Natural history of the cervical precancerous lesions and their evolutions
De Brux, J.
Clinical and Experimental Obstetrics and Gynecology 9(2): 106-112
1982
ISSN/ISBN: 0390-6663 PMID: 7160058 Document Number: 186517
The numerous epidemiologic studies confirm that precancerous cervical lesions and C.I.S. are dependent on multiple mutagenic factors (chemical, virus and other nucleo-proteins, radiations and co-carcinogens, hormones, infections). These studies demonstrate that cervical cancer is a "sexually transmissible" disease. The C.I.N. have a monomorphic mechanism. Their point of departure is the undifferentiated stem cells. According to the number of mitosis, their epidermoid differentiation and their capacity to mature, the morphology of these lesions will vary (C.I.N. 1, 2, 3, dysplasias: slight, moderate, severe, carcinoma in situ). The prognosis of these lesions is still unknown. Some are easily healed, others progress more or less rapidly, still others dramatically invade the stroma. These variables depend on the gravity of the DNA lesion caused by mutagen: some rapidly repair, others have a blocking effect on the DNA-synthesis and the cell dies, others present a definitive mutation able to be replicated. The DNA lesions induce an increase of the DNA-synthesis, and the cellular differentiation will be absent or delayed. The cytoplasmic protein-synthesis will also be modified (new glyco-proteins secretions: enzymes, globulins, angiogenesis factor, etc. . . .) favoring new cellular differentiation and/or invasive factors. So finally, the tumoral antigens induce a mediated cellular and humoral immunity of the host against his tumor. All these facts permit a better understanding of the histogenesis and the different evolutions of the precancerous cervical lesions.