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Cervical cancer is defined as carcinoma in cervix where it is located at the lower, narrow
portion of the uterus and it joins with the top end of vagina. The major causative agent of
cervical cancer is human papillomavirus, HPV (Schlecht et al. 2001). More than 100 different
strains of HPV are known to exist. However, persistent infection of high risk-HPV(HPV 16
and 18) may only leads to invasive cervical cancer while low risk-HPV (HPV6 and 11) might
cause genital warts (papillomas) or condylomas. The virus is spread by contact with skin and
membranes but not body fluids.
There are some risk factors which contribute to the development of cervical cancer.
Women who are having sex at an early age, having multiple sexual partners and multiparity
are seems to more likely to be infected by HPV. Irregular or never have Pap smears
examination might cause 1 in 90 women to develop cervical cancer and 1 in 200 women die
of cervical cancer. Those who did not getting HPV vaccine will have higher chance to get
cancer-causing HPV compared to those who accepted HPV vaccination. Cervical cancer are
found to be quite common cancer in developing countries. This may due to the poor
economic status which will unable to obtain adequate and effective screening system (Rostad
et al. 2002). Taking oral contraceptive, smoking and weak immune system are possible risk
factors which leads to cervical cancer.
Early cervical cancer might not give any significant symptoms. However, several
symptoms may occur if there is no proper treatment given to the patient. The symptoms are
abnormal vaginal bleeding or spotting between periods, after sexual intercourse or after
menopause and continuous vaginal discharge (pale, watery, pink, brown, bloody or foulsmelling). Some patients complain that they experienced pain during sex. At advanced stage,
cancerous cells might spread to other parts in the pelvic cavity or even distant organs such as
bone, lung, intestine, liver and extremities. The symptoms of metastasis cervical cancer
include back pain, bone pain or fractures, fatigue/loss of appetite/ weight loss, swollen lymph
nodes, urine/feces leaking from vagina, pelvic pain, leg pain and swollen leg.
The development of cervical cancer is gradual and begins as a precancerous condition
called dysplasia. Two major types of cervical cancer are squamous cell cancer and
adenocarcinoma (glandular cell cancer). In addition, squamous cell cancer is the most
common type of cervical cancer. After the cervix infected by high risk-HPV, the cervix will
Definition
IA
IA1
IA2
IB
Clinical lesions confined to the cervix or preclinical lesions greater than stage IA.
IB1
IB2
II
The carcinoma extends beyond the cervix but has not extended to the pelvic wall;
the carcinoma involves the vagina but not as far as the lower third.
IIA
No obvious parametrial involvement, the cancer may have grown into the upper part
of the vagina .
IIA1
Tumor size of less than or equal to 4 cm with involvement of less than the upper
two-thirds of the vagina.
IIA2
Tumor size of more than 4 cm with involvement of less than the upper two-thirds of
the vagina.
IIB
IIB1
IIB2
III
The carcinoma has extended to the pelvic wall; on rectal examination, there is no
cancer-free space between the tumor and the pelvic wall; the tumor involves the
lower third of the vagina; all cases with a hydronephrosis or nonfunctioning kidney
are included unless they are known to be due to other causes.
IIIA
The cancer has spread to the lower third of the vagina but not to the pelvic wall.
IIIB
The cancer has grown into the pelvic wall. If the tumor has blocked the ureters (a
condition called hydronephrosis) it is also a stage IIIB.
IV
The carcinoma has extended beyond the true pelvis or has clinically involved the
mucosa of the bladder or rectum; a bullous edema as such does not permit a case to
be allotted to stage IV.
IVA
IVB
(Adapted from New gynecologic cancer staging: FIGO Cancer Committee. Int J Gynecol
Obstet 2009; 105:107)
References
1. Hausen, H.Z. 2002. Papillomaviruses and cancer: from basic studies to clinical
application. Nature Publishing Group. 2: 342-360
2. Franco, E.L., Duarte-Franco, E., Ferenczy, A. 2001. Cervical cancer: epidemiology,
prevention and the role of human papillomavirus infection. CMAJ. 164 (7): 1017-25
3. Frazer, I.H. 2008. HPV vaccines and the prevention of cervical cancer. Cancer
Therapeutics. 3: 43-48
4. Bosch, X., Harper, D. 2006. Prevention strategies of cervical cancer in the HPV
vaccine era. Gynecologic oncology. 103: 21-24
5. Cramer, D.W. 1974. The role of cervical cytology in the declining morbidity and
mortility of cervical cancer. Cancer. 34: 2018-2027
6. Stark, A., Gregoire, L., Pilarski, R., Zarbo, A., Gaba, A., Lancaster, W.D. 2008.
Human papillomavirus, cervical cancer and womens knowledge. Cancer Detection
and Prevention. 32: 15-22
7. Armstrong, E.P. 2010. Prophylaxis of cervical cancer and related cervical disease: A
review of the cost-effectiveness of vaccination against oncogenic HPV types. J
Manag Care Pharm. 16(3): 217-30
8. Schlecht, N.F., Kulaga, S., Robitaille, J., Ferreira, S., Santos, M., Miyamura, R.A.,
Duarte-Franco, E., Rohan, T.E., Ferenczy, A., Villa, L.L., Franco, E.L. 2001.
Persistent human papillomavirus infection as a predictor of cervical intraepithelial
neoplasia. JAMA.286: 3106-3114
9. Svare, E.I., Kjaer, S.K., Smits, H.L., Poll, P., Tjong-A-Hung, S.P., Schegget, J. 1998.
Risk factors for HPV detection in Archival Pap Smears. A population-based study
from Greenland and Denmark. European Journal of Cancer. 34(8): 1230-1234
10. Omar, Z.A., Ali, Z.M, Tamin, N.S.I. 2006. Malaysian cancer statistics-Data and figure
peninsular Malaysia 2006. National Cancer Registry, Malaysia. 1-136
11. Lomalisa, P., Smith, T.S., Guidozzi, F. 2000. Human immunodeficiency virus
infection and invasive cervical cancer in South Africa. Gynecologic Oncology. 77:
460-463