What is precancer?

The morphogenesis of tumors, or the mechanism of their development in morphological terms, can be divided into precancer and the stage of tumor formation and growth.

Precancer is a change in an organ or tissue that develops into cancer with a higher probability than in unchanged organs or tissues. However, the presence of such a background as precancer does not mean that it will develop into cancer. Malignancy in precancer is observed in 0.1 - 5.0% of cases. Detection of such changes is not only theoretical but also of great practical importance. It allows identifying high-risk groups with respect to the possibility of developing a tumor in a particular organ, preventing the occurrence of a tumor and diagnosing it as early as possible.

Among precancer, morphologists distinguish the so-called background changes, manifested by dystrophy and atrophy, hyperplasia and metaplasia. This includes almost all chronic inflammatory specific and non-specific processes. For example, in the stomach - this is chronic gastritis of various etiologies; in the lungs - chronic bronchitis; in the liver - chronic hepatitis and cirrhosis; in the mammary gland - mastopathy; in the cervix - erosion and leukoplakia; in the thyroid gland - diffuse and nodular goiter, etc.

These changes, leading to structural reorganization of organs and tissues, become the basis for the emergence of foci of hyperplasia and dysplasia, which are considered as precancer.

Among precancers, the greatest importance has recently been given to cellular dysplasia (from the Greek dys - disorder and ptosis - formation), which always occurs in the depths of the dysregenerative process and is accompanied by insufficient and incomplete differentiation of tissue stem elements, and disruptions in the coordination between the processes of cell proliferation and maturation.

Depending on the severity of nuclear and cellular atypia, a three-stage gradation of dysplasia is most often used: mild (D1), moderate (D2), and severe (D3). The determining criterion for the degree of dysplasia is the severity of cellular atypia. As the degree of dysplasia increases, an increase in the size of the nuclei, their polymorphism, hyperchromia, coarsening and lumpy chromatin, an increase in the number and relative size of nucleoli, and increased mitotic activity are noted. Over time, dysplasia can regress, be stable, or progress. Mild dysplasia has virtually no relation to cancer, and the regression of mild and moderate dysplasia is observed everywhere. The more severe the dysplasia, the less likely it is to regress. The possibility of dysplasia turning into cancer in situ and, consequently, into cancer increases as its severity increases. Based on the fact that some precancerous conditions necessarily develop into cancer, while others do not, they are divided into obligatory and facultative precancer.

Obligate precancer, i.e. precancer that necessarily ends in cancer development, is more often associated with a hereditary predisposition. This is congenital polyposis of the colon, pigment xeroderma, neurofibromatosis (Recklinghausen's disease), retinal neuroblastoma, etc. Obligate precancer requires a mandatory set of preventive measures and even radical treatment, and patients with obligate precancer must be registered with an oncologist.

Optional precancer is a hyperplastic-dysplastic process, as well as some dysembryoplasia.

The so-called latent period of cancer, i.e. the period of existence of precancer before the development of cancer, is different for tumors of different localizations and is calculated in years (up to 30-40 years). The concept of "latent period of cancer" is applicable only to obligate precancer.

Thus, in early oncological pathology, four successive phases of cancer morphogenesis can be distinguished: I - precancerous conditions - facultative precancer; II - precancerous conditions - obligatory precancer; III - preinvasive cancer - carcinoma in situ and IV - early invasive cancer.

Tumor formation, or the transition of precancerous changes into cancer, has not been sufficiently studied. Based on experimental data, the following tumor development pattern can be assumed:

• violation of the regenerative process;
• precancerous changes characterized by hyperplasia and dysplasia;
• malignancy of proliferating cells that occurs in stages;
• the emergence of a tumor germ;
• tumor progression.

Recently, the theory of the "tumor field" has become widespread, revealing the staged nature of tumor development. According to this theory, multiple growth points - focal proliferates - arise in the organ, which constitute the "tumor field". Moreover, tumor transformation (malignancy) of focal proliferates occurs sequentially from the center to the periphery until the malignancy foci merge into one tumor node; however, primary multiple growth is also possible. After the "tumor field is spent", the tumor grows "on its own", it should be noted that this theory is controversial.