ICD-10 Specific code C53.1: Malignant neoplasm: Exocervix

Specific codes in ICD-10 are unique alphanumeric designations used to identify and categorize diseases, disorders, and conditions. They consist of 3-5 characters, including both letters and numbers, that provide a high level of detail and specificity.

Translations

Language Translation
Flag for English language  English Malignant neoplasm: Exocervix
Flag for French language  French Tumeur maligne de l'exocol

Hierarchical position

Level Code Title
1 II Neoplasms
2 C00-C97 Malignant neoplasms
3 C51-C58 Malignant neoplasms of female genital organs
4 C53 Malignant neoplasm of cervix uteri
5 C53.1 Malignant neoplasm: Exocervix

Indicated medicines

Active Ingredient Description
Bevacizumab

Bevacizumab binds to vascular endothelial growth factor (VEGF), the key driver of vasculogenesis and angiogenesis, and thereby inhibits the binding of VEGF to its receptors, Flt-1 (VEGFR-1) and KDR (VEGFR-2), on the surface of endothelial cells. Neutralising the biological activity of VEGF regresses the vascularisation of tumours, normalises remaining tumour vasculature, and inhibits the formation of new tumour vasculature, thereby inhibiting tumour growth.

Ifosfamide

Ifosfamide is an antineoplastic, a cytotoxic alkylating agent. It is a prodrug and shows no in vitro cytotoxic activity until activated by microsomal enzymes. The cytotoxic activity of ifosfamide (alkylation of the nucleophilic centres in the cells) is associated with the activated oxazaphosphorine ring hydroxylated at the C4 atom which interacts with DNA-DNA cross linking. This activity manifests itself by blocking the late S and early G2 phases of the cell cycle.

Tisotumab vedotin

Tisotumab vedotin is a tissue factor (TF)-directed antibody drug conjugate (ADC). The antibody is a human IgG1 directed against cell surface TF. TF is the primary initiator of the extrinsic blood coagulation cascade. The small molecule, MMAE, is a microtubule-disrupting agent, attached to the antibody via a protease-cleavable linker. Nonclinical data suggests that the anticancer activity of tisotumab vedotin is due to the binding of the ADC to TF expressing cancer cells, followed by internalization of the ADC-TF complex, and release of MMAE via proteolytic cleavage. MMAE disrupts the microtubule network of actively dividing cells, leading to cell cycle arrest and apoptotic cell death.