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The most significant risk factor for cSCC is extensive lifetime exposure to ultraviolet radiation from sunlight. The risk associated with UV radiation correlates with cumulative exposure rather than early life exposure. Tanning beds have emerged as a significant source of UV radiation. Genetic predispositions, such as xeroderma pigmentosum and certain forms of epidermolysis bullosa, also increase susceptibility to cSCC. The condition originates from squamous cells located in the skin's upper layers. Diagnosis typically relies on skin examination, and is confirmed through skin biopsy. Research, both in vivo and in vitro, indicates a crucial role for the upregulation of FGFR2, part of the fibroblast growth factor receptor immunoglobin family, in cSCC cell progression. Mutations in the TPL2 gene leads to overexpression of FGFR2, which activates the mTORC1 and AKT pathways in primary and metastatic cSCC cell lines. Utilization of a "pan FGFR inhibitor" has shown to reduce cell migration and proliferation in cSCC in vitro studies. Surgical removal is the typical treatment method, For cases with distant metastasis, chemotherapy or biologic therapy may be employed. constituting about 20% of all skin cancer cases. In the United States, approximately 12% of males and 7% of females are diagnosed with cSCC at some point in their lives. While prognosis remains favorable in the absence of metastasis, upon distant spread the five year survival rate is markedly reduced to ~34%. The average age at diagnosis is approximately 66 years. Following successful treatment of an initial cSCC lesion, there is a substantial risk of developing subsequent lesions. The lesion caused by cSCC is often asymptomatic
Ulcer or reddish skin plaque that is slow growing
Intermittent bleeding from the tumor, especially on the lip
The clinical appearance is highly variable
Usually the tumor presents as an ulcerated lesion with hard, raised edges
The tumor may be in the form of a hard plaque or a papule, often with an opalescent quality, with tiny blood vessels
The tumor can lie below the level of the surrounding skin, and eventually ulcerates and invades the underlying tissue
The tumor commonly presents on sun exposed areas (e. g. back of the hand, scalp, lip, and superior surface of pinna)
On the lip, the tumor forms a small ulcer, which fails to heal and bleeds intermittently
Evidence of chronic skin photodamage, as in multiple actinic keratoses (solar keratoses)
The tumor grows relatively slowly

People who have received solid organ transplants are at a significantly increased risk of developing squamous cell carcinoma due to the use of chronic immunosuppressive medication. While the risk of developing all skin cancers increases with these medications, this effect is particularly severe for cSCC, with hazard ratios as high as 250 being reported, versus 40 for basal cell carcinoma. The incidence of cSCC development increases with time posttransplant. Heart and lung transplant recipients are at the highest risk of developing cSCC due to more intensive immunosuppressive medications used. Cutaneous squamous cell carcinoma in individuals on immunotherapy or who have lymphoproliferative disorders (e. g. leukemia) tend to be much more aggressive, regardless of their location. The risk of cSCC, and non melanoma skin cancers generally, varies with the immunosuppressive drug regimen chosen. The risk is greatest with calcineurin inhibitors like cyclosporine and tacrolimus, and least with mTOR inhibitors, such as sirolimus and everolimus. The antimetabolites azathioprine and mycophenolic acid have an intermediate risk profile.

Diagnosis is confirmed via skin biopsy of the tissue or tissues suspected to be affected by SCC. The pathological appearance of a squamous cell cancer varies with the depth of the biopsy. For that reason, a biopsy including the subcutaneous tissue and basilar epithelium, to the surface is necessary for correct diagnosis. The performance of a shave biopsy (see skin biopsy) might not acquire enough information for a diagnosis. An inadequate biopsy might be read as actinic keratosis with follicular involvement. A deeper biopsy down to the dermis or subcutaneous tissue might reveal the true cancer. An excision biopsy is ideal, but not practical in most cases. An incisional or punch biopsy is preferred. A shave biopsy is least ideal, especially if only the superficial portion is acquired.

Histopathologically, the epidermis in cSCC in situ (Bowen's disease) will show hyperkeratosis and parakeratosis. There will also be marked acanthosis with elongation and thickening of the rete ridges. These changes will overly keratinocytic cells which are often highly atypical and may in fact have a more unusual appearance than invasive cSCC. The atypia spans the full thickness of the epidermis, with the keratinocytes demonstrating intense mitotic activity, pleomorphism, and greatly enlarged nuclei. They will also show a loss of maturity and polarity, giving the epidermis a disordered or "windblown" appearance. Two types of multinucleated cells may be seen: the first will present as a multinucleated giant cell, and the second will appear as a dyskeratotic cell engulfed in the cytoplasm of a keratinocyte. Occasionally, cells of the upper epidermis will undergo vacuolization, demonstrating an abundant and strongly eosinophilic cytoplasm. There may be a mild to moderate lymphohistiocytic infiltrate detected in the upper dermis. In cSCC in situ (Bowen's disease), atypical squamous cells proliferate through the whole thickness of the epidermis. and the vulva in females. It mainly occurs in uncircumcised males, over the age of 40.

In invasive cSCC, tumor cells infiltrate through the basement membrane. The infiltrate can be somewhat difficult to detect in the early stages of invasion: however, additional indicators such as full thickness epidermal atypia and the involvement of hair follicles can be used to facilitate the diagnosis. Later stages of invasion are characterized by the formation of nests of atypical tumor cells in the dermis, often with a corresponding inflammatory infiltrate. A 2016 review of sunscreen for preventing cutaneous squamous cell carcinoma found insufficient evidence to demonstrate whether it was effective.

Most cutaneous squamous cell carcinomas are removed with surgery. A few selected cases are treated with topical medication. Surgical excision with a free margin of healthy tissue is a frequent treatment modality. Radiotherapy, given as external beam radiotherapy or as brachytherapy (internal radiotherapy), can also be used to treat cSCC. There is little evidence comparing the effectiveness of different treatments for non metastatic cSCC. Mohs surgery is frequently utilized; considered the treatment of choice for squamous cell carcinoma of the skin, physicians have also utilized the method for the treatment of squamous cell carcinoma of the mouth, throat, and neck. An equivalent method of the CCPDMA standards can be utilized by a pathologist in the absence of a Mohs trained physician. Radiation therapy is often used afterward in high risk cancer or patient types. Radiation or radiotherapy can also be a standalone option in treating cSCC. As a non invasive option brachytherapy serves a painless possibility to treat in particular but not only difficult to operate areas like the earlobes or genitals. An example of this kind of therapy is the high dose brachytherapy Rhenium SCT which makes use of the beta rays emitting property of rhenium 188. The radiation source is enclosed in a compound which is applied to a thin protection foile directly over the lesion. This way the radiation source can be applied to complex locations and minimize radiation to healthy tissue. After removal of the cancer, closure of the skin for patients with a decreased amount of skin laxity involves a split thickness skin graft. A donor site is chosen and enough skin is removed so that the donor site can heal on its own. Only the epidermis and a partial amount of dermis is taken from the donor site which allows the donor site to heal. Skin can be harvested using either a mechanical dermatome or Humby knife. Electrodessication and curettage (EDC) can be done on selected squamous cell carcinoma of the skin. In areas where cSCC is known to be non aggressive, and where the patient is not immunosuppressed, EDC can be performed with good to adequate cure rate. Treatment options for cSCC in situ (Bowen's disease) include photodynamic therapy with 5 aminolevulinic acid, cryotherapy, topical 5 fluorouracil or imiquimod, and excision. A meta analysis showed evidence that PDT is more effective than cryotherapy and has better cosmetic outcomes. There is generally a lack of evidence comparing the effectiveness of all treatment options. Frequent skin exams with a dermatologist is recommended after treatment.

The long term outcome of squamous cell carcinoma is dependent upon several factors: the sub type of the carcinoma, available treatments, location and severity, and various patient health related variables (accompanying diseases, age, etc.). Generally, the long term outcome is positive, with a metastasis rate of 1.9 5.2% and a mortality rate of 1.5 3.4%. When it does metastasize, the most commonly involved organs are the lungs, brain, bone and other skin locations. Squamous cell carcinoma occurring in immunosuppressed people (such as those with organ transplant, human immunodeficiency virus infection, or chronic lymphocytic leukemia) the risk of developing cSCC and having metastasis is much higher than the general population. One study found squamous cell carcinoma of the penis had a much greater rate of mortality than some other forms of squamous cell carcinoma, that is, about 23%, although this relatively high mortality rate may be associated with possibly latent diagnosis of the disease due to patients avoiding genital exams until the symptoms are debilitating, or refusal to submit to a possibly scarring operation upon the genitalia.

The incidence of cutaneous squamous cell carcinoma continues to rise around the world. This is theorized to be due to several factors; including an aging population, a greater incidence of those who are immunocompromised and the increasing use of tanning beds. A recent study estimated that there are between 180,000 and 400,000 cases of cSCC in the United States in 2013. Risk factors for cSCC varies with age, gender, race, geography, and genetics. The incidence of cSCC increases with age and with those 75 years or older eing at a 5 10 times increased risk of developing cSCC as compared with those who are younger than 55 years old. Solid organ transplant recipients (heart, lung, liver, pancreas, among others) are also at a heightened risk of developing aggressive, high risk cSCC. There are also a few rare congenital diseases predisposed to cutaneous malignancy. In certain geographic locations, exposure to arsenic in well water or from industrial sources may significantly increase the risk of cSCC.