Basal cell carcinoma (BCC) is the most common type of human cancer worldwide, and it is a subtype of nonmelanoma skin cancer that is on the rise due to an aging population and widespread sun exposure. Although the fatality rate from BCC is low, this tumor can cause significant morbidity and cost. Over time, BCC diagnosis has been greatly improved by dermoscopy and, more recently, reflectance confocal microscopy.
Although surgery is the first-line treatment for localized BCC, additional nonsurgical local therapeutic options exist. BCC etiology is determined by the interaction of the patient’s environmental and genetic features. The pathophysiology of this disease is thought to be caused by abnormal stimulation of the Hedgehog signaling system.
Notably, Hedgehog pathway inhibitors such as vismodegib and sonidegib have been utilized successfully as targeted therapy for advanced or metastatic BCC. Furthermore, the introduction of preventative interventions has been shown to be beneficial for in-patient treatment.
BCC is the most common type of skin cancer in humans, with a growing global incidence rate. Men are more likely than women to develop it. BCC is more common in areas with increased UV exposure, such as those at higher or lower latitudes. A history of squamous cell carcinoma (SCC) or BCC is the most common predictor of BCC development.
Patients with a BCC history are at least 10 times more likely to acquire a second BCC diagnosis than patients without a history of non-melanoma skin cancer. Estimated incidence rates have climbed between 20%-80% in the last 30 years. BCC incidence rates rise with age, with the median age of diagnosis being 68 years. BCC-related deaths are uncommon and occur mostly only in immunocompromised patients.
Metastatic BCC (1% of all cases) is more likely to be caused by malignancies with aggressive histopathologic characteristics. When a BCC spreads, it frequently involves regional lymph nodes, bone, the lungs, and the skin. The mean age of death is greater than in Squamous Cell Carcinoma, and the age-adjusted mortality rate is estimated to be 0.12 per 100 000. The risk of death is elevated for older individuals, the male gender (more than double the rate of occurrence compared to women), and for the white race phenotype.
Chronic sun exposure is one of the most important risk factors for BCC development. Between the time of UV exposure and clinical manifestation, BCCs often have a diagnostic delay of 15 to 20 years.Direct DNA damage, indirect DNA damage via reactive oxygen species, and immunological suppression are the mechanisms of BCC formation caused by UV exposure.
Melanin absorbs UVA and, as a result, causes free radical damage to DNA. UVB directly damages DNA and RNA by causing a C/T or CC/TT change. UV radiation also suppresses the cutaneous immune system in a dose-dependent manner, compromising immunological monitoring of skin cancer.
Exposure to UV light, particularly UVB wavelengths, is the most important etiological component in developing basal cell carcinoma, but UVA wavelengths can also play a role. A thorough evaluation of the literature, including meta-analysis and sensitivity analysis, reveals that outdoor workers have a much higher risk, with an inverse connection between occupational UV exposure and BCC risk with latitude.
Among white-skinned individuals, the Fitzpatrick skin type is a strong predictor of the relative risk of BCC. The cumulative UV dose and skin type are not the only predictors of BCC development; exposure duration and intensity, particularly in early infancy and adolescence, also play a role. Recreational sun exposure and the usage of indoor tanning salons are factors that contribute to the development of BCCs.
UV light therapy may potentially result in the development of BCC. Intermittent severe sun exposure, as evidenced by prior sunburns; a positive family history of BCC; a pale complexion, particularly red hair; facile sunburning (skin types I or II); and blistering sunburns as a youngster are all risk factors for the formation of BCC. UV light exposure is not the main risk factor — 20% of BCCs develop on non–sun-exposed skin.
Other factors that contribute to BCCs include ionizing radiation exposure, arsenic exposure, immunosuppression, and genetic susceptibility. Xeroderma pigmentosum, basal cell nevus syndrome (also known as Gorlin syndrome), Bazex–Dupre–Christol syndrome, and Rombo syndrome are several genetic syndromes linked to an elevated incidence of BCCs. There is no risk linked to nutrition, however, smoking appears to be a risk factor in women.
According to the literature, the cells of origin from which BCC develops are immature, pluripotent cells connected with the hair follicle. It is worth noting that the PTCH1 gene is the most frequently changed in BCCs. PTCH1 gene mutations are found in 70% of patients with sporadic BCC. Smoothened (SMO) mutations are found in 10% to 20% of patients with sporadic BCC.
According to the literature, a sufficiently high expression level of Gli in a responsive cell caused by activating mutations of SMO or homozygous inactivation of PTCH1 is sufficient to promote the formation of BCC. The P53 gene is the site of the second most prevalent mutation in BCCs. Mutations in the CDKN2A gene have also been found in a limited percentage of sporadic BCCs.
Basal Cell Carcinoma is very rarely fatal. BCC prognosis is mostly dependent on the risk of recurrence after treatment. This risk of recurrence is dependent on the location as well as the clinical and histopathological features of Basal Cell Carcinoma. The trunk and limbs are low-risk locations, whereas the cheeks, forehead, neck, scalp, and chin present an intermediate risk of recurrence.
Anatomical regions such as the nose, ears, centofacial, and periorificial areas are high-risk locations. A poor prognosis of the tumor is expected if a nodular Basal Cell Carcinoma larger than 1cm exists in a high-risk location, morpheaform, infiltrative or histologically aggressive, and recurrent tumors have a poor prognosis.
Intermediate prognosis is expected with recurrent superficial Basal Cell Carcinomas, with nodular BCC’s smaller than 1cm in high-risk locations or nodular BCCs smaller than 2cm in intermediate locations. Primary superficial BCCs, primary nodular BCCs under 2cm in low-risk locations, and primary nodular Basal Cell Carcinomas smaller than 1cm all indicate a good prognosis.
sonidegib is indicated for the treatment of basal cell carcinoma (advanced) in patients who have received radiation therapy
200 mg orally each day
The medication is continued until the disease reaches progression or toxicity is reduced
Dose Adjustments
In the case of hepatic or renal impairment, no dose reduction is required
If severe musculoskeletal adverse reactions are observed, interrupt the treatment
If 1st occurrence of the serum CK elevation is between 2.5 and 10 times the standard upper limit
Recurrent serum CK elevation should be between 2.5 and 5 times the standard upper limit
Restart the dose at 200 mg per day after the resolution of clinical symptoms and signs
Permanently discontinue the treatment if
serum CK elevation is more than 10 times the standard upper limit
Basal cell carcinoma (BCC) is the most common type of human cancer worldwide, and it is a subtype of nonmelanoma skin cancer that is on the rise due to an aging population and widespread sun exposure. Although the fatality rate from BCC is low, this tumor can cause significant morbidity and cost. Over time, BCC diagnosis has been greatly improved by dermoscopy and, more recently, reflectance confocal microscopy.
Although surgery is the first-line treatment for localized BCC, additional nonsurgical local therapeutic options exist. BCC etiology is determined by the interaction of the patient’s environmental and genetic features. The pathophysiology of this disease is thought to be caused by abnormal stimulation of the Hedgehog signaling system.
Notably, Hedgehog pathway inhibitors such as vismodegib and sonidegib have been utilized successfully as targeted therapy for advanced or metastatic BCC. Furthermore, the introduction of preventative interventions has been shown to be beneficial for in-patient treatment.
BCC is the most common type of skin cancer in humans, with a growing global incidence rate. Men are more likely than women to develop it. BCC is more common in areas with increased UV exposure, such as those at higher or lower latitudes. A history of squamous cell carcinoma (SCC) or BCC is the most common predictor of BCC development.
Patients with a BCC history are at least 10 times more likely to acquire a second BCC diagnosis than patients without a history of non-melanoma skin cancer. Estimated incidence rates have climbed between 20%-80% in the last 30 years. BCC incidence rates rise with age, with the median age of diagnosis being 68 years. BCC-related deaths are uncommon and occur mostly only in immunocompromised patients.
Metastatic BCC (1% of all cases) is more likely to be caused by malignancies with aggressive histopathologic characteristics. When a BCC spreads, it frequently involves regional lymph nodes, bone, the lungs, and the skin. The mean age of death is greater than in Squamous Cell Carcinoma, and the age-adjusted mortality rate is estimated to be 0.12 per 100 000. The risk of death is elevated for older individuals, the male gender (more than double the rate of occurrence compared to women), and for the white race phenotype.
Chronic sun exposure is one of the most important risk factors for BCC development. Between the time of UV exposure and clinical manifestation, BCCs often have a diagnostic delay of 15 to 20 years.Direct DNA damage, indirect DNA damage via reactive oxygen species, and immunological suppression are the mechanisms of BCC formation caused by UV exposure.
Melanin absorbs UVA and, as a result, causes free radical damage to DNA. UVB directly damages DNA and RNA by causing a C/T or CC/TT change. UV radiation also suppresses the cutaneous immune system in a dose-dependent manner, compromising immunological monitoring of skin cancer.
Exposure to UV light, particularly UVB wavelengths, is the most important etiological component in developing basal cell carcinoma, but UVA wavelengths can also play a role. A thorough evaluation of the literature, including meta-analysis and sensitivity analysis, reveals that outdoor workers have a much higher risk, with an inverse connection between occupational UV exposure and BCC risk with latitude.
Among white-skinned individuals, the Fitzpatrick skin type is a strong predictor of the relative risk of BCC. The cumulative UV dose and skin type are not the only predictors of BCC development; exposure duration and intensity, particularly in early infancy and adolescence, also play a role. Recreational sun exposure and the usage of indoor tanning salons are factors that contribute to the development of BCCs.
UV light therapy may potentially result in the development of BCC. Intermittent severe sun exposure, as evidenced by prior sunburns; a positive family history of BCC; a pale complexion, particularly red hair; facile sunburning (skin types I or II); and blistering sunburns as a youngster are all risk factors for the formation of BCC. UV light exposure is not the main risk factor — 20% of BCCs develop on non–sun-exposed skin.
Other factors that contribute to BCCs include ionizing radiation exposure, arsenic exposure, immunosuppression, and genetic susceptibility. Xeroderma pigmentosum, basal cell nevus syndrome (also known as Gorlin syndrome), Bazex–Dupre–Christol syndrome, and Rombo syndrome are several genetic syndromes linked to an elevated incidence of BCCs. There is no risk linked to nutrition, however, smoking appears to be a risk factor in women.
According to the literature, the cells of origin from which BCC develops are immature, pluripotent cells connected with the hair follicle. It is worth noting that the PTCH1 gene is the most frequently changed in BCCs. PTCH1 gene mutations are found in 70% of patients with sporadic BCC. Smoothened (SMO) mutations are found in 10% to 20% of patients with sporadic BCC.
According to the literature, a sufficiently high expression level of Gli in a responsive cell caused by activating mutations of SMO or homozygous inactivation of PTCH1 is sufficient to promote the formation of BCC. The P53 gene is the site of the second most prevalent mutation in BCCs. Mutations in the CDKN2A gene have also been found in a limited percentage of sporadic BCCs.
Basal Cell Carcinoma is very rarely fatal. BCC prognosis is mostly dependent on the risk of recurrence after treatment. This risk of recurrence is dependent on the location as well as the clinical and histopathological features of Basal Cell Carcinoma. The trunk and limbs are low-risk locations, whereas the cheeks, forehead, neck, scalp, and chin present an intermediate risk of recurrence.
Anatomical regions such as the nose, ears, centofacial, and periorificial areas are high-risk locations. A poor prognosis of the tumor is expected if a nodular Basal Cell Carcinoma larger than 1cm exists in a high-risk location, morpheaform, infiltrative or histologically aggressive, and recurrent tumors have a poor prognosis.
Intermediate prognosis is expected with recurrent superficial Basal Cell Carcinomas, with nodular BCC’s smaller than 1cm in high-risk locations or nodular BCCs smaller than 2cm in intermediate locations. Primary superficial BCCs, primary nodular BCCs under 2cm in low-risk locations, and primary nodular Basal Cell Carcinomas smaller than 1cm all indicate a good prognosis.
sonidegib is indicated for the treatment of basal cell carcinoma (advanced) in patients who have received radiation therapy
200 mg orally each day
The medication is continued until the disease reaches progression or toxicity is reduced
Dose Adjustments
In the case of hepatic or renal impairment, no dose reduction is required
If severe musculoskeletal adverse reactions are observed, interrupt the treatment
If 1st occurrence of the serum CK elevation is between 2.5 and 10 times the standard upper limit
Recurrent serum CK elevation should be between 2.5 and 5 times the standard upper limit
Restart the dose at 200 mg per day after the resolution of clinical symptoms and signs
Permanently discontinue the treatment if
serum CK elevation is more than 10 times the standard upper limit
Basal cell carcinoma (BCC) is the most common type of human cancer worldwide, and it is a subtype of nonmelanoma skin cancer that is on the rise due to an aging population and widespread sun exposure. Although the fatality rate from BCC is low, this tumor can cause significant morbidity and cost. Over time, BCC diagnosis has been greatly improved by dermoscopy and, more recently, reflectance confocal microscopy.
Although surgery is the first-line treatment for localized BCC, additional nonsurgical local therapeutic options exist. BCC etiology is determined by the interaction of the patient’s environmental and genetic features. The pathophysiology of this disease is thought to be caused by abnormal stimulation of the Hedgehog signaling system.
Notably, Hedgehog pathway inhibitors such as vismodegib and sonidegib have been utilized successfully as targeted therapy for advanced or metastatic BCC. Furthermore, the introduction of preventative interventions has been shown to be beneficial for in-patient treatment.
BCC is the most common type of skin cancer in humans, with a growing global incidence rate. Men are more likely than women to develop it. BCC is more common in areas with increased UV exposure, such as those at higher or lower latitudes. A history of squamous cell carcinoma (SCC) or BCC is the most common predictor of BCC development.
Patients with a BCC history are at least 10 times more likely to acquire a second BCC diagnosis than patients without a history of non-melanoma skin cancer. Estimated incidence rates have climbed between 20%-80% in the last 30 years. BCC incidence rates rise with age, with the median age of diagnosis being 68 years. BCC-related deaths are uncommon and occur mostly only in immunocompromised patients.
Metastatic BCC (1% of all cases) is more likely to be caused by malignancies with aggressive histopathologic characteristics. When a BCC spreads, it frequently involves regional lymph nodes, bone, the lungs, and the skin. The mean age of death is greater than in Squamous Cell Carcinoma, and the age-adjusted mortality rate is estimated to be 0.12 per 100 000. The risk of death is elevated for older individuals, the male gender (more than double the rate of occurrence compared to women), and for the white race phenotype.
Chronic sun exposure is one of the most important risk factors for BCC development. Between the time of UV exposure and clinical manifestation, BCCs often have a diagnostic delay of 15 to 20 years.Direct DNA damage, indirect DNA damage via reactive oxygen species, and immunological suppression are the mechanisms of BCC formation caused by UV exposure.
Melanin absorbs UVA and, as a result, causes free radical damage to DNA. UVB directly damages DNA and RNA by causing a C/T or CC/TT change. UV radiation also suppresses the cutaneous immune system in a dose-dependent manner, compromising immunological monitoring of skin cancer.
Exposure to UV light, particularly UVB wavelengths, is the most important etiological component in developing basal cell carcinoma, but UVA wavelengths can also play a role. A thorough evaluation of the literature, including meta-analysis and sensitivity analysis, reveals that outdoor workers have a much higher risk, with an inverse connection between occupational UV exposure and BCC risk with latitude.
Among white-skinned individuals, the Fitzpatrick skin type is a strong predictor of the relative risk of BCC. The cumulative UV dose and skin type are not the only predictors of BCC development; exposure duration and intensity, particularly in early infancy and adolescence, also play a role. Recreational sun exposure and the usage of indoor tanning salons are factors that contribute to the development of BCCs.
UV light therapy may potentially result in the development of BCC. Intermittent severe sun exposure, as evidenced by prior sunburns; a positive family history of BCC; a pale complexion, particularly red hair; facile sunburning (skin types I or II); and blistering sunburns as a youngster are all risk factors for the formation of BCC. UV light exposure is not the main risk factor — 20% of BCCs develop on non–sun-exposed skin.
Other factors that contribute to BCCs include ionizing radiation exposure, arsenic exposure, immunosuppression, and genetic susceptibility. Xeroderma pigmentosum, basal cell nevus syndrome (also known as Gorlin syndrome), Bazex–Dupre–Christol syndrome, and Rombo syndrome are several genetic syndromes linked to an elevated incidence of BCCs. There is no risk linked to nutrition, however, smoking appears to be a risk factor in women.
According to the literature, the cells of origin from which BCC develops are immature, pluripotent cells connected with the hair follicle. It is worth noting that the PTCH1 gene is the most frequently changed in BCCs. PTCH1 gene mutations are found in 70% of patients with sporadic BCC. Smoothened (SMO) mutations are found in 10% to 20% of patients with sporadic BCC.
According to the literature, a sufficiently high expression level of Gli in a responsive cell caused by activating mutations of SMO or homozygous inactivation of PTCH1 is sufficient to promote the formation of BCC. The P53 gene is the site of the second most prevalent mutation in BCCs. Mutations in the CDKN2A gene have also been found in a limited percentage of sporadic BCCs.
Basal Cell Carcinoma is very rarely fatal. BCC prognosis is mostly dependent on the risk of recurrence after treatment. This risk of recurrence is dependent on the location as well as the clinical and histopathological features of Basal Cell Carcinoma. The trunk and limbs are low-risk locations, whereas the cheeks, forehead, neck, scalp, and chin present an intermediate risk of recurrence.
Anatomical regions such as the nose, ears, centofacial, and periorificial areas are high-risk locations. A poor prognosis of the tumor is expected if a nodular Basal Cell Carcinoma larger than 1cm exists in a high-risk location, morpheaform, infiltrative or histologically aggressive, and recurrent tumors have a poor prognosis.
Intermediate prognosis is expected with recurrent superficial Basal Cell Carcinomas, with nodular BCC’s smaller than 1cm in high-risk locations or nodular BCCs smaller than 2cm in intermediate locations. Primary superficial BCCs, primary nodular BCCs under 2cm in low-risk locations, and primary nodular Basal Cell Carcinomas smaller than 1cm all indicate a good prognosis.
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