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Mensen met BCNS kunnen veel basaalcelcarcinomen (BCC’s) krijgen.
Een basaalcelcarcinoom is een vorm van huidkanker die over het algemeen goed te behandelen is. Bij BCNS verschillen deze carcinomen qua leeftijd en qua uiterlijk waarop ze ontstaan van de ‘normale’ BCC’s. Want normaliter komen BCC’s voornamelijk voor boven de 40 jaar, maar bij BCNS ontstaan ze al op jonge(re) leeftijd, meestal al vanaf het tiende tot het vijftiende levensjaar.
Gewoonlijk zijn BCC’s langzaam groeiende bobbeltjes die er meestal rood, bruin of huidkleurig uitzien. In het midden van deze bobbeltjes ontstaat na enige tijd een niet-genezend wondje met een korstje erop.
Bij BCNS zien de BCC’s er in eerste instantie anders uit. Ze lijken dan meer op kleine moedervlekken (naevi). Deze naevi kunnen in principe overal op het lichaam voorkomen, maar zijn meestal te vinden in de nek, hals en gezicht of op schouders, en in mindere mate op de romp. In een later stadium gaan deze vlekken meer op ‘gewone’ BCC’s lijken. Na de puberteit nemen de BCC’s in aantal toe.
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]
If you have areas of your skin that you’re concerned about, or if you have patches of skin that aren’t healing within three to six months, you should schedule a skin cancer screening with a dermatology provider. And if you’re an adult who’s never had a skin cancer screening before, you may want to consider the option.
“Roughly 75% of your sun exposure happens before you turn 21, which means skin cancer begins developing many years before you may notice it appearing on the surface of your skin,” Dr. Poblete-Lopez explains.
And as always, sun protection is key. Wearing the right sunscreen every day and wearing sun-protective clothing helps minimize your risk for skin cancer. Other strategies like avoiding direct sun exposure during peak hours when the sun is highest can also help.
“We always advocate for sun protection,” says Dr. Poblete-Lopez. “You should make a habit of using sun protection on your sun-exposed skin 24/7 much like you take the time to brush your teeth twice a day.”
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.