Precancerous condition

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Definition

Precancerous disease is a condition that precedes the development of a malignant tumor - a standard morphological alteration of the tissue, in which the tumor process occurs statistically significantly more often than in healthy tissue of the same histogenetic origin and the same anatomical location.

A common feature of precancerous conditions is the acceleration of cell proliferation, making there a greater likelihood of a genetic error in the division of the initiated cell. Thus, proliferation becomes precancerous in:

metaplasias (caused by prolonged inflammatory irritation) - e.g. Barrett's esophagus, squamous metaplasia of the bronchial epithelium, leukoplakia in the oral cavity, intestinal metaplasia of the gastric mucosa
inflammation - e.g. pseudoepitheliomatous hyperplasia, formation of inflammatory hyperplastic polyps in the intestine in ulcerative colitis, HPV infection of the cervix
hyperplasia of hormone-dependent organs - endometrium, prostate, mammary gland

Some precancerous lesions also arise on the basis of congenital developmental abnormalities (e.g. cryptorchidism - undescended testes - in 90% of cases spermatogonia atrophy, in the remaining cases they turn into atypical cells that can malignantly transform, various hamartia, familial adenomatous polyposis, etc.)

Classification

stationary - low risk of malignant reversal, may not have a special microscopy or proliferative character from the beginning, this includes pseudoepitheliomatous hyperplasia around chronic skin ulcers, retinal testicular tissue at the beginning, Paget's disease
progressive - higher to high risk of malignant reversal, microscopic tissue and cell atypia, increased proliferation, this includes further development in retinal testicular tissue, cervical dysplasia, mammary gland, colon polyposis, bone marrow myelodysplastic syndrome
preinvasive - the highest degree of risk of malignant reversal (carcinoma in situ) - tissue and cellular atypia are identical to the malignant tumor, but the basement membrane is preserved, invasion of surrounding structures is missing and metastasis is missing, this includes ca situ in cervical, ductal or lobular epithelium ca in situ mammary glands, etc.

Precancerous changes can develop in any tissue, they are best characterized in epithelial tissue, where progressive and part of stationary precancerous lesions are referred to as dysplasia (loss of cell uniformity and oriented tissue arrangement - cells have different shape and size, more basophilic nuclei, shift of nucleoplasmic ratio in favor nuclei, more frequent mitoses - according to the degree of cellular atypia and the risk of transition to invasive carcinoma are divided into mild, moderate and severe), respectively. intraepithelial neoplasia (as well as dysplasia is divided into three stages, called I, II, III) - these can be:

cervical (CIN)
vaginal (VAIN)
vulvar (VIN)
oral (OIN)
prostate (PIN)

Perimaligní tissue changes

Changes in the environment of a growing tumor, which are the same as in precancerous lesion, can lead to successive primary multiplicity, even after the first tumor has healed.

Examples

Cervical intraepithelial neoplasia (CIN)

It is a dysplasia of the stratified squamous non-corneal epithelium of the cervix (portio vaginalis cervicis uteri) - they are distinguished here: stratum basale, spinosum et superficiale.

Microscopically, from a depth to the surface, the regularly stratified squamous epithelium is gradually replaced by undifferentiated cells resembling the epithelium of the basal layers.

According to the height of the disease, dysplasia is divided into mild (CIN I - affects less than 1/3 of the thickness), medium (CIN II - 2/3 of the thickness) and severe (CIN IIIa - almost the entire epithelium except the superficial flattened layer), when replacing the epithelium atypical cells in the whole range are already carcinoma in situ (CIN IIIb)

Cervical CINs are often associated with HPV (human papilloma virus) infection. This virus attacks skin and mucous membrane cells and undergoes either a lytic (non-transforming HPV) or lysogenic (transforming HPV) cycle:

LSIL (Low-grade Squamous Intraepithelial Lesions)

benign HPV forest (verruca vulgaris, condyloma accuminatum, laryngeal papillomatosis) + CIN I
corresponds to the lytic cycle, koilocytes are morphologically characteristic (large cells with pycnotic hyperchromic nucleus and perinuclear clearing)

HSIL (High-grade)

CIN II + CIN III + ca in situ
corresponds to the lysogenic cycle in which the viral genome integrates into the genome of the host cell, it can progress to the stage of invasive carcinoma

Barret's esophagus

Iron

It is a metaplasia of the distal esophageal mucosa (non-corneal layered squamous epithelium) into a single-layered cylindrical epithelium resembling the gastric mucosa (junction type - resembling a normal cardiac mucosa, corporate type - similar to the mucosa in the fundus and body of the stomach) or intestinal mucosa with goblet cells

The cause is long-term irritation of the mucosa during gastroesophageal reflux (reflux oesophagitis - in slippery hiatal hernia, weakness of the lower esophageal sphincter, increased intra-abdominal pressure) or decreased resistance of the gastric mucosa (smoking, alcohol).

It starts as inflammation (basal cell hyperplasia, stromal papilla elongation, inflammatory cellulization), erosions to ulcers, later dysplasia to metaplasia (which arises from pluripotent undifferentiated cells of the original esophageal glands) can form. This is a typical precancerous lesion that can lead to adenocarcinoma.

Intestinal metaplasia of the gastric mucosa

In chronic atrophic gastritis (with the disappearance of the gastric glands), the normal epithelium of the gastric mucosa (single-layered cylindrical of mucus-forming cells) can be replaced by epithelium of the intestinal type:

complete intestinal metaplasia - goblet cells, resorption cells (enterocytes), Paneth cells
incomplete intestinal metaplasia - instead of resorbing cells, the cells are mucus-forming, increases the risk of gastric adenocarcinoma

Links

References

STŘÍTESKÝ, Jan. Patologie. 1. vydání. 2001. https://www.wikiskripta.eu/w/Speci%C3%A1ln%C3%AD:Zdroje_knih/80-86297-06-3