eMedicine Specialties > Dermatology > Malignant Neoplasms

Squamous Cell Carcinoma: Treatment & Medication

Author: Debjani Sahni, MBBS, MRCP, Cutaneous Oncology Fellow, Brigham and Women's Hospital, Dana Farber Cancer Institute
Coauthor(s): Chrysalyne D Schmults, MD, Instructor in Dermatology, Harvard Medical School; Director, Mohs Micrographic Surgery Center, Department of Dermatology, Brigham and Women's Hospital
Contributor Information and Disclosures

Updated: Mar 18, 2009

Treatment

Medical Care

Nonsurgical options for the treatment of cutaneous squamous cell carcinoma (SCC) include topical chemotherapy, topical immune response modifiers, photodynamic therapy (PDT), radiotherapy, and systemic chemotherapy. The use of topical therapy and PDT is generally limited to premalignant (ie, actinic keratoses [AKs]) and in situ lesions. Radiation therapy is a primary treatment option for patients in whom surgery is not feasible and is an adjuvant therapy for those with metastatic or high-risk cutaneous squamous cell carcinoma. In current practice, systemic chemotherapy is used exclusively for patients with metastatic disease. However, newer more targeted drugs, such as epidermal growth factor receptor (EGFR) antagonists (eg, cetuximab), have favorable adverse effect profiles and await trails to determine if they are beneficial in high-risk squamous cell carcinoma.

Topical chemotherapy

Topical formulations of 5-fluorouracil (5-FU) are available for the treatment of AKs and superficial basal cell carcinomas (BCCs). Successful treatment of in situ squamous cell carcinoma has also been reported.39 Invasive squamous cell carcinoma should not be treated with topical chemotherapy. An oral form of 5-FU (capecitabine), which is approved by the US Food and Drug Administration (FDA) for other forms of cancer, may be considered in patients with diffuse in situ squamous cell carcinoma over large skin areas, on which topical 5-FU is difficult to apply. However, studies of efficacy have not yet been performed.

Topical immune response modifiers

Imiquimod is an imidazoquinoline that enhances cell-mediated immune responses via the induction of proinflammatory cytokines. It is approved by the FDA for the treatment of genital warts (ie, condylomata acuminata), AKs, and superficial BCC. Imiquimod cream has also shown effectiveness in the treatment of Bowen disease as monotherapy and in combination with topical 5-FU. However, systemic flulike symptoms and other adverse effects can occur when applied to large surface areas; therefore, using this agent in patients with diffuse in situ squamous cell carcinoma is difficult.40,41

Photodynamic therapy

Treatment with PDT involves the application of a photosensitizer (given topically or systemically) followed by exposure to a light source. The resulting photochemical reaction causes inflammation and destruction of the targeted lesion(s). PDT is used primarily to treat large numbers of AKs in a single session. Squamous cell carcinoma in situ is also amenable to PDT, although a wide range of recurrence rates (0-52%) have been reported. At this time, PDT is not recommended for treatment of invasive squamous cell carcinoma.42

Radiation therapy

Radiation therapy offers the potential advantage of avoiding the deformity and trauma of a surgical procedure. Cure rates for T1 lesions range from 85-95%. However, a number of disadvantages are associated with radiation therapy. For example, radiation therapy is expensive and requires a significant time commitment because treatments are usually given 3-5 times per week for 4-8 weeks. Most patients experience significant irritation at the radiation site, and they frequently develop erythema, erosions, alopecia, and pain, which may require narcotic-level analgesia. Although the initial cosmetic result following radiation is usually good, the long-term outcome is often poor, owing to the development of cutaneous atrophy, dyspigmentation, and telangiectasia in the radiation field. Patients treated with radiation also have a slightly increased risk of developing cutaneous carcinoma (most commonly squamous cell carcinoma) or sarcoma later in life.

Radiation therapy does not involve histologic margin control and has a lower cure rate compared with surgery. For these reasons, as well as those discussed in the preceding paragraph, primary radiation therapy for squamous cell carcinoma is generally restricted to older patients who cannot tolerate or who refuse surgery.

In contrast, radiation is routinely used as an adjunct to surgical treatment in cases of nodal metastasis, and the reported 5-year cure rate is 73% for combined surgical and radiation therapy to involved nodal basins.14

The use of adjuvant radiotherapy in high-risk cutaneous squamous cell carcinoma in the absence of known metastasis is more controversial because studies have not been conducted to verify its benefit. In the setting of high-risk squamous cell carcinoma, every attempt should be made to obtain clear surgical margins. Administration of adjuvant radiotherapy, which may include both the primary site and the draining nodal basins, is usually reserved for cases in which surgical margins are in doubt or when the patient has substantial nerve involvement.43

Systemic chemotherapy
 
A variety of different chemotherapeutic agents have been used to treat metastatic cutaneous squamous cell carcinoma. Many of the current protocols have been adapted from those used to treat metastatic head and neck squamous cell carcinoma. Capecitabine (Xeloda), an oral formation of 5-FU, either alone or in combination with interferon alfa, has shown some efficacy in the treatment of advanced cutaneous squamous cell carcinoma.44

Reduction in immunosuppression

In OTRs, a reduction in the magnitude of immunosuppression may be an effective adjuvant therapeutic strategy in the treatment of aggressive squamous cell carcinoma. Because a decrease in immunosuppression may increase the risk for rejection of the transplanted organ, this strategy should only be considered in selected high-risk patients and under the careful management of the transplantation physician, who must closely monitor the patient for signs and symptoms of organ rejection.45

Surgical Care

Most squamous cell carcinomas (SCCs) are readily treated in the physician's office by surgical or destructive methods, with a high expectation of cure. The treatment of squamous cell carcinoma must take into account multiple patient- and lesion-specific factors. The standard modalities available for the treatment of localized (primary) invasive squamous cell carcinoma are described below. Because squamous cell carcinoma is a lesion that can recur, metastasize, and cause death, and because recurrent squamous cell carcinoma carries a worse prognosis, every opportunity should be taken to effect complete tumor extirpation at first presentation.

Cryotherapy

Cryotherapy with liquid nitrogen is a safe and low-cost procedure for the ablation of selected in situ squamous cell carcinomas. The 5-year cure rate for squamous cell carcinoma can be 95% or greater with proper tumor selection and technique. In the United States, cryosurgery is routinely used for in situ disease and AKs. It is not often used for invasive squamous cell carcinoma because deeper portions of the tumor may not be eradicated by this technique and because the development of scar tissue at the site of cryotherapy might obscure a recurrence. The risks associated with cryotherapy include transient pain, edema, and blistering. Hypopigmentation and alopecia are also common and may be permanent, so treatment of hair-bearing areas and in darkly pigmented individuals is generally not recommended.46

Electrodesiccation and curettage

Electrodesiccation and curettage (ED&C) is a simple technique that can be used to treat low-risk squamous cell carcinoma on the trunk and extremities. The tumor indications are similar to those of cryotherapy. In addition, ED&C can be used to treat superficially invasive squamous cell carcinomas without high-risk characteristics. However, the thick scars that often occur after ED&C can delay the diagnosis of cancer recurrence. Subsequently, ED&C should be used with caution in invasive squamous cell carcinoma. It is not appropriate for certain anatomic locations (ie, eyelids, genitalia, lips, ears).

The technique is based on the delineation of tumor margins with a curette because tumor tissue is generally more friable than the surrounding normal tissue. ED&C is known to be very technique-dependent, and cure rates improve with a practitioner's experience. The main disadvantage of ED&C is a lack of histologic margin control, and most dermatologic surgeons believe the actual long-term cure rate for invasive squamous cell carcinoma is much lower than that quoted in the literature. Tumor recurrence may result from failure of ED&C treatment to eradicate atypical cells residing deep in the hair follicles or in the dermis. Nonetheless, the procedure is fast, minimally invasive, well tolerated, and effective for properly selected lesions.

Excision with conventional margins

Standard excision with conventional permanent (ie, fixed) tissue sections is an excellent, highly effective, and well-tolerated therapy for many primary squamous cell carcinomas. Cure rates following simple excision of well-defined T1 lesions may be as high as 95-99%. The generally accepted 5-year cure rate for primary squamous cell carcinoma treated with standard excision is 92%; this rate drops to 77% for recurrent squamous cell carcinoma.

A 4-mm margin of normal tissue is recommended for lower-risk lesions (<2 cm, well-differentiated, without subcutaneous fat invasion) on the trunk and extremities. For lesions larger than 2 cm, invasive to fat, and in high-risk locations (ie, central face, ears, scalp, genitalia, hands, feet), a 6-mm margin of normal tissue is recommended. Given the cosmetic and functional impact of these wider margins, tumors in this latter category are often removed via Mohs surgery (see below) to achieve high cure rates while sparing normal tissue. The depth of an excision should always include a portion of the subcutaneous fat.

One pitfall of standard excision is that histologic margins can be reported to be negative when they are, in fact, positive (false negative) because the traditional "bread-loaf" method of tissue sectioning typically results in evaluation of less than 1% of the specimen’s margins. More commonly, a greater amount of healthy tissue is removed than is necessary for complete tumor extirpation. Therefore, simple excision is most valuable in the treatment of small primary squamous cell carcinomas on the trunk, extremities, or neck, where tissue sparing is less essential.47

Mohs micrographic surgery

Mohs micrographic surgery (MMS) is a specialized technique for removing many forms of skin cancer, including squamous cell carcinoma. Because of its many advantages, MMS is the procedure of choice for squamous cell carcinoma in which tissue preservation is needed, for ill-defined squamous cell carcinoma, and for high-risk squamous cell carcinoma. The main advantage of MMS over simple excision is the ability to histologically examine nearly 100% of the surgical margins and to carefully map residual foci of invasive carcinoma. This residual tumor is removed in a step-wise fashion until clear margins are obtained.

MMS provides the best available cure rates (94-99%) for squamous cell carcinoma and has been of particular value in curing squamous cell carcinoma associated with perineural invasion. In a comprehensive historical review, Rowe et al48 noted that local recurrences are less frequent when squamous cell carcinoma is treated with MMS compared with all non-Mohs modalities. This local recurrence rate differential in favor of MMS was observed in primary squamous cell carcinoma of the skin and lip (3.1% vs 10.9%), for locally recurrent squamous cell carcinoma (10% vs 23.3%), for poorly differentiated squamous cell carcinoma (32.6% vs 53.6%), and for squamous cell carcinoma with perineural involvement (0% vs 47%). MMS offers the added benefit of preserving healthy tissue, thus facilitating reconstruction and optimizing cosmetic and functional outcomes.

MMS is routinely performed in an outpatient setting with local anesthesia and, therefore, is safe and cost effective. As a result of the fellowship training programs in Mohs surgery overseen by the American College of Mohs Surgery and the new Accreditation Council for Graduate Medical Education (ACGME)–accredited Procedural Dermatology Fellowship programs, MMS has become widely available throughout the United States.49,50

Care of patients with diffuse actinic keratosis and in situ squamous cell carcinoma

Many patients with a history of extensive sun exposure and light skin develop epidermal atypia in the form of AK and in situ squamous cell carcinoma over large areas of their skin. Most of these patients also develop multiple invasive squamous cell carcinomas. The management of such patients is highly labor intensive and involves the following steps:
  • Surgically remove all tumors that clinically appear to have to have an invasive (dermal) component and confirm clearance of histologic margins.
  • Evaluate for underlying immunosuppression, such as from CLL or an overly impaired immune system from immunosuppressive or immunomodulatory therapy. If this is suspected, discuss with the patient’s other doctors whether the immunosuppression can be safely remedied or lessened.
  • Perform field treatment of the areas of epidermal atypia. Treatment options include topical chemotherapy with 5-FU or PDT. Imiquimod has limited utility in diffuse disease because adverse effects increase when applied to large surface areas. If 5-FU therapy is planned, remove any hyperkeratotic lesions with a curette just prior to beginning therapy to enhance penetration of the medication to the basal layer. A full course of 5-FU therapy is twice-daily administration for 4 weeks. Patients who cannot tolerate this duration may try shorter courses and then resume treatment after a healing phase. Subsequent treatments become more tolerable as the epidermal damage is corrected.
  • Follow the patient closely for recurrence of actinic keratosis/squamous cell carcinoma in situ and for new invasive squamous cell carcinomas. Field treatment may need to be repeated every 6-12 months to keep precursor actinic keratosis and squamous cell carcinoma in situ lesions to a minimum.
  • Oral retinoids in the form of low-dose acitretin can decrease new cancer formation, although they do not generally alter the course of existing tumors.51 Although most patients do not require retinoids if the above measures are taken, patients who are still developing multiple cancers 6-12 months after beginning an intensive program to clear disease may benefit from retinoid therapy. Once the desired effect is achieved, considering a dose reduction of long-term maintenance therapy rather than discontinuing therapy is better because the latter typically leads to a rebound of multiple squamous cell carcinoma formation.

Treatment of patients with high-risk tumors

Management of primary tumors

See "High-risk squamous cell carcinoma" in Prognosis. The use of ED&C in the treatment of high-risk squamous cell carcinoma, particularly in immunocompromised individuals, is best avoided, because histologic margin status cannot be evaluated. Clear margins must be obtained for optimal outcomes.

Ensuring clear surgical margins wherever possible is highly recommended. A systematic review of available data for high-risk squamous cell carcinoma compared cases with clear surgical margins (n = 943) versus those in which margins were not specified (n = 1506) and demonstrated statistically better outcomes in cases in which clear margins were documented, with risks of local recurrence, regional metastasis, distant metastasis, and disease-specific death of 5%, 5%, 1%, and 1%, respectively, in clear-margin cases versus 8%, 14%, 7%, and 7% in cases with undocumented margins.43

A prospective study identified several risk factors for incomplete excision of squamous cell carcinomas, namely, ear lesions, invasive lesions, and previously incompletely excised lesions referred for reexcision. The study also recommended more care with tumor markings, taking margins of at least 5 mm, deeper margins, and referring such lesions to centers with personnel who have more experience.52

No controlled comparative studies of Mohs versus excision in high-risk squamous cell carcinoma have been performed, but case series data suggest that Mohs is superior to excision for high-risk squamous cell carcinoma patients.49

Adjuvant therapy

No comparative studies of surgery versus surgery plus adjuvant radiotherapy for high-risk squamous cell carcinoma have been performed. With no clear evidence of benefit and the potential of significant morbidity, clinical judgment is required in deciding which patients should receive adjuvant radiation. One systematic review of available outcome data suggests that adjuvant radiation be considered in patients with uncertain or positive surgical margins or advanced nerve involvement (eg, involvement of named nerves, nerves 0.1 mm or greater in diameter, or with clinical or radiologic evidence of nerve invasion).43 Adjuvant medication may also be considered in select highest-risk cases. Options include oral 5-FU (Xeloda) and EGFR inhibitors via oncology treatment centers. Although survival data are lacking, these medications are generally well-tolerated with few adverse effects.

Consultations

Most cases of squamous cell carcinoma are easily and successfully treated by dermatologists or Mohs surgeons. However, in certain cases, a multidisciplinary approach may be needed (see "High-risk squamous cell carcinoma" in Prognosis). Such cases include the following:

  • Large or deep tumors in which excision and reconstruction under local anesthesia is not feasible
  • When clear surgical margins are not achieved or are in doubt
  • Cases of nodal or distant metastasis
A multidisciplinary approach using MMS performed in conjunction with an otolaryngologist and/or a plastic surgeon may aid in completely removing deeply invasive squamous cell carcinoma, preserving a vital structure (eg, facial nerve), and facilitating the reconstruction of a large operative defect. For example, Mohs surgery may be used in cases of squamous cell carcinoma of the scalp involving bone to establish peripheral margins to the level of the galea. Mohs is then followed by resection of the deep margin, including bone, with the patient under general anesthesia, performed by a head and neck or plastic surgeon. Because the peripheral margins are established in advance, the head and neck or plastic surgeon can then focus on the deep margin and reconstruction. The patient is often spared hours of anesthesia time, lowering surgical morbidity.

Metastatic disease also requires aggressive management by a multidisciplinary team. Surgical treatment of metastatic disease may require the expertise of an otolaryngologist, a general surgeon, or a surgical oncologist. Adjuvant or palliative radiotherapy may be administered by a radiation oncologist. A medical oncologist should be consulted if systemic chemotherapy is considered for metastatic disease.

More on Squamous Cell Carcinoma

Overview: Squamous Cell Carcinoma
Differential Diagnoses & Workup: Squamous Cell Carcinoma
Treatment & Medication: Squamous Cell Carcinoma
Follow-up: Squamous Cell Carcinoma
Multimedia: Squamous Cell Carcinoma
References
[ CLOSE WINDOW ]

References

  1. Johnson TM, Rowe DE, Nelson BR, Swanson NA. Squamous cell carcinoma of the skin (excluding lip and oral mucosa). J Am Acad Dermatol. Mar 1992;26(3 Pt 2):467-84. [Medline].

  2. Leiter U, Garbe C. Epidemiology of melanoma and nonmelanoma skin cancer--the role of sunlight. Adv Exp Med Biol. 2008;624:89-103. [Medline].

  3. Masini C, Fuchs PG, Gabrielli F, et al. Evidence for the association of human papillomavirus infection and cutaneous squamous cell carcinoma in immunocompetent individuals. Arch Dermatol. Jul 2003;139(7):890-4. [Medline].

  4. Wong SS, Tan KC, Goh CL. Cutaneous manifestations of chronic arsenicism: review of seventeen cases. J Am Acad Dermatol. Feb 1998;38(2 Pt 1):179-85. [Medline].

  5. Herman S, Rogers HD, Ratner D. Immunosuppression and squamous cell carcinoma: a focus on solid organ transplant recipients. Skinmed. Sep-Oct 2007;6(5):234-8. [Medline].

  6. Mehrany K, Weenig RH, Pittelkow MR, Roenigk RK, Otley CC. High recurrence rates of squamous cell carcinoma after Mohs' surgery in patients with chronic lymphocytic leukemia. Dermatol Surg. Jan 2005;31(1):38-42; discussion 42. [Medline].

  7. Nguyen P, Vin-Christian K, Ming ME, Berger T. Aggressive squamous cell carcinomas in persons infected with the human immunodeficiency virus. Arch Dermatol. Jun 2002;138(6):758-63. [Medline].

  8. Mallipeddi R. Epidermolysis bullosa and cancer. Clin Exp Dermatol. Nov 2002;27(8):616-23. [Medline].

  9. Newman MD, Weinberg JM. Topical therapy in the treatment of actinic keratosis and basal cell carcinoma. Cutis. Apr 2007;79(4 Suppl):18-28. [Medline].

  10. Miller DL, Weinstock MA. Nonmelanoma skin cancer in the United States: incidence. J Am Acad Dermatol. May 1994;30(5 Pt 1):774-8. [Medline].

  11. Gray DT, Suman VJ, Su WP, Clay RP, Harmsen WS, Roenigk RK. Trends in the population-based incidence of squamous cell carcinoma of the skin first diagnosed between 1984 and 1992. Arch Dermatol. Jun 1997;133(6):735-40. [Medline].

  12. Hampton T. Skin cancer's ranks rise: immunosuppression to blame. JAMA. Sep 28 2005;294(12):1476-80. [Medline].

  13. Buettner PG, Raasch BA. Incidence rates of skin cancer in Townsville, Australia. Int J Cancer. Nov 23 1998;78(5):587-93. [Medline].

  14. Veness MJ, Morgan GJ, Palme CE, Gebski V. Surgery and adjuvant radiotherapy in patients with cutaneous head and neck squamous cell carcinoma metastatic to lymph nodes: combined treatment should be considered best practice. Laryngoscope. May 2005;115(5):870-5. [Medline].

  15. McCall CO, Chen SC. Squamous cell carcinoma of the legs in African Americans. J Am Acad Dermatol. Oct 2002;47(4):524-9. [Medline].

  16. Williams LS, Mancuso AA, Mendenhall WM. Perineural spread of cutaneous squamous and basal cell carcinoma: CT and MR detection and its impact on patient management and prognosis. Int J Radiat Oncol Biol Phys. Mar 15 2001;49(4):1061-9. [Medline].

  17. de Gruijl FR, Rebel H. Early events in UV carcinogenesis--DNA damage, target cells and mutant p53 foci. Photochem Photobiol. Mar-Apr 2008;84(2):382-7. [Medline].

  18. Katiyar SK. UV-induced immune suppression and photocarcinogenesis: chemoprevention by dietary botanical agents. Cancer Lett. 2007;255:1-11. [Medline].

  19. Ziegler A, Jonason AS, Leffell DJ, et al. Sunburn and p53 in the onset of skin cancer. Nature. Dec 22-29 1994;372(6508):773-6. [Medline].

  20. Brown VL, Harwood CA, Crook T, Cronin JG, Kelsell DP, Proby CM. p16INK4a and p14ARF tumor suppressor genes are commonly inactivated in cutaneous squamous cell carcinoma. J Invest Dermatol. May 2004;122(5):1284-92. [Medline].

  21. Ziegler A, Jonason AS, Leffell DJ, et al. Sunburn and p53 in the onset of skin cancer. Nature. Dec 22-29 1994;372(6508):773-6. [Medline].

  22. Perry PK, Silverberg NB. Cutaneous malignancy in albinism. Cutis. May 2001;67(5):427-30. [Medline].

  23. Karagas MR, Nelson HH, Zens MS, et al. Squamous cell and basal cell carcinoma of the skin in relation to radiation therapy and potential modification of risk by sun exposure. Epidemiology. Nov 2007;18(6):776-84. [Medline].

  24. Zghal M, El-Fekih N, Fazaa B, et al. [Xeroderma pigmentosum. Cutaneous, ocular, and neurologic abnormalities in 49 Tunisian cases]. Tunis Med. Dec 2005;83(12):760-3. [Medline].

  25. Berg D, Otley CC. Skin cancer in organ transplant recipients: Epidemiology, pathogenesis, and management. J Am Acad Dermatol. Jul 2002;47(1):1-17; quiz 18-20. [Medline].

  26. Black AP, Bailey A, Jones L, Turner RJ, Hollowood K, Ogg GS. p53-specific CD8+ T-cell responses in individuals with cutaneous squamous cell carcinoma. Br J Dermatol. Nov 2005;153(5):987-91. [Medline].

  27. Alam M, Caldwell JB, Eliezri YD. Human papillomavirus-associated digital squamous cell carcinoma: literature review and report of 21 new cases. J Am Acad Dermatol. Mar 2003;48(3):385-93. [Medline].

  28. Della Torre G, Donghi R, Longoni A, et al. HPV DNA in intraepithelial neoplasia and carcinoma of the vulva and penis. Diagn Mol Pathol. Mar 1992;1(1):25-30. [Medline].

  29. Stockfleth E, Nindl I, Sterry W, Ulrich C, Schmook T, Meyer T. Human papillomaviruses in transplant-associated skin cancers. Dermatol Surg. Apr 2004;30(4 Pt 2):604-9. [Medline].

  30. Mallipeddi R, Keane FM, McGrath JA, Mayou BJ, Eady RA. Increased risk of squamous cell carcinoma in junctional epidermolysis bullosa. J Eur Acad Dermatol Venereol. Sep 2004;18(5):521-6. [Medline].

  31. Arbiser JL, Fan CY, Su X, et al. Involvement of p53 and p16 tumor suppressor genes in recessive dystrophic epidermolysis bullosa-associated squamous cell carcinoma. J Invest Dermatol. Oct 2004;123(4):788-90. [Medline].

  32. Jambusaria-Pahlajani A, Hess S, Berg D, Schmults CD. Equipoise exists in the peri-operative management of cutaneous squamous cell carcinoma with perineural invasion: A survey study of American College of Mohs Surgery surgeons. Manuscript under review.

  33. Hess SD, Jambusaria A, Katz K, Schmults CD. Clinical equipoise exists in the peri-operative management of high-risk cutaneous squamous cell carcinoma: A survey study of American College of Mohs Surgery surgeons. Manuscript under review.

  34. Williams LS, Mancuso AA, Mendenhall WM. Perineural spread of cutaneous squamous and basal cell carcinoma: CT and MR detection and its impact on patient management and prognosis. Int J Radiat Oncol Biol Phys. Mar 15 2001;49(4):1061-9. [Medline].

  35. Land R, Herod J, Moskovic E, et al. Routine computerized tomography scanning, groin ultrasound with or without fine needle aspiration cytology in the surgical management of primary squamous cell carcinoma of the vulva. Int J Gynecol Cancer. Jan-Feb 2006;16(1):312-7. [Medline].

  36. Cho SB, Chung WG, Yun M, Lee JD, Lee MG, Chung KY. Fluorodeoxyglucose positron emission tomography in cutaneous squamous cell carcinoma: retrospective analysis of 12 patients. Dermatol Surg. Apr 2005;31(4):442-6; discussion 446-7. [Medline].

  37. Brantsch KD, Meisner C, Schonfisch B, et al. Analysis of risk factors determining prognosis of cutaneous squamous-cell carcinoma: a prospective study. Lancet Oncol. Aug 2008;9(8):713-20. [Medline].

  38. Ross AS, Schmults CD. Sentinel lymph node biopsy in cutaneous squamous cell carcinoma: a systematic review of the English literature. Dermatol Surg. Nov 2006;32(11):1309-21. [Medline].

  39. Bargman H, Hochman J. Topical treatment of Bowen's disease with 5-Fluorouracil. J Cutan Med Surg. Mar-Apr 2003;7(2):101-5. [Medline].

  40. Mackenzie-Wood A, Kossard S, de Launey J, Wilkinson B, Owens ML. Imiquimod 5% cream in the treatment of Bowen's disease. J Am Acad Dermatol. Mar 2001;44(3):462-70. [Medline].

  41. Smith KJ, Hamza S, Skelton H. Topical imidazoquinoline therapy of cutaneous squamous cell carcinoma polarizes lymphoid and monocyte/macrophage populations to a Th1 and M1 cytokine pattern. Clin Exp Dermatol. Sep 2004;29(5):505-12. [Medline].

  42. Marmur ES, Schmults CD, Goldberg DJ. A review of laser and photodynamic therapy for the treatment of nonmelanoma skin cancer. Dermatol Surg. Feb 2004;30(2 Pt 2):264-71. [Medline].

  43. Jambusaria-Pahlajani A, Miller C, Quon H. Surgical monotherapy versus surgery plus radiotherapy in high risk cutaneous squamous cell carcinoma: A systematic review of outcomes. Dermatol Surg. In press.

  44. Wollina U, Hansel G, Koch A, Kostler E. Oral capecitabine plus subcutaneous interferon alpha in advanced squamous cell carcinoma of the skin. J Cancer Res Clin Oncol. May 2005;131(5):300-4. [Medline].

  45. Otley CC, Cherikh WS, Salasche SJ, McBride MA, Christenson LJ, Kauffman HM. Skin cancer in organ transplant recipients: effect of pretransplant end-organ disease. J Am Acad Dermatol. Nov 2005;53(5):783-90. [Medline].

  46. Kuflik EG, Gage AA. The five-year cure rate achieved by cryosurgery for skin cancer. J Am Acad Dermatol. Jun 1991;24(6 Pt 1):1002-4. [Medline].

  47. Brodland DG, Zitelli JA. Surgical margins for excision of primary cutaneous squamous cell carcinoma. J Am Acad Dermatol. Aug 1992;27(2 Pt 1):241-8. [Medline].

  48. Rowe DE, Carroll RJ, Day CL Jr. Prognostic factors for local recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol. Jun 1992;26(6):976-90. [Medline].

  49. Holmkvist KA, Roenigk RK. Squamous cell carcinoma of the lip treated with Mohs micrographic surgery: outcome at 5 years. J Am Acad Dermatol. Jun 1998;38(6 Pt 1):960-6. [Medline].

  50. Robins P, Dzubow LM, Rigel DS. Squamous-cell carcinoma treated by Mohs' surgery: an experience with 414 cases in a period of 15 years. J Dermatol Surg Oncol. Oct 1981;7(10):800-1. [Medline].

  51. Harwood CA, Leedham-Green M, Leigh IM, Proby CM. Low-dose retinoids in the prevention of cutaneous squamous cell carcinomas in organ transplant recipients: a 16-year retrospective study. Arch Dermatol. Apr 2005;141(4):456-64. [Medline].

  52. Tan PY, Ek E, Su S, Giorlando F, Dieu T. Incomplete excision of squamous cell carcinoma of the skin: a prospective observational study. Plast Reconstr Surg. Sep 15 2007;120(4):910-6. [Medline].

  53. Chen K, Craig JC, Shumack S. Oral retinoids for the prevention of skin cancers in solid organ transplant recipients: a systematic review of randomized controlled trials. Br J Dermatol. Mar 2005;152(3):518-23. [Medline].

  54. Mrass P, Rendl M, Mildner M, et al. Retinoic acid increases the expression of p53 and proapoptotic caspases and sensitizes keratinocytes to apoptosis: a possible explanation for tumor preventive action of retinoids. Cancer Res. Sep 15 2004;64(18):6542-8. [Medline].

  55. Papoutsaki M, Lanza M, Marinari B, et al. The p73 gene is an anti-tumoral target of the RARbeta/gamma-selective retinoid tazarotene. J Invest Dermatol. Dec 2004;123(6):1162-8. [Medline].

  56. Clayman GL, Lee JJ, Holsinger FC, et al. Mortality risk from squamous cell skin cancer. J Clin Oncol. Feb 1 2005;23(4):759-65. [Medline].

  57. Brantsch KD, Meisner C, Schonfisch B, et al. Analysis of risk factors determining prognosis of cutaneous squamous-cell carcinoma: a prospective study. Lancet Oncol. Aug 2008;9(8):713-20. [Medline].

  58. Ross AS , Miller F, Elenitsas R, Xu X, Troxel AB, Schmults CD. Diameter of involved nerves predicts outcome in cutaneous squamous cell carcinoma with perineural invasion: an investigative-blinded retrospective cohort study. Under review.

  59. Jensen P, Hansen S, Moller B, et al. Skin cancer in kidney and heart transplant recipients and different long-term immunosuppressive therapy regimens. J Am Acad Dermatol. Feb 1999;40(2 Pt 1):177-86. [Medline].

  60. Euvrard S, Kanitakis J, Decullier E, et al. Subsequent skin cancers in kidney and heart transplant recipients after the first squamous cell carcinoma. Transplantation. Apr 27 2006;81(8):1093-100. [Medline].

  61. Veness MJ, Quinn DI, Ong CS, et al. Aggressive cutaneous malignancies following cardiothoracic transplantation: the Australian experience. Cancer. Apr 15 1999;85(8):1758-64. [Medline].

  62. Mehrany K, Weenig RH, Pittelkow MR, Roenigk RK, Otley CC. High recurrence rates of squamous cell carcinoma after Mohs' surgery in patients with chronic lymphocytic leukemia. Dermatol Surg. Jan 2005;31(1):38-42; discussion 42. [Medline].

  63. Frierson HF Jr, Deutsch BD, Levine PA. Clinicopathologic features of cutaneous squamous cell carcinomas of the head and neck in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma. Hum Pathol. Dec 1988;19(12):1397-402. [Medline].

  64. Lobo DV, Chu P, Grekin RC, Berger TG. Nonmelanoma skin cancers and infection with the human immunodeficiency virus. Arch Dermatol. May 1992;128(5):623-7. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

squamous cell carcinoma, skin cancer, SCC, actinic keratoses, SCC in situ, Bowen disease, Bowen's disease, keratotic invasive SCC, leukoplakia, erythroplasia of Queyrat, nodular SCC, periungual SCC, Marjolin ulcer, actinically derived SCC, adenoid squamous cell carcinoma, ASCC, adenosquamous cell carcinoma, verrucous carcinoma,  keratoacanthoma,  oral florid papillomatosis, epithelioma cuniculatum, giant condyloma of Buschke and Löwenstein, malignant tumor of keratinocytes, sun-induced cancerous lesions

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Debjani Sahni, MBBS, MRCP, Cutaneous Oncology Fellow, Brigham and Women's Hospital, Dana Farber Cancer Institute
Debjani Sahni, MBBS, MRCP is a member of the following medical societies: British Association of Dermatologists, Royal College of Physicians, and St John's Dermatological Society
Disclosure: Nothing to disclose.

Coauthor(s)

Chrysalyne D Schmults, MD, Instructor in Dermatology, Harvard Medical School; Director, Mohs Micrographic Surgery Center, Department of Dermatology, Brigham and Women's Hospital
Chrysalyne D Schmults, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American Society for Dermatologic Surgery, and International Society for Dermatologic Surgery
Disclosure: Nothing to disclose.

Medical Editor

R Stan Taylor, MD, Professor of Dermatology, University of Texas Southwestern Medical School; Director of Skin Surgery and Oncology Clinic, Department of Dermatology, University of Texas Southwestern Medical Center
R Stan Taylor, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Dermatological Association, American Medical Association, American Society for Dermatologic Surgery, Christian Medical & Dental Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Mary Farley, MD, Dermatologic Surgeon/Mohs Surgeon, Anne Arundel Surgery Center
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.