cancer is made on examination of cytological
samples taken from the endocervix with
a cytobrush and from the ectocervix with an
Ayre’s spatula (an ectocervical or a
Papanicolaou smear) [7]. A tissue specimen
may also be obtained by colposcopy and
biopsy, which may be the loop electrosurgical
excision procedure. In the course of
screening, false negatives are common so
all suspicious lesions are biopsied. If clinical
cancer is apparent, a punch biopsy specimen
is evaluated. Patients with abnormal
Pap smear and no visible lesion require colposcopy
and biopsy. The diagnosis of
microinvasive carcinoma is made from cone
biopsy or hysterectomy specimen pathology.
High risk Low risk
High risk 16, 18, 31, 33, 35, 39, 70
45, 51, 52, 56, 58, 59,
68, 82, 26, *53, *66*
Low risk 6, 11, 40, 42, 43, 44,
73 54, 61, 72, 81,
CP6108
* The epidemiologic classification of these types as probable high-risk types is based
on zero controls and one to three positive cases.
Table. 5.2 B. Phylogenetic and Epidemiologic Classification of HPV Types. Munoz et al. N Engl J Med 348:518-
527 (2003).
Cervical cancer does not tend to produce
any symptoms in the early stages. Only
when invasive disease is established do
symptoms such as vaginal bleeding, discharge
and pain become manifest.
Fig. 5.60 Histology of cervical intraepithelial neoplasia
stage I (CIN1). Note that dysplastic cells
(arrow) are confined to the lower third of the
epithelium.
EX
Fig. 5.61 A well-differentiated mucinous adenocarcinoma
(arrow) with a papillary architecture
developing from the endocervical mucosa, deep
under the normal squamous epithelium of the exocervical
mucosa (EX).