Squamous cell carcinoma - Karsinoma Sél Skuamosahttps://en.wikipedia.org/wiki/Squamous_cell_carcinoma
Karsinoma Sél Skuamosa (Squamous cell carcinoma) ilaharna mangrupa lesi beureum, skala, jeung beurat dina kulit anu kakeunaan panonpoé. Sababaraha nodulna teuas, teguh, sarta ngabentuk kubah kawas keratoacanthoma. Borok jeung perdarahan tiasa lumangsung. Lamun karsinoma sél skuamosa (Squamous cell carcinoma) teu dirawat, éta bisa jadi massa anu gedé. Squamous-sél nyaéta kanker kulit kadua paling umum. Éta bahaya, tapi teu sabanding bahaya melanoma. Sanggeus biopsi, éta bakal dipiceun sacara bedah.

Diagnosis sareng Perawatan
#Dermoscopy
#Skin biopsy
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  • Squamous cell carcinoma well differentiated — Keratosis actinic perlu dipantau.
  • Keratoacanthoma
  • Keratoacanthoma
  • Karsinoma Sel Skuamosa (Squamous cell carcinoma) – Leungeun
  • Lamun tatu teu cageur lila, kanker kulit kudu disangka.
  • Lamun tatu teu cageur lila, kanker kulit kudu dipikiran.
References Squamous Cell Skin Cancer 28722968 
NIH
Squamous cell carcinoma (SCC) mangrupa kanker kulit kadua paling umum di Amérika Serikat, sanggeus basal cell carcinoma. Biasana dimimitian tina lesi prekanker anu disebut actinic keratosis, sarta tiasa nyebar ka bagian awak séjén. Faktor utama nu nyababkeun nyaéta paparan sinar ultraviolét (UV) ti panonpoé, nu akumulasi sapanjang waktos. Perawatan biasana ngalibatkeun panyabutan bedah, hususna pikeun SCC dina sirah jeung beuheung. Terapi radiasi mangrupakeun pilihan pikeun pasien sepuh atawa nu teu tiasa dioperasi. Immunosuppression ningkatkeun résiko SCC. Sanajan jarang, SCC bisa nyebar, utamana dina penderita sistem imun lemah. Pamariksaan rutin jeung panyalindungan ti panonpoé penting pikeun anu boga 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) mangrupikeun kanker anu paling umum kadua di antara jalma, sareng jumlahna terus naék. Sanajan CSCC biasana némbongkeun paripolah klinis anu benign, éta tiasa sumebar boh sacara lokal boh ka bagian séjén awak. Élmuwan geus ngaidentifikasi jalur husus anu aub dina ngembangkeun CSCC, anu ngarah kana perlakuan anyar. Jumlah mutasi anu luhur sareng résiko anu ningkat dina penderita anu immunosuppressed parantos nyababkeun ngembangna immunotherapy. Tinjauan ieu ningali akar genetik CSCC sareng pangobatan panganyarna anu nargétkeun molekul khusus sareng sistem imun.
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