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Rak podstawnokomórkowy - Prognozy i leczenie
Rak podstawnokomórkowy (carcinoma basocellulare)
Rak podstawnokomórkowy (carcinoma basocellulare) jest jednym z najczęstszych nowotworów skóry. To rak o miejscowej złośliwości, tzn. cechuje go powolny przebieg – rozrasta się miejscowo, naciekając podłoże i może wywołać zniszczenie tkanek otoczenia. Rak podstawnokomórkowy niezwykle rzadko powoduje przerzuty (jeden przerzut na 4000 raków). Częściej występuje u osób w starszym wieku. Objawem raka podstawnokomórkowego jest perełkowaty guzek o błyszczącej i gładkiej powierzchni. Guzek taki może się rozrastać odśrodkowo, tworząc większą zmianę. Raki podstawnokomórkowe zwykle są umiejscowione na twarzy – głównie na czole, w okolicach oczodołów i nosa, na plecach, rzadziej na kończynach górnych i dolnych. Wyróżnia się kilka odmian raków podstawnokomórkowych.
Fot. Rak podstawnokomórkowy (owrzodzenie w okolicy ciemieniowej skóry owłosionej głowy)
Histopathology
The characteristic feature seen in BCCs is islands or nests of basaloid cells, with cells palisading at the periphery in a haphazard arrangement in the centers of the islands. Each of these small pleomorphic cells is composed of a basophilic nucleus without a discernible nucleolus and scanty cytoplasm. Retraction artifact, also referred to as clefting, is usually is seen between the tumor and its surrounding stroma on paraffin-embedded sections. Mucin deposition may be present within the tumor and in the stroma around the tumor. Mitotic figures also may be present. Perineural growth, also known to as perineural invasion, can be an indicator of aggressive disease.
The histologic differential diagnosis may include trichoepithelioma or trichoblastoma. Various morphological subtypes have been defined, including nodular (solid), micronodular, superficial, cystic, infiltrating, infundibulocystic, pigmented, adenoid, sclerosing, metatypical, basosquamous, and fibroepitheliomatous (see Image. Pigmented Basal Cell Carcinoma). Mixed patterns of the above-listed types are also common.
The superficial subtype has multiple, small buds of basaloid cells descending from the epidermis with no dermal invasion.[8][9]
The nodular variant accounts for the majority of all cases. Nodular BCCs are composed of islands of cells with peripheral palisading and a haphazard arrangement of the more central cells. Ulceration may be present in larger lesions (see Image. Basal Cell Carcinoma, Nodular).[8][9]
The micronodular subtype has histologic features similar to those of the nodular subtype, except that it is composed of multiple small nodules. The micronodular type has a much greater risk for local recurrence than the solid type (see Image. Basal Cell Carcinoma with Micronodular and Morpheaform Features).[8][9]
The sclerosing (morphea-like) subtype is composed of spiky, basaloid, thin strands of cells that invade the dermis, surrounded by dense fibrous stroma. The histologic differential diagnosis may include microcystic adnexal carcinoma, desmoplastic trichoepithelioma, or metastatic cancer. When most of the tumor nests have spiky projections, the tumor may invade deeply, referred to as an infiltrative BCC (see Image. Basal Cell Carcinoma, Morpheaform).[9]
Epidemiology
BCC is the most common skin cancer in humans, with increasing incidence rates worldwide. Men generally have higher rates of BCC than women. BCC is more frequent in geographic locations with greater UV exposure, such as those at higher or lower latitudes. The most common predictor of BCC development is a history of squamous cell carcinoma (SCC) or BCC. Patients are at least ten times more likely to develop a second BCC if they have a BCC history compared to patients without a history of non-melanoma skin cancer.[5][6]
The mechanism of BCC formation via ultraviolet radiation is direct DNA damage, indirect DNA damage through reactive oxygen species, and immune suppression. Melanin absorbs UVA and indirectly damages DNA through free radicals. UVB directly damages DNA and RNA with a characteristic C/T or CC/TT transition. Ultraviolet exposure also causes dose-dependent suppression of the cutaneous immune system, impairing immune surveillance of skin cancer.
Literature suggests that the cells of origin from which BCC arises are immature, pluripotent cells associated with the hair follicle. Of note, the gene most often altered in BCCs is the PTCH1 gene. PTCH1 gene mutations occur in 70% of people with sporadic BCC. Ten percent to 20% of people with sporadic BCC have smoothened (SMO) mutations. Literature suggests that a sufficiently elevated expression level of Gli, by activating mutations of SMO or by homozygous inactivation of PTCH1 in a responding cell, is sufficient to drive the formation of BCC. The second most common mutation found in BCCs is in the P53 gene. Mutations in CDKN2A locus also have been detected in a smaller number of sporadic BCCs.