Squamous cell carcinoma - Karsinom Selil Squamoushttps://en.wikipedia.org/wiki/Squamous_cell_carcinoma
Karsinom Selil Squamous (Squamous cell carcinoma) se souvan yon blesi wouj, dekale, epè sou po solèy la ekspoze. Gen kèk ki fèm nodil difisil ak bòl ki gen fòm keratoakantom. Ilsè ak senyen ka rive. Lè karsinom selil squamous (squamous cell carcinoma) yo pa trete, li ka devlope nan yon gwo mas. Selil squamous se dezyèm kansè po ki pi komen. Li danjere, men se pa prèske osi danjere ke yon melanom. Apre byopsi a, li pral retire yon operasyon.

Dyagnostik ak Tretman
#Dermoscopy
#Skin biopsy
☆ Nan rezilta Stiftung Warentest 2022 ki soti nan Almay, satisfaksyon konsomatè yo ak ModelDerm te sèlman yon ti kras pi ba pase ak konsiltasyon telemedsin peye.
  • Squamous cell carcinoma well differentiated ― Yo obsève yon keratoz aktinik adjasan.
  • Keratoacanthoma
  • Keratoacanthoma
  • Karsinom Selil Squamous (Squamous cell carcinoma) ― Avantbra
  • Si yon blesi pa geri pou yon tan long, yo ta dwe sispèk kansè po.
  • Si yon blesi pa geri pou yon tan long, yo ta dwe sispèk kansè po.
References Squamous Cell Skin Cancer 28722968 
NIH
Squamous cell carcinoma (SCC) se dezyèm kansè po ki pi komen nan peyi Etazini, apre basal cell carcinoma. Anjeneral li kòmanse nan blesi prekansè yo rele actinic keratosis , epi li ka pwopaje nan lòt pati nan kò a. Kòz prensipal la se ekspoze a radyasyon iltravyolèt (UV) ki soti nan solèy la, ki akimile sou tan. Tretman anjeneral enplike nan retire chirijikal, espesyalman pou SCC sou tèt la ak kou. Terapi radyasyon se yon opsyon pou pasyan ki pi gran oswa moun ki pa ka fè operasyon. Imunosuppresyon ogmante risk pou SCC. Malgre ke ra, SCC ka gaye, espesyalman nan pasyan ki gen sistèm iminitè febli. Tèks regilye ak pwoteksyon solèy yo enpòtan pou moun ki gen SCC.
Squamous cell carcinoma of the skin or cutaneous squamous cell carcinoma is the second most common form of skin cancer in the United States, behind basal cell carcinoma. Squamous cell carcinoma has precursor lesions called actinic keratosis, exhibits tumor progression and has the potential to metastasize in the body. Ultraviolet (UV) solar radiation is the primary risk factor in the development of cutaneous squamous cell carcinoma and the cumulative exposure received over a lifetime plays a major part in the development of this cancer. Surgical excision is the primary treatment modality for cutaneous squamous cell carcinoma, with Mohs micrographic surgery being the preferred excisional technique for squamous cell carcinoma of the head and neck, and in other areas of high risk or squamous cell carcinoma with high-risk characteristics. Radiation therapy is reserved for squamous cell carcinoma in older patients or those who will not tolerate surgery, or when it has not been possible to obtain clear margins surgically. Adjuvant radiotherapy is commonly after surgical treatment in very high tumors. Immunosuppression significantly increases the risk of squamous cell carcinoma over the course of an individual’s life. Metastasis is uncommon for squamous cell carcinomas arising in areas of chronic sun exposure, but it can take place, and the risk is increased in immunosuppressed patients. Patients with cutaneous squamous cell carcinoma should be examined regularly and remember to use measures to protect from UV damage.
 Cutaneous Squamous Cell Carcinoma: From Biology to Therapy 32331425 
NIH
Cutaneous squamous cell carcinoma (CSCC) se dezyèm kansè ki pi komen nan moun, epi nimewo li yo ap ogmante. Malgre ke CSCC anjeneral montre yon konpòtman benign klinik, li ka gaye tou de lokalman ak nan lòt pati nan kò a. Syantis yo te idantifye chemen espesifik ki enplike nan devlopman CSCC, ki mennen nan nouvo tretman. Gwo kantite mitasyon ak risk ogmante nan pasyan imunosupprime yo te pouse devlopman imunoterapi. Revizyon sa a gade rasin jenetik CSCC ak dènye tretman ki vize molekil espesifik ak sistèm iminitè a.
Cutaneous squamous cell carcinoma (CSCC) is the second most frequent cancer in humans and its incidence continues to rise. Although CSCC usually display a benign clinical behavior, it can be both locally invasive and metastatic. The signaling pathways involved in CSCC development have given rise to targetable molecules in recent decades. In addition, the high mutational burden and increased risk of CSCC in patients under immunosuppression were part of the rationale for developing the immunotherapy for CSCC that has changed the therapeutic landscape. This review focuses on the molecular basis of CSCC and the current biology-based approaches of targeted therapies and immune checkpoint inhibitors