- Published on
Pathology - Cervical carcinoma
Definition • A malignant epithelial neoplasm originating in the cervix.
Epidemiology • Globally, cervical carcinoma represents the predominant malignancy of the female genital tract and the second most prevalent non-cutaneous malignancy in women, following breast cancer. • In developed nations, cervical carcinoma ranks as the third most common malignancy of the female genital tract, subsequent to endometrial and ovarian carcinoma. The reduced incidence is primarily due to the effectiveness of cervical screening programs.
Aetiology: Nearly all cases are attributable to high-risk HPV infection, specifically strains 16 and 18. Other risk factors encompass smoking and the use of oral contraceptives, perhaps contributing to the persistence of HPV in the cervix. Carcinogenesis: 80% of cases are squamous cell carcinomas originating from a precursor lesion termed cervical intraepithelial neoplasia (CIN). Twenty percent are adenocarcinomas that originate from a precursor lesion termed cervical glandular intraepithelial neoplasia (CGIN). HPV-induced cervical carcinogenesis is associated with the expression of two viral genes, E6 and E7. The E6 and E7 proteins interact with the tumor suppressor proteins, P53 and RB, facilitating their destruction. The dysfunction of these proteins leads to unregulated growth of the infected cells.
Presentation: Non-menstrual vaginal hemorrhage and secretion. Macroscopy • Observable tumors present as a solid mass on the cervix, which may exhibit exophytic or endophytic growth patterns.
Histopathology • Squamous cell carcinomas are distinguished by infiltrating irregular nests of malignant epithelial cells demonstrating squamous differentiation. Residual CIN may be observed next to diminutive tumors. Adenocarcinomas are defined by the infiltration of malignant epithelial cells that create glandular structures. Residual CGIN may be observed close to diminutive tumors.
Prognosis is contingent upon several criteria, including age, stage, and the presence or absence of lymphovascular invasion.
FIGO staging of cervical carcinomas
IA1: microscopic tumour with stromal invasion d 3mm in depth, d 7mm
in horizontal spread.
IA2: microscopic tumour with stromal invasion > 3mm in depth and not
more than 5mm with a horizontal spread d 7mm.
IB: any clinically visible lesion confi ned to the cervix or microscopic
lesion greater than IA1/2.
II: tumour invades beyond the uterus, but not to the pelvic side wall or
to the lower third of the vagina.
IIIA: tumour involves the lower third of vagina, no extension to the
pelvic side wall.
IIIB: tumour extends to the pelvic side wall and/or causes hydronephrosis
or non-functioning kidney.
IVA: tumour invades the mucosa of bladder or rectum and/or extends
beyond the true pelvis.
IVB: distant metastasis
Definition • A malignant epithelial neoplasm originating in the cervix.
Epidemiology • Globally, cervical carcinoma represents the predominant malignancy of the female genital tract and the second most prevalent non-cutaneous malignancy in women, following breast cancer. • In developed nations, cervical carcinoma ranks as the third most common malignancy of the female genital tract, subsequent to endometrial and ovarian carcinoma. The reduced incidence is primarily due to the effectiveness of cervical screening programs.
Aetiology: Nearly all cases are attributable to high-risk HPV infection, specifically strains 16 and 18. Other risk factors encompass smoking and the use of oral contraceptives, perhaps contributing to the persistence of HPV in the cervix. Carcinogenesis: 80% of cases are squamous cell carcinomas originating from a precursor lesion termed cervical intraepithelial neoplasia (CIN). Twenty percent are adenocarcinomas that originate from a precursor lesion termed cervical glandular intraepithelial neoplasia (CGIN). HPV-induced cervical carcinogenesis is associated with the expression of two viral genes, E6 and E7. The E6 and E7 proteins interact with the tumor suppressor proteins, P53 and RB, facilitating their destruction. The dysfunction of these proteins leads to unregulated growth of the infected cells.
Presentation: Non-menstrual vaginal hemorrhage and secretion. Macroscopy • Observable tumors present as a solid mass on the cervix, which may exhibit exophytic or endophytic growth patterns.
Histopathology • Squamous cell carcinomas are distinguished by infiltrating irregular nests of malignant epithelial cells demonstrating squamous differentiation. Residual CIN may be observed next to diminutive tumors. Adenocarcinomas are defined by the infiltration of malignant epithelial cells that create glandular structures. Residual CGIN may be observed close to diminutive tumors.
Prognosis is contingent upon several criteria, including age, stage, and the presence or absence of lymphovascular invasion.
FIGO staging of cervical carcinomas
IA1: microscopic tumour with stromal invasion d 3mm in depth, d 7mm
in horizontal spread.
IA2: microscopic tumour with stromal invasion > 3mm in depth and not
more than 5mm with a horizontal spread d 7mm.
IB: any clinically visible lesion confi ned to the cervix or microscopic
lesion greater than IA1/2.
II: tumour invades beyond the uterus, but not to the pelvic side wall or
to the lower third of the vagina.
IIIA: tumour involves the lower third of vagina, no extension to the
pelvic side wall.
IIIB: tumour extends to the pelvic side wall and/or causes hydronephrosis
or non-functioning kidney.
IVA: tumour invades the mucosa of bladder or rectum and/or extends
beyond the true pelvis.
IVB: distant metastasis
0 Comments
