BASAL CELL CARCINOMA AND ITS VARIANTS. !
CARCINOMA BASOCELULAR Y SUS VARIANTES. !
PUBLICADO 2017-ACTUALIZADO 2025
EDITORIAL ENGLISH
==================
Hello friends of the network, DERMAGIC today with the fascinating
topic: BASAL CELL CARCINOMA.
Long ago, it was believed that this tumor did not occur in children, that it was not related to viruses, that it was benign, that it did not produce metastases, that it was not related to genetics (HLA antigens).
In this 2025 update, we will decipher these mysteries:
HISTORY:
BASAL CELL CARCINOMA (BCC) was first described by the Irish surgeon Arthur Jacob in 1827, who reported a peculiar ulcer-like lesion affecting the eyelid and other facial areas.
Before that, ancient evidence can be found in Egyptian papyri dating back thousands of years, where these lesions are referred to as "touch me not," due to their refusal to heal and recurrence.
In 1903, the German pathologist Odon Krompecher made the first microscopic description of the lesion and proposed the term "basal cell epithelioma" due to its resemblance to epidermal basal cells.
During the 20th century, its cellular origin and the behavior of the lesions became clearer, and it was recognized as a "semi-malignant" tumor due to its slow growth and rare metastasis.
In 1974, the WHO ratified the name BASAL CELL CARCINOMA (EPITHELIOMA) (BCC).
Long ago, it was believed that this tumor did not occur in children, that it was not related to viruses, that it was benign, that it did not produce metastases, that it was not related to genetics (HLA antigens).
In this 2025 update, we will decipher these mysteries:
HISTORY:
BASAL CELL CARCINOMA (BCC) was first described by the Irish surgeon Arthur Jacob in 1827, who reported a peculiar ulcer-like lesion affecting the eyelid and other facial areas.
Before that, ancient evidence can be found in Egyptian papyri dating back thousands of years, where these lesions are referred to as "touch me not," due to their refusal to heal and recurrence.
In 1903, the German pathologist Odon Krompecher made the first microscopic description of the lesion and proposed the term "basal cell epithelioma" due to its resemblance to epidermal basal cells.
During the 20th century, its cellular origin and the behavior of the lesions became clearer, and it was recognized as a "semi-malignant" tumor due to its slow growth and rare metastasis.
In 1974, the WHO ratified the name BASAL CELL CARCINOMA (EPITHELIOMA) (BCC).
CLINICAL FEATURES:
The lesion presents clinically as a pearly nodular or plaque-like lesion with a translucent, pearly, ridged border with telangiectasias, which may ulcerate over time.
Typically, the lesion most frequently occurs in sun-exposed areas such as the head, neck, and face, especially in white people and those over 60 years of age.
This criterion for people over 60 years of age was clarified over time. Today, BASAL CELL CARCINOMA can occur in adolescents, young adults, and even children, and also in people of color, although less frequently.
The growth of the lesions is slow and localized, and it has been estimated that it takes 9 to 11 years to metastasize, even though it causes significant destruction of surrounding tissues. This is why it is considered "semi-malignant."
The most important risk factor is prolonged exposure to ultraviolet light, i.e., sunlight: common in people who work with excessive sun exposure: fishermen, farmers, mountaineers, athletes, etc.
CLASSIFICATION: (See photos)
BASAL CELL CARCINOMA is classified according to its clinical appearance and specific histological pattern for each type, which determines its aggressiveness and therapeutic management.
1.) NODULAR: This is a nodule-shaped lesion, or papule (at first), raised with telangiectasias and a pearly appearance.
2.) SUPERFICIAL EXTENSION or SPREAD: This is a macule that later evolves into an erythematous plaque with irregularly bordered scales, which slowly spreads centrifugally (laterally).
3.) MORPHEIFORM (sclerodermiform or atrophic): It presents as a plaque that is hardened to the touch, somewhat depressed (sunken), scarred, brown, infiltrated, and more aggressive than the previous ones.
4.) ULCERATED: The typical lesion is a crusted ulcer; this variant is generally the chronic evolution of all BASAL CELL CARCINOMAS, meaning they tend to ulcerate over time if not treated promptly.
5.) PIGMENTED: The lesion is a plaque similar to classic BCC, but the border is hyperpigmented, and the entire lesion may even appear pigmented.
6.) HYPERPIGMENTED OF PINKUS: With dark pigmentation, it may resemble melanoma.
PINKUS EPITHELIOMA, also known as PINKUS FIBROEPITHELIOMA, is a rare variant of basal cell carcinoma (BCC) with distinctive clinical and histopathological features.
It was first described by Hermann Pinkus in 1953, who called it a "premalignant fibroepithelial tumor."
Originally considered a separate entity from BCC, it is now accepted as a variant of BASAL CELL CARCINOMA.
Although there is still controversy in the scientific community and literature, some claim that the lesion is similar to a TRICHOBLASTOMA, a benign tumor originating in the hair follicle.
It usually presents in adults between 40 and 60 years of age, with no marked preference for male or female sex. It is usually located primarily in the lumbosacral region. However, like BASAL CELL CARCINOMA, it also presents on the head, abdomen, extremities, and rarely on the genitals.
Clinically, there are two types: it presents as a single, pedunculated, or sessile nodular lesion, 1.) skin-colored or pinkish, and 2.) the pigmented form, also pedunculated or plaque-like, with a smooth and sometimes eroded surface, very similar to pigmented BCC (see photo).
The main difference with pigmented basal cell carcinoma is in the biopsy of the lesion, which shows thin, elongated cords of basaloid cells that anastomose, forming a typical "honeycomb" structure. Immunohistochemical markers are also used to differentiate it.
SIGNS OF MALIGNANCY IN BASAL CELL CARCINOMA:
1.) Rapid growth: The lesion, which usually grows slowly, evolves into "violent" growth over the course of months.
2.) Bleeding: BCC usually does not bleed, except for the ulcerated type. Frequent bleeding or bleeding with minor trauma is a sign of a slow progression.
3.) Increased telangiectasias: Telangiectasias are small blood vessels that appear on the surface of the lesion and increase considerably in size over time.
4.) Color changes: Changes in color appear on the lesion, with bluish, blackish, or brown areas.
5.) Appearance of indurated plaques: with irregular borders.
6.) Time of progression: A BASAL CELL CARCINOMA that has progressed for more than 9 to 11 years without treatment can metastasize or evolve into SQUAMOUS CELL CARCINOMA, which is malignant.
TREATMENTS:
Treatment of BASAL CELL CARCINOMA (BCC) depends primarily on tumor risk (low vs. high), the location of the lesion, its size, the histological type of the tumor, and the patient's characteristics.
1.) SURGICAL TREATMENTS:
A. Standard surgical excision with a scalpel: This is the first-line treatment for most BCCs, especially low-risk ones. The recurrence rate is low (around 3-4%). Margins of at least 1 cm, even 2 cm, are recommended for well-defined lesions.
B. Mohs micrographic surgery: This type of surgery is performed in the operating room and is indicated for high-risk and recurrent BCCs located in anatomically critical areas (e.g., the facial "H zone") or with poorly defined borders.
It involves removing the primary tumor, which is "frozen" with liquid nitrogen. Incisions are made in the operating room. A specialized pathologist observes them under a microscope and determines the extent of the excision, reaching healthy skin.
This method allows for intraoperative evaluation of margins and maximizes tissue preservation, with recurrence rates similar to or lower than standard excision (scalpel) in high-risk facial tumors.
2.) NON-SURGICAL TREATMENTS:
A. Electrodesiccation and curettage: Useful for superficial or small nodular BCCs in non-critical areas. The cure rate is high, making it one of the most commonly used methods for small lesions.
B. Cryotherapy: Less commonly used, it consists of cooling the tumor with liquid nitrogen, placing a temperature-measuring needle underneath it until the cooling point reaches a temperature between -40 and -60 degrees Celsius.
This causes the destruction of tumor cells. Recurrence in these cases is estimated at 22%, and cosmetic results are variable, as the main side effects are blistering (frost burns) at the procedure site, which can leave scarring.
C. Radiotherapy: An alternative for patients who are not candidates for surgery, especially for tumors located in areas where surgery would be disfiguring or for elderly patients.
The recurrence rate is comparable to surgery in low-risk BCCs, but cosmetic results may be inferior. There is also a risk of telangiectasias and loss of skin color (radiation dermatitis).
D. Photodynamic therapy (PDT): Indicated for superficial and some low-risk nodular BCCs. It uses photosensitizing agents (e.g., methylaminolevulinate, known as MAL) and ultraviolet light to destroy the tumor.
How does this method work? Methylaminolevulinate (MAL) is a photosensitizing agent and a precursor to protoporphyrin IX (PpIX), a substance that selectively accumulates in tumor cells.
This is applied topically to the lesions in the form of a cream, left on for 2 to 3 hours, and then exposed to red light with a wavelength between 570 and 670 nm. The light activates protoporphyrin IX (PpIX), producing the release of free radicals that cause the destruction of tumor cells.
It has a higher recurrence rate than surgery, but better cosmetic results.
3.) TOPICAL TREATMENTS:
A. Imiquimod 5%: Approved for use in superficial and some low-risk nodular BCCs. It consists of applying the cream to the lesion for 6 weeks. Application is NOT USUALLY DAILY; it can be every 2 or 3 days. The recurrence rate is higher than surgery, but the cosmetic result is acceptable.
B. 5-Fluorouracil: This medication comes in 2.5% cream and 5% ointment forms and represents a topical alternative for superficial BCCs, with lower efficacy than surgery.
It can be used in COMPOUND preparations and alternated with IMIQUIMOD, using the following regimen: 3 days IMIQUIMOD, 2 days 5-FLUOROURACIL.
4.) SYSTEMIC TREATMENTS (advanced disease):
A.- Hedgehog pathway inhibitors (Vismodegib, Sonidegib): Approved by the FDA in the USA for locally advanced BCC and metastatic BCC in which surgery or radiation therapy is not appropriate or indicated.
The Hedgehog pathway is a cell signaling pathway essential for embryonic development and cell maintenance. In most basal cell carcinomas, this pathway is activated, causing uncontrolled tumor cell growth.
What are Vismodegib and Sonidegib, and how do they work?
These are two oral medications and are first-line in these cases, although they present significant adverse effects such as muscle spasms, hair loss, gastrointestinal discomfort, and taste disturbances.
- Vismodegib: oral capsules, usually at a dose of 150 mg.
- Sonidegib: oral capsules, typically at a dose of 200 mg.
Both inhibitors work by blocking a protein called Smoothened (SMO), thereby blocking the Hedgehog pathway and thereby slowing tumor proliferation and growth.
B.- Immunotherapy (Cemiplimab, PD-1 inhibitor):
Cemiplimab is an immunoglobulin G4 monoclonal antibody that blocks the PD-1 (programmed cell death protein 1) receptor on T cells of the immune system.
When this PD-1 blockade occurs, it prevents tumor cells from diminishing or "turning off" the immune response, thereby reactivating the immune system to detect and destroy tumor or cancer cells.
It is indicated for adult patients with locally advanced or METASTATIC CARCINOMA (BCC), in whom radiotherapy is not feasible, or who cannot tolerate Hedgehog pathway inhibitors (Vismodegib, Sonidegib).
This immunotherapy is the first approved for the treatment of advanced BCC in these settings.
Administration and Dosage:
Cemiplimab comes in vials under the brand name LIBTAYO and is administered by intravenous infusion, usually 350 mg every 3 weeks.
Treatment can be extended for up to almost 2 years (93 weeks) or until disease progression or significant toxicity occurs.
The most common side effects of this therapy are musculoskeletal pain, fatigue, itching, diarrhea, and rashes. Severe organ effects may also occur in the intestines, lungs, kidneys, skin, and endocrine glands due to immune imbalance.
CONCLUSIONS:
Basal cell carcinoma is the MOST COMMON SKIN CANCER, and if treated early, the risk of malignancy is low. It can occur in both women and men, mostly adults.
Sun exposure is a determining factor in its development, and in some cases, an association with Histocompatibility Antigens (HLA) has been described, which could indicate a genetic predisposition.
The time to malignancy is long, between 9 and 11 years, but if you have a suspicious lesion, consult your doctor as soon as possible.
A. Imiquimod 5%: Approved for use in superficial and some low-risk nodular BCCs. It consists of applying the cream to the lesion for 6 weeks. Application is NOT USUALLY DAILY; it can be every 2 or 3 days. The recurrence rate is higher than surgery, but the cosmetic result is acceptable.
B. 5-Fluorouracil: This medication comes in 2.5% cream and 5% ointment forms and represents a topical alternative for superficial BCCs, with lower efficacy than surgery.
It can be used in COMPOUND preparations and alternated with IMIQUIMOD, using the following regimen: 3 days IMIQUIMOD, 2 days 5-FLUOROURACIL.
4.) SYSTEMIC TREATMENTS (advanced disease):
A.- Hedgehog pathway inhibitors (Vismodegib, Sonidegib): Approved by the FDA in the USA for locally advanced BCC and metastatic BCC in which surgery or radiation therapy is not appropriate or indicated.
The Hedgehog pathway is a cell signaling pathway essential for embryonic development and cell maintenance. In most basal cell carcinomas, this pathway is activated, causing uncontrolled tumor cell growth.
What are Vismodegib and Sonidegib, and how do they work?
These are two oral medications and are first-line in these cases, although they present significant adverse effects such as muscle spasms, hair loss, gastrointestinal discomfort, and taste disturbances.
- Vismodegib: oral capsules, usually at a dose of 150 mg.
- Sonidegib: oral capsules, typically at a dose of 200 mg.
Both inhibitors work by blocking a protein called Smoothened (SMO), thereby blocking the Hedgehog pathway and thereby slowing tumor proliferation and growth.
B.- Immunotherapy (Cemiplimab, PD-1 inhibitor):
Cemiplimab is an immunoglobulin G4 monoclonal antibody that blocks the PD-1 (programmed cell death protein 1) receptor on T cells of the immune system.
When this PD-1 blockade occurs, it prevents tumor cells from diminishing or "turning off" the immune response, thereby reactivating the immune system to detect and destroy tumor or cancer cells.
It is indicated for adult patients with locally advanced or METASTATIC CARCINOMA (BCC), in whom radiotherapy is not feasible, or who cannot tolerate Hedgehog pathway inhibitors (Vismodegib, Sonidegib).
This immunotherapy is the first approved for the treatment of advanced BCC in these settings.
Administration and Dosage:
Cemiplimab comes in vials under the brand name LIBTAYO and is administered by intravenous infusion, usually 350 mg every 3 weeks.
Treatment can be extended for up to almost 2 years (93 weeks) or until disease progression or significant toxicity occurs.
The most common side effects of this therapy are musculoskeletal pain, fatigue, itching, diarrhea, and rashes. Severe organ effects may also occur in the intestines, lungs, kidneys, skin, and endocrine glands due to immune imbalance.
CONCLUSIONS:
Basal cell carcinoma is the MOST COMMON SKIN CANCER, and if treated early, the risk of malignancy is low. It can occur in both women and men, mostly adults.
Sun exposure is a determining factor in its development, and in some cases, an association with Histocompatibility Antigens (HLA) has been described, which could indicate a genetic predisposition.
The time to malignancy is long, between 9 and 11 years, but if you have a suspicious lesion, consult your doctor as soon as possible.
The facts are in the references...
Greetings to all.
Dr, Jose Lapenta.
EDITORIAL ESPAÑOL
=================
Hola amigos de la red, DERMAGIC hoy con el apasionante tema: CARCINOMA BASO CELULAR.
Dr, Jose Lapenta.
Dr. José M. Lapenta.
EDITORIAL ESPAÑOL
=================
Hola amigos de la red, DERMAGIC hoy con el apasionante tema: CARCINOMA BASO CELULAR.
Hace mucho tiempo se creía que este tumor NO se presentaba en
NIÑOS, que NO tenia relación con VIRUS, que era BENIGNO, que que
NO producía METÁSTASIS., que NO tenia relación con la GENÉTICA
(Antígenos HLA).
En esta actualización año 2025, vamos a descifrar estas
incógnitas:
El CARCINOMA BASOCELULAR (CBC) fue descrito por primera vez por el cirujano Irlandés Arthur Jacob en 1827, quien reportó una lesion tipo úlcera peculiar que afectaba el párpado y otras áreas faciales.
Antes de eso, se encuentran indicios ancestrales en papiros de Egipto,
de hace miles de años, donde se hacen referencias a estas lesiones bajo
los nombres "no me toques", por su rechazo a la curación y
recurrencia.
En 1903, el alemán Odon Krompecher (patólogo), hizo la primera descripción microscópica de la lesion, y propuso
el término de "epitelioma basocelular" por su semejanza con las células
basales epidérmicas.
En el transcurso del siglo XX, se clarificó su origen celular y también
se aclaro el comportamiento de la las lesiones, siendo reconocido como
un tumor
"semi-maligno" debido a su lento crecimiento y rara metástasis.
Para 1974, la OMS ratifica el nombre de CARCINOMA o EPITELIOMA BASOCELULAR (CBC).
CARACTERÍSTICAS CLÍNICAS:
La lesion se presenta clínicamente como una lesion nodular perlada o
tipo placa con un borde en rodete, traslucido y perlado con
telangiectasias, la cual puede ulcerarse con el tiempo.
Típicamente la lesion se presenta con mayor frecuencia en zonas
expuestas al sol como cabeza, cuello y rostro, especialmente en personas
blancas y mayores de 60 años.
Este criterio de personas mayores de 60 años, fue aclarado con el tiempo, hoy dia el CARCINOMA BASOCELULAR, se puede presentar en adolescentes, adultos jóvenes e incluso niños, también en personas de color, ciertamente con menor frecuencia.
El crecimiento de las lesiones es lento y localizado, y se ha estimado un tiempo que oscila entre 9 a 11 años para producir metastasis, aun produciendo destrucción importante de los tejidos circundantes, es por ello que se le considera "semi maligno".
El factor de riesgo mas importante es la exposición prolongada a la luz ultravioleta, es decir luz solar: frecuente en personas que trabajan con una
exposición solar excesiva: pescadores agricultores, alpinistas,
deportistas, etc.
CLASIFICACIÓN: (Ver fotos)
CLASIFICACIÓN: (Ver fotos)
El CARCINOMA BASOCELULAR se clasifica según su aspecto clínico y patron
histológico especifico para cada tipo, y de ello depende su agresividad
y manejo terapéutico.
1.) NODULAR:
Es una lesion en forma de nódulo, o papula (al comienzo), elevada con
telagiectasias y aspecto perlado.
2.) EXTENSION SUPERFICIAL: Es una macula que luego evoluciona a placa eritematosa con escamas de borde irregular, la cual se extiende lentamente en forma centrifuga (hacia los lados).
2.) EXTENSION SUPERFICIAL: Es una macula que luego evoluciona a placa eritematosa con escamas de borde irregular, la cual se extiende lentamente en forma centrifuga (hacia los lados).
3.) MORFEIFORME:
(esclerodermiforme o atrófico): Se presenta como una placa endurecida al
tacto, algo deprimida (hundida), de aspecto cicatricial, color pardo,
infiltrada, siendo mas agresivo que los anteriores.
4.) ULCERADO: La lesion típica es una ulcera con costras; por lo general esta
variante es la evolución crónica de todos los CARCINOMAS BASOCELULARES,
es decir con el tiempo tienden a ulcerarse si no son tratados a
tiempo.
5.) PIGMENTADO: La lesion es una placa similar al CBC clásico, pero el borde es hiper-pigmentado, incluso toda la lesion puede presentarse pigmentada.
6.) HIPERPIGMENTADO DE PINKUS: con pigmentación oscura, puede parecer un melanoma.
El epitelioma O CARCINOMA BASOCELULAR DE PINKUS, también se le conoce
con el nombre de
"FIBROEPITELIOMA DE PINKUS", es una variante poco frecuente del carcinoma basocelular (CBC), que
presenta una clínica y características histopatológicas
distintivas.
Fue descrito por por Hermann Pinkus, en 1953 por primera vez, quien lo denominó “tumor fibroepitelial premaligno”.
Originalmente fue considerado una entidad separada del CBC, pero hoy dia se acepta que es una variante del CARCINOMA BASOCELULAR.
Fue descrito por por Hermann Pinkus, en 1953 por primera vez, quien lo denominó “tumor fibroepitelial premaligno”.
Originalmente fue considerado una entidad separada del CBC, pero hoy dia se acepta que es una variante del CARCINOMA BASOCELULAR.
Aunque sigue existiendo controversia en el medio científico y
literatura, quienes afirman que la lesion es similar a un
TRICOBLASTOMA, el cual es un tumor benigno que se origina el el folículo
piloso.
Se presenta por lo general en adultos entre 40
y 60 años, sin preferencia marcada por sexo masculino o femenino, y
suele localizarse principalmente en la region lumbo sacra, pero al igual
que el CARCINOMA BASOCELULAR, también se presenta en cabeza, abdomen,
extremidades y raramente en genitales.
Clínicamente hay dos tipos: se presenta como una lesión nodular única, pediculada o sésil, de 1.) color piel, o color rosada, y 2.) la forma pigmentada, también pediculada o tipo placa, con superficie lisa y a veces erosionada, muy similar al CBC PIGMENTADO (ver foto).
Clínicamente hay dos tipos: se presenta como una lesión nodular única, pediculada o sésil, de 1.) color piel, o color rosada, y 2.) la forma pigmentada, también pediculada o tipo placa, con superficie lisa y a veces erosionada, muy similar al CBC PIGMENTADO (ver foto).
La gran diferencia con el CARCINOMA BASOCELULAR PIGMENTADO esta en la
BIOPSIA de la lesion, la cual muestra cordones finos y alargados de
células basaloides que se anastomosan formando una estructura típica en
“panal de abejas”. También se usan marcadores inmunohistoquímicos
para diferenciarlo.
INDICIOS DE MALIGNIZACION DEL CARCINOMA BASOCELULAR:
1.) Crecimiento rápido:
la lesion que por lo generalmente crece lentamente, evoluciona a un
crecimiento "violento", en el curso de meses.
2.) Sangramiento: Por lo general el CBC no sangra, a excepción del tipo ULCERADO.
Sangramientos frecuentes, o con leves traumatismos son señal de una
evolución torpida.
3.) Telangiectasias aumentadas: las telagiectasias que son vasos sanguíneos pequeños que se ven en la
superficie de la lesion y con el tiempo aumentan considerablemente
de tamaño.
4.) Cambios de coloración:
aparecen en la lesion cambios en la tonalidad del color, areas azuladas,
negruzcas, o marrones.
5.) Aparición de placas induradas: con bordes irregulares.
6.) Tiempo de evolución: un CARCINOMA BASOCELULAR con mas de 9 a 11 años de evolución sin
tratamiento, puede dar metastasis o evolucionar a un CARCINOMA
ESPINOCELULAR, el cual si es maligno.
TRATAMIENTOS:
El tratamiento del CARCINOMA BASOCELULAR (CBC) depende principalmente
del riesgo tumoral (bajo vs. alto), la localización de la lesion, el
tamaño, el tipo histológico del tumor, y las características del
paciente.
1. ) TRATAMIENTOS QUIRÚRGICOS:
A.- Escisión quirúrgica estándar con bisturi:
Es el tratamiento de primera línea para la mayoría de los CBC,
especialmente los de bajo riesgo. La tasa de recurrencia es
baja(alrededor del 3-4%). Se recomienda márgenes de mínimo 1 Cm incluso
2 Cm para lesiones bien delimitadas.
B.- Cirugía micrográfica de Mohs: Este tipo de cirugía se realiza en pabellón quirúrgico y esta indicada en CBC de alto riesgo y recurrentes, localizados en áreas anatómicamente críticas (por ejemplo, la “zona H” facial), o con bordes mal definidos.
B.- Cirugía micrográfica de Mohs: Este tipo de cirugía se realiza en pabellón quirúrgico y esta indicada en CBC de alto riesgo y recurrentes, localizados en áreas anatómicamente críticas (por ejemplo, la “zona H” facial), o con bordes mal definidos.
Consiste en eliminar el tumor principal, el cual se "congela" con
nitrógeno liquido, y se van haciendo cortes, que en el mismo quirófano
un patólogo especializado observa al microscopio, y determina hasta
donde debe llegar la escisión, hasta llegar a piel sana.
Este método permite la evaluación intraoperatoria de los márgenes y
maximiza la conservación del tejido, con tasas de recurrencia similares
o menores a la escisión estándar (bisturí), en tumores faciales de alto
riesgo.
2.) TRATAMIENTOS NO QUIRÚRGICOS:
A.- Electrodesecación y curetaje: Útil en CBC superficiales o nodulares pequeños, en zonas no críticas. La tasa de curación es alta, siendo uno de los métodos mas utilizados en lesiones de pequeño tamaño.
A.- Electrodesecación y curetaje: Útil en CBC superficiales o nodulares pequeños, en zonas no críticas. La tasa de curación es alta, siendo uno de los métodos mas utilizados en lesiones de pequeño tamaño.
B.- Crioterapia:
Menos utilizada, consiste en enfriar el tumor con nitrógeno liquido,
colocando debajo del mismo una aguja que mide la temperatura, hasta que
el punto de enfriamiento alcance una temperatura entre -40 y -60
grados centígrados.
Esto provoca la destrucción de las células tumorales. La
recurrencia en estos casos esta estimada en un 22%, y los resultados
cosméticos son variables, porque los principales efectos secundarios son
la formación de ampollas (quemaduras por frio), en el sitio del
procedimiento, que pueden dejar secuelas
cicatriciales.
C.- Radioterapia:
Alternativa para pacientes no candidatos a cirugía, especialmente en
tumores localizados en áreas donde la cirugía sería desfigurante o en
pacientes de edad avanzada.
La tasa de recurrencia ES comparables a la cirugía en los CBC de bajo
riesgo, pero los resultados cosméticos pueden ser inferiores. También
existe riesgo de telangiectasias y perdida de la coloración de la
piel (radio dermitis).
D.- Terapia fotodinámica (TFD): Indicada en CBC superficiales y algunos nodulares de bajo riesgo. Utiliza agentes fotosensibilizantes (por ejemplo, metil-aminolevulinato, conocido como MAL) y luz ultravioleta para destruir el tumor.
D.- Terapia fotodinámica (TFD): Indicada en CBC superficiales y algunos nodulares de bajo riesgo. Utiliza agentes fotosensibilizantes (por ejemplo, metil-aminolevulinato, conocido como MAL) y luz ultravioleta para destruir el tumor.
Como funciona este metodo?:
El metil-aminolevulinato (MAL) es un agente fotosensibilizante,
precursor de la protoporfirina IX (PpIX), una sustancia que se acumula
selectivamente en las células tumorales.
Este se aplica tópicamente en las lesiones en forma de crema, se deja unas 2 a 3 horas y
luego se expone a a una luz roja con una longitud de onda entre 570nm
y 670nm. La luz activa
la protoporfirina IX (PpIX) produciendo esta la liberación de
radicales libres que causan la destrucción de las células
tumorales.
Presenta una tasa de recurrencia superior a la cirugía, pero mejores
resultados cosméticos.
3.) TRATAMIENTOS TÓPICOS:
A.- Imiquimod 5%: Aprobado para su uso en los CBC superficiales y algunos nodulares de bajo riesgo. Consiste en aplicar la crema en la lesion durante 6 semanas. La aplicación NO SUELE SER DIARIA, puede ser cada 2 o 3 días. Las tasa de recurrencia es mayor que la cirugía, pero el resultado cosmético es aceptable.
B.-) 5-fluorouracilo: Este medicamento viene en presentación al 2.5% en crema y al 5% en ungüento, y representa una alternativa tópica en los CBC superficiales, con eficacia inferior a la cirugía.
3.) TRATAMIENTOS TÓPICOS:
A.- Imiquimod 5%: Aprobado para su uso en los CBC superficiales y algunos nodulares de bajo riesgo. Consiste en aplicar la crema en la lesion durante 6 semanas. La aplicación NO SUELE SER DIARIA, puede ser cada 2 o 3 días. Las tasa de recurrencia es mayor que la cirugía, pero el resultado cosmético es aceptable.
B.-) 5-fluorouracilo: Este medicamento viene en presentación al 2.5% en crema y al 5% en ungüento, y representa una alternativa tópica en los CBC superficiales, con eficacia inferior a la cirugía.
Se puede utilizar en preparaciones MAGISTRALES e intercalar su uso con
el IMIQUIMOD, bajo el siguiente esquema: 3 días IMIQUIMOD, 2
días 5-FLUORACILO.
4.) TRATAMIENTOS SISTÉMICOS: (enfermedad avanzada):
4.) TRATAMIENTOS SISTÉMICOS: (enfermedad avanzada):
A.- Inhibidores de la vía Hedgehog (Vismodegib, Sonidegib): Aprobados por la FDA en USA. para los CBC localmente avanzados, CBC metastásico en los cuales la cirugía o radioterapia no es la apropiada o indicada.
La vía Hedgehog es una ruta de señalización celular fundamental para el desarrollo
embrionario y el mantenimiento celular. En la mayoría de los carcinomas
basocelulares esta via se encuentra activada, provocando un crecimiento
descontrolado de las células tumorales.
Que son el Vismodegib, Sonidegib, y como actuan:
Son dos medicamentos que vienen en presentación oral, y de primera
línea en estos casos, aunque presentan efectos adversos significativos
como: espasmos musculares, alopecia, molestias gastrointestinales y
alteración sensorial del gusto.
- Vismodegib: cápsulas orales, comúnmente en dosis de 150 mg.
- Sonidegib: cápsulas orales, típicamente en dosis de 200 mg.
Ambos inhibidores actúan bloqueando una proteína llamada
Smoothened (SMO), logrando con esto el bloqueo de de la vía
Hedgehog, por lo tanto se frena la proliferación y crecimiento del
tumor.
B.- Inmunoterapia (Cemiplimab, inhibidor de PD-1):
El Cemiplimab es un anticuerpo monoclonal de tipo inmunoglobulina G4 el
cual bloquea el receptor PD-1 (programmed cell death protein 1), en las
células T del sistema inmunitario.
Al presentarse este bloqueo de PD-1
impide que las células tumorales disminuyan o "apaguen" la respuesta
inmune, logrando con ello una reactivación del sistema inmune, para
detectar y destruir las células tumorales o cancerosas.
Esta indicado en pacientes adultos con CARCINOMA BASOCELULAR (CBC) localmente avanzado, o con metastasis, en aquellos que la radioterapia no es viable, o no toleran los inhibidores de la via Hedgehog (Vismodegib, Sonidegib).
Esta inmunoterapia es la primera aprobada para tratar el CBC avanzado en estos contextos.
Administración y dosis:
El Cemiplimab viene en presentación de viales bajo el nombre comercial de LIBTAYO, y se administra mediante infusión intravenosa, generalmente 350 mg cada 3 semanas.
Esta indicado en pacientes adultos con CARCINOMA BASOCELULAR (CBC) localmente avanzado, o con metastasis, en aquellos que la radioterapia no es viable, o no toleran los inhibidores de la via Hedgehog (Vismodegib, Sonidegib).
Esta inmunoterapia es la primera aprobada para tratar el CBC avanzado en estos contextos.
Administración y dosis:
El Cemiplimab viene en presentación de viales bajo el nombre comercial de LIBTAYO, y se administra mediante infusión intravenosa, generalmente 350 mg cada 3 semanas.
El tratamiento puede extenderse hasta casi 2 años (93 semanas) o
hasta que la enfermedad progrese o se presente toxicidad
importante.
Los efectos secundarios mas frecuentes de esta terapia son:
Dolor musculo esquelético, fatiga, picazón, diarrea y erupciones cutáneas, pero también pueden
presentarse efectos severos orgánicos en: intestino, pulmón, riñón,
piel, y glándulas endocrinas, debido a un descontrol inmunitario.
CONCLUSIONES:
El CARCINOMA BASOCELULAR es el CANCER DE PIEL MAS COMÚN, y si se trata a
tiempo el riesgo de malignidad es bajo, puede presentarse tanto en mujeres
como hombres, mayormente adultos.
La exposición al sol es determinante en su aparición, y se ha descrito en
algunos casos asociación con los Antígenos de Histocompatibilidad (HLA),
lo que pudiera indicar predisposición genética.
El tiempo para convertirse en maligno es LARGO, entre 9 y 11 años, pero
si tienes una lesion sospechosa, no tardes en consultar al
medico.
En las referencias los hechos..
Saludos a todos.
Dr. José Lapenta.
Dr. José M. Lapenta.
==================================================================
REFERENCIAS BIBLIOGRÁFICAS / BIBLIOGRAPHICAL REFERENCES
==================================================================
REFERENCIAS BIBLIOGRÁFICAS / BIBLIOGRAPHICAL REFERENCES
==================================================================
N.- HLA-G expression in basal cell carcinomas of the skin recurring
after radiotherapy (2005).
==================================================================
==================================================================
1.) Basal Cell Carcinoma in Children Report of 3 Cases
2.) Papillomaviruses in non-melanoma skin cancer: epidemiological aspects.
3.) Reconstruction of the scalp and cranium using multiple free-tissue transfers following recurrent basal cell carcinoma.
4.) Prognostic value of apoptotic index in cutaneous basal cell carcinomas of head and neck.
5.) Low levels of urokinase plasminogen activator components in basal cell carcinoma of the skin.
6.) Folliculotropic T cells in regressive basal cell carcinoma of skin.
7.) Repeated 5-aminolevulinic acid-based photodynamic therapy following electro-curettage for pigmented basal cell carcinoma.
8.) Sporadic Bazex-Dupre-Christol-like Syndrome: Early Onset Basal Cell Carcinoma, Hypohidrosis, Hypotrichosis, and Prominent Milia.
9.) Reporting basal cell carcinoma: a survey of the attitudes of histopathologists.
10.) Host-related and environmental risk factors for cutaneous basal cell carcinoma: evidence from an italian case-control study.
11.) Collagenolytic and gelatinolytic matrix metalloproteinases and their inhibitors in basal cell carcinoma of skin: comparison with normal skin.
12.) A Cancer-Registry-Assisted Evaluation of the Accuracy of Digital Epiluminescence Microscopy Associated with Clinical Examination ofPigmented Skin Lesions.
13.) Expression of p53 in arsenic-related and sporadic basal cell carcinoma.
14.) Decision support software to help primary care physicians triage skin cancer: a pilot study.
15.) A randomized, 12-year primary-prevention trial of beta carotene supplementation for nonmelanoma skin cancer in the physician's health study.
16.) Photofrin photodynamic therapy can significantly deplete or preserve oxygenation in human basal cell carcinomas during treatment, depending on fluence rate.
17.) Gamma-irradiation deregulates cell cycle control and apoptosis in nevoid basal cell carcinoma syndrome-derived cells.
18.) Expression of desmoglein I and plakoglobin in skin carcinomas.
19.) Expression of basement membrane antigens and matrix metalloproteinases 2 and 9 in cutaneous basal and squamous cell carcinomas.
20.) Detoxifying enzyme genotypes and susceptibility to cutaneous malignancy.
21.) Tumors arising in nevus sebaceus: A study of 596 cases.
22.) Liposome-mediated gene transfer into human basal cell carcinoma.
23.) Proliferative Actinic Keratosis: Three Representative Cases.
24.) Diet and basal cell carcinoma of the skin in a prospective cohort of men.
25.) Preliminary observations on the use of topical tazarotene to treat basal-cell carcinoma.
26.)HLA phenotypes and multiple basal cell carcinomas.
27.) Multiple non-melanoma skin cancer: evidence that different MHC genes are associated with different cancers.
28.) HLA DR4 is associated with the development of multiple basal cell carcinomas and malignant melanoma.
29.) Multiple basal cell carcinoma in tropical Australia.
30.) HLA-DR1 is not a sign of poor prognosis for the development of multiple basal cell carcinomas.
31.) Multiple basal cell carcinomas and HLA frequencies in southern Australia.
32.) Expression of human lymphocyte antigen (HLA)-DR on tumor cells in basal cell carcinoma.
33.) Human leukocyte antigen associations in basal cell carcinoma.
34.) Translocation (4; 14) and concomitant inv(14) in a basal cell carcinoma.
35.) Long-term therapy with low-dose isotretinoin for prevention of basal cell carcinoma: a multicenter clinical trial. Isotretinoin-Basal Cell Carcinoma Study Group [see comments]
36.) Treatment and prevention of basal cell carcinoma with oral isotretinoin.
37.) Chemoprevention of basal cell carcinoma with isotretinoin.
38.) Chemoprevention of skin cancer in xeroderma pigmentosum.
39.) Relative importance of prior basal cell carcinomas, continuing sun
exposure, and circulating T lymphocytes on the development of basal cell carcinoma.
40.) Topical tretinoin in actinic keratosis and basal cell carcinoma.
41.) Margin assessment of selected basal cell carcinomas utilizing laser Doppler velocimetry.
42.) Carbon dioxide laser vaporization and curettage in the treatment of large or multiple superficial basal cell carcinomas.
43.) The effect of intralesional 5-fluorouracil therapeutic implant (MPI 5003) for treatment of basal cell carcinoma.
44.) Cryosurgery and topical fluorouracil: a treatment method for widespread basal cell epithelioma in basal cell nevus syndrome.
45.) Selective cytotoxic effect of topical 5-fluorouracil.
46.) Nodular superficial pigmented basal cell epitheliomas.
47.) Metastatic basal cell carcinoma: response to chemotherapy.
48.) Basal cell carcinoma of the vulva with lymph node and skin metastasis--report of a case and review of 20 Japanese cases.
49.) Basal cell carcinoma of the scalp resulting in spine metastasis in a black patient.
50.) Long-term survival following bony metastases from basal cell carcinoma. Report of a case.
51.)Giant basal cell carcinoma with metastasis and secondary amyloidosis: report of case.
52.) Pulmonary metastases from a basal cell carcinoma.
53.) Nonrecurrent primary basal cell carcinoma of the lower extremity with late metastasis.
54.) [Metastatic basal cell carcinoma]
55.) Metastatic basal cell carcinoma: report of twelve cases with a review of the literature [see comments]
56.) Rapid development of metastases from basal cell carcinoma presenting as cranial nerve palsies.
57.) Photodynamic therapy by topical aminolevulinic acid, dimethylsulphoxide and curettage in nodular basal cell carcinoma: a one-year follow-up study.
58.) Epidemiologic characteristics and clinical course of patients with malignant eyelid tumors in an incidence cohort in Olmstead County, Minnesota.
59.) Does wound healing contribute to the eradication of basal cell carcinoma following curettage and electrodessication?
60.)Does inflammation contribute to the eradication of basal cell carcinoma following curettage and electrodesiccation?
61.) Cryosurgery in dermatology.
62.) [The treatment of basal cell carcinoma patients by dermatologists in Netherland].
63.) [Therapy of non-melanocytic skin tumors].
64.) [High resolution ultrasound imaging: value in treatment of basocellular carcinoma by cryosurgery].
65.) Recurrent basal cell carcinoma treated with cryosurgery.
66.) Fractional cryosurgery. A new technique for basal cell carcinoma of the eyelids and periorbital area.
67.) Long-term follow-up of cryosurgery of basal cell carcinoma of the eyelid.
68.) Five-year results of curettage-cryosurgery of selected large primarybasal cell carcinomas on the nose: an alternative treatment in a geographical area underserved by Mohs' surgery.
69.) Laser microsurgery for superficial T1-T2 basal cell carcinoma of the eyelid margins.
70.)[Use of Nd:YAG laser for treatment of basal-cell carcinomas and some
premalignant conditions].
71.) Laser therapy of skin tumors.
72.) Treatment of superficial basal cell carcinoma and squamous cell carcinoma in situ with a high-energy pulsed carbon dioxide laser.
73.) Prediction of subclinical tumor infiltration in basal cell carcinoma.
74.) Recurrence rates of treated basal cell carcinomas. Part 3: Surgical excision.
75.) Human papillomavirus type 2-associated basal cell carcinoma in two immunosuppressed patients.
76.) Occurrence of human papillomavirus type 16 DNA in cutaneous squamous and basal cell neoplasms.
77.) Basal cell carcinoma of the genitalia.
78.) Detection of human papillomavirus DNA in PUVA-associated non-melanoma skin cancers.
79.)Premalignant lesions and cancers of the skin in the general population:
evaluation of the role of human papillomaviruses.
80.) Human papillomavirus type 2-associated basal cell carcinoma in two immunosuppressed patients.
============================================================
2.) Papillomaviruses in non-melanoma skin cancer: epidemiological aspects.
3.) Reconstruction of the scalp and cranium using multiple free-tissue transfers following recurrent basal cell carcinoma.
4.) Prognostic value of apoptotic index in cutaneous basal cell carcinomas of head and neck.
5.) Low levels of urokinase plasminogen activator components in basal cell carcinoma of the skin.
6.) Folliculotropic T cells in regressive basal cell carcinoma of skin.
7.) Repeated 5-aminolevulinic acid-based photodynamic therapy following electro-curettage for pigmented basal cell carcinoma.
8.) Sporadic Bazex-Dupre-Christol-like Syndrome: Early Onset Basal Cell Carcinoma, Hypohidrosis, Hypotrichosis, and Prominent Milia.
9.) Reporting basal cell carcinoma: a survey of the attitudes of histopathologists.
10.) Host-related and environmental risk factors for cutaneous basal cell carcinoma: evidence from an italian case-control study.
11.) Collagenolytic and gelatinolytic matrix metalloproteinases and their inhibitors in basal cell carcinoma of skin: comparison with normal skin.
12.) A Cancer-Registry-Assisted Evaluation of the Accuracy of Digital Epiluminescence Microscopy Associated with Clinical Examination ofPigmented Skin Lesions.
13.) Expression of p53 in arsenic-related and sporadic basal cell carcinoma.
14.) Decision support software to help primary care physicians triage skin cancer: a pilot study.
15.) A randomized, 12-year primary-prevention trial of beta carotene supplementation for nonmelanoma skin cancer in the physician's health study.
16.) Photofrin photodynamic therapy can significantly deplete or preserve oxygenation in human basal cell carcinomas during treatment, depending on fluence rate.
17.) Gamma-irradiation deregulates cell cycle control and apoptosis in nevoid basal cell carcinoma syndrome-derived cells.
18.) Expression of desmoglein I and plakoglobin in skin carcinomas.
19.) Expression of basement membrane antigens and matrix metalloproteinases 2 and 9 in cutaneous basal and squamous cell carcinomas.
20.) Detoxifying enzyme genotypes and susceptibility to cutaneous malignancy.
21.) Tumors arising in nevus sebaceus: A study of 596 cases.
22.) Liposome-mediated gene transfer into human basal cell carcinoma.
23.) Proliferative Actinic Keratosis: Three Representative Cases.
24.) Diet and basal cell carcinoma of the skin in a prospective cohort of men.
25.) Preliminary observations on the use of topical tazarotene to treat basal-cell carcinoma.
26.)HLA phenotypes and multiple basal cell carcinomas.
27.) Multiple non-melanoma skin cancer: evidence that different MHC genes are associated with different cancers.
28.) HLA DR4 is associated with the development of multiple basal cell carcinomas and malignant melanoma.
29.) Multiple basal cell carcinoma in tropical Australia.
30.) HLA-DR1 is not a sign of poor prognosis for the development of multiple basal cell carcinomas.
31.) Multiple basal cell carcinomas and HLA frequencies in southern Australia.
32.) Expression of human lymphocyte antigen (HLA)-DR on tumor cells in basal cell carcinoma.
33.) Human leukocyte antigen associations in basal cell carcinoma.
34.) Translocation (4; 14) and concomitant inv(14) in a basal cell carcinoma.
35.) Long-term therapy with low-dose isotretinoin for prevention of basal cell carcinoma: a multicenter clinical trial. Isotretinoin-Basal Cell Carcinoma Study Group [see comments]
36.) Treatment and prevention of basal cell carcinoma with oral isotretinoin.
37.) Chemoprevention of basal cell carcinoma with isotretinoin.
38.) Chemoprevention of skin cancer in xeroderma pigmentosum.
39.) Relative importance of prior basal cell carcinomas, continuing sun
exposure, and circulating T lymphocytes on the development of basal cell carcinoma.
40.) Topical tretinoin in actinic keratosis and basal cell carcinoma.
41.) Margin assessment of selected basal cell carcinomas utilizing laser Doppler velocimetry.
42.) Carbon dioxide laser vaporization and curettage in the treatment of large or multiple superficial basal cell carcinomas.
43.) The effect of intralesional 5-fluorouracil therapeutic implant (MPI 5003) for treatment of basal cell carcinoma.
44.) Cryosurgery and topical fluorouracil: a treatment method for widespread basal cell epithelioma in basal cell nevus syndrome.
45.) Selective cytotoxic effect of topical 5-fluorouracil.
46.) Nodular superficial pigmented basal cell epitheliomas.
47.) Metastatic basal cell carcinoma: response to chemotherapy.
48.) Basal cell carcinoma of the vulva with lymph node and skin metastasis--report of a case and review of 20 Japanese cases.
49.) Basal cell carcinoma of the scalp resulting in spine metastasis in a black patient.
50.) Long-term survival following bony metastases from basal cell carcinoma. Report of a case.
51.)Giant basal cell carcinoma with metastasis and secondary amyloidosis: report of case.
52.) Pulmonary metastases from a basal cell carcinoma.
53.) Nonrecurrent primary basal cell carcinoma of the lower extremity with late metastasis.
54.) [Metastatic basal cell carcinoma]
55.) Metastatic basal cell carcinoma: report of twelve cases with a review of the literature [see comments]
56.) Rapid development of metastases from basal cell carcinoma presenting as cranial nerve palsies.
57.) Photodynamic therapy by topical aminolevulinic acid, dimethylsulphoxide and curettage in nodular basal cell carcinoma: a one-year follow-up study.
58.) Epidemiologic characteristics and clinical course of patients with malignant eyelid tumors in an incidence cohort in Olmstead County, Minnesota.
59.) Does wound healing contribute to the eradication of basal cell carcinoma following curettage and electrodessication?
60.)Does inflammation contribute to the eradication of basal cell carcinoma following curettage and electrodesiccation?
61.) Cryosurgery in dermatology.
62.) [The treatment of basal cell carcinoma patients by dermatologists in Netherland].
63.) [Therapy of non-melanocytic skin tumors].
64.) [High resolution ultrasound imaging: value in treatment of basocellular carcinoma by cryosurgery].
65.) Recurrent basal cell carcinoma treated with cryosurgery.
66.) Fractional cryosurgery. A new technique for basal cell carcinoma of the eyelids and periorbital area.
67.) Long-term follow-up of cryosurgery of basal cell carcinoma of the eyelid.
68.) Five-year results of curettage-cryosurgery of selected large primarybasal cell carcinomas on the nose: an alternative treatment in a geographical area underserved by Mohs' surgery.
69.) Laser microsurgery for superficial T1-T2 basal cell carcinoma of the eyelid margins.
70.)[Use of Nd:YAG laser for treatment of basal-cell carcinomas and some
premalignant conditions].
71.) Laser therapy of skin tumors.
72.) Treatment of superficial basal cell carcinoma and squamous cell carcinoma in situ with a high-energy pulsed carbon dioxide laser.
73.) Prediction of subclinical tumor infiltration in basal cell carcinoma.
74.) Recurrence rates of treated basal cell carcinomas. Part 3: Surgical excision.
75.) Human papillomavirus type 2-associated basal cell carcinoma in two immunosuppressed patients.
76.) Occurrence of human papillomavirus type 16 DNA in cutaneous squamous and basal cell neoplasms.
77.) Basal cell carcinoma of the genitalia.
78.) Detection of human papillomavirus DNA in PUVA-associated non-melanoma skin cancers.
79.)Premalignant lesions and cancers of the skin in the general population:
evaluation of the role of human papillomaviruses.
80.) Human papillomavirus type 2-associated basal cell carcinoma in two immunosuppressed patients.
============================================================
