Skin Cancer: Non-Melanoma Skin Cancer

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[restab title=”Objectives” active=”active”]

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The following module was designed to supplement medical students’ learning in the clinic. Please take the time to read through each module by clicking the headings below. Information on epidemiology, screening & testing, classification, signs & symptoms, diagnosis, staging, treatment and follow-up of non-melanoma skin cancers is provided.

By the end of the tutorial, the following objectives should be addressed:
  1. Understand the burden of disease attributed to non-melanoma skin cancers
  2. Describe the role of UV radiation in the pathogenesis of non-melanoma skin cancer
  3. Understand the role of environmental risk factors besides UV radiation in non-melanoma skin cancer
  4. Describe the role of genetics in the development of non-melanoma skin cancer
  5. Describe the factors that can decrease the risk of non-melanoma skin cancer
  6. Understand the appropriate approach and timing for skin examinations
  7. Demonstrate a suggested approach for a full body skin examination
  8. Be able to inform patients how to conduct a self-skin examination
  9. Name the subtypes of basal cell carcinomas
  10. Describe the pathology of basal cell carcinomas
  11. Understand the spectrum of disease for cutaneous squamous cell carcinomas
  12. Describe the pathology of cutaneous squamous cell carcinoma and its precursors
  13. Take a comprehensive history from a patient presenting with a skin lesion suspicious for malignancy
  14. Understand the elements of a physical examination for a patient with a skin lesion
  15. Describe the role of biopsy in the diagnosis of non-melanoma skin cancer
  16. Understand the role of laboratory tests and imaging in the diagnosis of non-melanoma skin cancer
  17. Understand the TNM classification system for non-melanoma skin cancers
  18. Describe the features that make non-melanoma skin cancers high risk
  19. Understand the protocol for staging high-risk non-melanoma skin cancers
  20. Understand the prognosis for non-melanoma skin cancers
  21. Describe the treatment modalities used to treat non-melanoma skin cancers
  22. Understand when the different treatment modalities are used
  23. Describe the follow-up protocol for non-melanoma skin cancers

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[restab title=”Epidemiology”]

Epidemiology

Non-melanoma skin cancer is the most common type of cancer in the world. The two most common types of non-melanoma skin cancers are basal cell carcinoma (~80%) and cutaneous squamous cell carcinoma (~20%) [1,2].

It is difficult to know the true incidence of non-melanoma skin cancers as very few cancer registries worldwide maintain statistics on these cancers [1,2]. According to the Canadian Cancer agency, it is estimated that there will be 81,300 new cases of non-melanoma skin cancer in Canada in 2012, with 320 deaths [3]. Despite the low rate of mortality from these cancers, they demand treatment. Australian statistics indicate that the incidence of treated non-melanoma skin cancers is more than 5 times the incidence of all other skin cancers combined [4].

Epidemiologic studies have revealed patterns common to both basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC). Both BCC and cSCC have higher rates of incidence in populations located closer to the equator. Incidence also increases exponentially with age, although cases of BCC before age 40 are becoming more frequent.  Additionally, both BCC and cSCC are significantly more frequent in light skinned populations than darker skinned individuals [1,2,4,5,6].

Risk Factors

Image from reference [7]

Image from reference [7]

UV Light Exposure

By far the biggest risk factor for both BCC and cSCC is UV light exposure [1,2,7,8]. UV light is divided by wavelength into three subtypes: UVA (320-400nm), UVB (290-320nm) and UVC (200-290nm). It is estimated that 95% of UV rays that reach the earth are UVA, with the vast majority remaining being UVB rays. UVC rays do not reach the earth’s surface in appreciable amounts, as they cannot pass through the ozone layer [7].

The depth of UV light penetration through the skin is proportional to its wavelength. It is estimated that 20-30% of UVA rays penetrate to the deep dermis. Conversely, only 10% of UVB rays penetrate to the superficial dermis (see image) [7].

Traditionally it has been thought that UVB is responsible for carcinogenesis, while UVA exposure results in other effects such as photoaging. UVB is absorbed directly by DNA, ultimately leading to mutations in the tumor suppressor gene p53. However, there is increasing evidence that UVA also contributes to carcinogenesis. It is hypothesized that UVA indirectly alters DNA through the creation of reactive oxygen species [7,8].

Although UV light exposure is a major risk factor for both BCC and cSCC, there is a difference in the timing of exposure that produces the risk of carcinogenesis. BCC is associated with childhood sun exposure, whereas cSCC is associated with chronic sun exposure in the 10 years prior to diagnosis [5,6,7].

Other Environmental Risk Factors

Chronic arsenic exposure has been shown to lead to both cSCC and BCC [1,2]. Arsenic exposure can be as a result of occupational exposure or environmental exposure, such as drinking contaminated water or eating contaminated food. Evidence suggests that BCC occurs 30-40 years after exposure [2].

Studies have demonstrated that ionizing radiation also increases the incidence of both BCC and cSCC, with a higher risk of BCC development [1,2]. Ionizing radiation is used for a variety of therapeutic purposes, including the treatment of acne and cancer. The risk of developing a non-melanoma skin cancer increases with increasing dose of radiation and when it is delivered over sun exposed areas of skin [4].

Chronic immunosuppression is another risk factor for non-melanoma skin cancer, particularly cSCC [1,2]. Studies from Europe indicated that patients who received heart and kidney transplants were 65-250 times more likely to develop a cSCC than the general population [1,2,4]. The pathogenesis of this risk is complex and likely relates to the inability of the skin to repair the damage caused by UV rays [4].

Approximately 1% of skin cancers occur in chronically inflamed skin, with the vast majority of these being cSCCs [1].

There is increasing evidence that lifestyle factors may play a role in the pathogenesis of non-melanoma skin cancers. It is known that smoking leads to an increased risk of cSCC and it may be contributory in BCC as well. The potential risks and/or benefits of other dietary and social factors are also currently being investigated [1,2,4].

Genetic Factors

In addition to environmental risk factors, there are genetic disorders and polymorphisms that increase susceptibility to non-melanoma skin cancers [1,2,4].

Xeroderma pigmentosa (XP) is an autosomal recessive disorder that leads to an increased risk of both cSCC and BCC. The genetic defect associated with XP manifests as a defective DNA repair mechanism to UV radiation leading to increased sun sensitivity [4]. It is estimated that the rate of skin cancers in this population before age 20 is 2000 times the rate of skin cancer in the rest of the population [4].

Epidermolysis bullosa is a group of syndromes that are characterized by blister formation in response to minimal injury. Certain subtypes of this condition increase risk for both BCC and cSCC. The cSCCs that arise in patients with these syndromes are extremely aggressive, with a 80% mortality rate [1].

Basal cell nevus (Gorlin’s) syndrome is an autosomal dominant disorder that arises due to mutations of the human patched gene. It is characterized by developmental anomalies and multiple BCC’s developing at a young age (between age 2 to 35). There are other characteristic clinical features associated with this syndrome [1,2,4].

Other genes have been implicated in the pathogenesis of cSCC and BCC. These include the p53 tumor suppressor gene, polymorphisms in the glutathione-S-peroxidase enzymes and melanocortin-1 receptor. The role of these genes is the subject of much current research [1,2,4].

Factors that Decrease Risk of Non-Melanoma Skin Cancers

Sun Protection

The basic principles of UV protection are [8]:

  • Avoid the sun during peak hours (10am to 4pm)
  • Wear long clothing when in the sun
  • Do not use tanning beds
  • Use broad spectrum, water resistant sunscreen with an SPF factor of at least 30.

Sunscreen impedes UV radiation from penetrating through the skin’s layers. The use of sunscreen has been proven to decrease the risk of actinic keratoses (the precursor lesion for cSCC) and cSCC. The evidence is inconclusive as to the impact of sunscreen on BCCs [8].

A handout for patients on the proper use of sunscreen can be found by clicking here [8].

Diet

There is evidence that certain dietary factors may play a role in preventing non-melanoma skin cancers, including: low dietary fat intake and high antioxidant intake. However, these results have not yet been supported by large studies and thus cannot be used to inform dietary choices [4].

References:

[1] Lim, J.L., & Asgari M. (2012). Epidemiology and risk factors for cutaneous squamous cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[2] Stern, R.S. (2012). Epidemiology and clinical features of basal cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[3] Canadian Cancer Encyclopedia: Canadian Cancer Society. Statistics for non-melanoma skin cancer overview. Retrieved from: http://info.cancer.ca/cce-ecc/default.aspx?Lang=E&toc=47&cceid=1377. Accessed July 25th, 2012.

[4] Basal cell carcinoma, squamous cell carcinoma (and related lesions) – a guide to clinical management in Australia. Cancer Council Australia and Australian Cancer Network, Sydney, 2008.

[5] Gallagher, R.P., Hill, G.B., Badjdik, C., Fincham, S., Coldman, A.J., McLean, D.I., & Threlfall, W.J. (1995). Sunlight Exposure, Pigmentary Factors and Risk of Nonmelnocytic Skin Cancer: I. Basal Cell Carcinoma. Archives of Dermatology, 131(2), 157-63.

[6] Gallagher, R.P., Hill, G.B., Badjdik, C., Coldman, A.J., Fincham, S., McLean, D.I., & Threlfall, W.J. (1995). Sunlight Exposure, Pigmentary Factors and Risk of Nonmelnocytic Skin Cancer: II. Squamous Cell Carcinoma. Archives of Dermatology, 131(2), 164-69.

[7] Battie C., & Verschoore M. (2012). Cutaneous solar ultraviolet exposure and clinical aspects of photodamage. Indian J Dermatol Venereol Leprol, 78, 9-14. Available from: http://www.ijdvl.com/text.asp?2012/78/7/9/97350

[8] Jou, P.C., Feldman, R. J., & Tomecki, K.J. (2012). UV protection and sunscreens: What to Tell Patients. Cleveland Clinic Journal of Medicine, 79(6), 427-436. doi: 10.3949/ccjm.79a.11110.[/restab]
[restab title=”Screening”]

Screening

To date, Canada has not set out screening guidelines for non-melanoma skin cancer in the general population. Australian practice guidelines suggest that skin cancer screening should be a routine part of the annual check-up. Early detection of non-melanoma skin cancers can reduce morbidity and mortality as well as the costs associated with treatment [1].

Clinical Approach

The most important part of the clinical assessment for skin cancer is the physical examination.

A suggested approach for a full body skin examination is as follows [2]:

i) With the patient sitting on the examination table:

  • Examine the face, head, neck and scalp
  • Examine the arms and hands (all surfaces)

ii) With the patient lying on his or her back:

  • Examine the chest, abdomen, anterior thighs and legs, dorsal feet, soles and toe webs

iii) With the patient either lying on his or her abdomen or standing:

  • Examine the calves, posterior thighs, buttocks, and back.

It is important to ensure complete visualization of any lesion in order to give a thorough description. Every skin lesion should be described noting the following features: location, type, colour, shape, arrangement, distribution, consistency and feel. The two most useful characteristics in terms of forming a differential diagnosis are the type and distribution of lesions. Palpation of the lesion can reveal scale and tenderness. Stretching the skin around the lesion can help expose distinguishing features [3].

Self Skin Examination

Patients may also participate in monitoring their own skin through self-examinations. A useful tool for conducting a self-skin examination is a body map. Patients mark all of their skin lesions on a drawing of a human body. Each time that they examine themselves they mark down new spots and monitor for changes to previously existing spots. There are a number of websites that offer information for patients on how to conduct a proper skin examination [2]:

References:

[1] Basal cell carcinoma, squamous cell carcinoma (and related lesions) – a guide to clinical management in Australia. Cancer Council Australia and Australian Cancer Network, Sydney, 2008.

[2] Geller, A.C, & Swetter, S. (2012). Screening and early detection of melanoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[3] Internet Curriculum for Melanoma Early Detection group. (2011). INFORMED Skin Cancer Education Series. Retrieved from: http://www.skinsight.com/info/for_professionals/skin-cancer-detection-informed/skin-cancer-education.

[4] Jou, P.C., Feldman, R. J., & Tomecki, K.J. (2012). UV protection and sunscreens: What to Tell Patients. Cleveland Clinic Journal of Medicine, 79(6), 427-436. doi: 10.3949/ccjm.79a.11110.[/restab]
[restab title=”Classification”]

Classification

Basal Cell Carcinomas

Subtypes

BCCs are cancers that arise from the non-keratinizing cells of the basal layer of the epidermis. There are three major subtypes of BCC: nodular (~60%), superficial (~30%) and morpheaform/sclerosing (~5-10%) [1]. These subtypes can usually be distinguished from one another based on their appearance (see Signs and Symptoms module).

Pathology

Pathologic evaluation confirms the diagnosis and subtype of BCC. BCCs appear histologically as nests of basaloid cells with hyperchromatic nuclei and scanty cytoplasm within the dermis. Most BCCs have peripheral nuclear palisading. Pigmented BCCs contain melanin [1].

Cutaneous Squamous Cell Carcinomas

Spectrum of Disease

cSCCs are cancers of the keratinocyte, which is the major cell type of the epidermis [2]. cSCC’s can arise spontaneously, however at least 60% of them arise from actinic keratoses (AK). It should be noted, however, that <1% of AKs become cSCCs [3]. cSCC’s can be subdivided into cutaneous squamous cell carcinomas in situ (bowen’s disease) and invasive squamous cell carcinomas [2].

Pathology

These lesions do have characteristic clinical features (see Signs and Symptoms module), however they can only be definitively distinguished histologically. All three of these lesions show nuclear atypia of the keratinocyte [2]. Additionally all may show hyperkeratosis, which produces the rough scales seen clinically. Actinic keratoses and cSCC in situ are distinct from invasive cSCC in that only invasive cSCC penetrates from the epidermis into the dermis [2,3].

References:

[1] Stern, R.S. (2012). Epidemiology and clinical features of basal cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[2] Lim, J.L., & Asgari M. (2012). Epidemiology and risk factors for cutaneous squamous cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate

[3] Basal cell carcinoma, squamous cell carcinoma (and related lesions) – a guide to clinical management in Australia. Cancer Council Australia and Australian Cancer Network, Sydney, 2008.[/restab]
[restab title=”Signs & Symptoms”]

Signs & Symptoms

Non-melanoma skin cancers vary in their appearances and presentations. Clinical examination plays a key role in determining management of skin lesions, thus it is essential to be able to recognize and distinguish between benign skin lesions and non-melanoma skin cancers. It is beyond the scope of this module to describe the features of benign skin lesions; however, students should familiarize themselves with these.

Basal Cell Carcinoma

Basal cell carcinomas can be divided into 3 subtypes: nodular, superficial and morpheaform [1]. Any of these subtypes can present in a pigmented form. In this case they must be distinguished from malignant melanoma [2]. The common presentation of each of these subtypes will be described below.

a) Nodular BCC (60%) [1,2,3]

nodular table

nodular BCC

Image from BC Cancer Skin Atlas [4]

b) Superficial BCC (30%) [1,2,3]

superficial table

superficial BCC

Image from BC Cancer Skin Atlas [4]

c) Morpheaform/Sclerosing (5-10%) [1,2,3]

morpheaform table

morpheaform BCC

Image from BC Cancer Skin Atlas [4]

Cutaneous Squamous Cell Carcinoma

cSCC has a spectrum of disease. 60% of invasive SCCs originate from actinic keratoses [5]. Bowen’s disease is cSCC in situ, where the disease has not penetrated into the dermis through the basement membrane. Invasive cSCC involves both the epidermis and dermis [2,3,6,7]. The spectrum of cSCC can often be distinguished clinically. The characteristic clinical features are described below:

a) Actinic Keratosis [2,3,6]

AK table

AK

Image from BC Cancer Skin Atlas [4]

b) Cutaneous Squamous Cell Carcinoma in-situ (Bowen’s Disease) [2,3,7]

bowens table

bowen's disease

Image from www.dermquest.com

c) Invasive Cutaneous Squamous Cell Carcinoma [2,3,7]

cSCC table

SCC 2

Image from BC Cancer Skin Atlas [4]

SCC 1

Image from BC Cancer Skin Atlas [4]

References:

[1] Stern, R.S. (2012). Epidemiology and clinical features of basal cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[2] Lim, J.L., & Asgari M. (2012). Epidemiology and risk factors for cutaneous squamous cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate

[3] Basal cell carcinoma, squamous cell carcinoma (and related lesions) – a guide to clinical management in Australia. Cancer Council Australia and Australian Cancer Network, Sydney, 2008.[/restab]
[restab title=”Diagnosis”]

Diagnosis

History

 The first step in establishing a diagnosis of skin cancer is to gather a history. Below is a suggested approach to gathering a comprehensive history for a suspected skin cancer [1,2,3]:

History of Presenting Illness

  • Characterize the lesion: size, colour, shape, onset, duration, location/distribution
  • Changes to the lesion: growth, bleeding, other symptoms
  • Associated sensory symptoms (ie. pruritus, pain)
  • Aggravating and alleviating factors
  • Systemic symptoms: weight loss, fever, night sweats
  • Risk factors for skin cancer
  • Prior management of this lesion
  • Use of new skin products

Past medical history

Prior skin lesions: appearance and management

Medications

Prescription, over the counter, supplements

Allergies

Previous cutaneous reactions

Family History

  • Skin cancers: non-melanoma vs. melanoma
  • Actinic keratoses
  • Heritage

Social History

  • Living situation
  • Occupation
  • Travel
  • Hobbies

Review of systems

Physical Exam

The most important part of the clinical assessment for skin cancer is the physical examination. Students should review the approach outlined in the screening module.

It is important to note that cSCCs metastasize in 1-5% of cases [2,4]. The most common locations for metastasis are to the local lymph nodes. As such, the regional lymph nodes should be examined any time that a lesion is suspicion for cSCC [4,5].

A full body skin examination should be performed anytime an examination of a single skin lesion is done. This aids not only in characterizing the distribution of lesions, but it provides the opportunity to screen for other skin lesions [4].

Biopsy

A biopsy is needed in order to definitively establish the diagnosis of BCC or cSCC. All of the following techniques may be used [6]:

Technique

Description

Benefits

Excisional Total removal of a skin lesion including a small margin of normal tissue One step diagnosis and treatment of skin tumors
Incisional Similar to an excisional biopsy, but only part of the lesion is removed
Punch Remove a cone shaped section of tissue that contains the epidermis and full thickness of dermis
  • Minimal scarring
  • Low interference with function
  • Provides information about tumor depth
Shave Removal of the protruding portion of raised skin
  • Quick
  • No suturing needed
  • Good cosmesis

 The choice of which biopsy technique to use is dependent on the clinical situation and the judgment of the treating physician [4,6]. Consideration should be given to choosing a technique that will provide the maximal information regarding the skin cancer and its prognosis, and insight into the optimal treatment modality. For instance, an excisional biopsy may be preferable with small lesions where the clinician suspects that excision may be curative. For lesions that are suspected to be malignant it is preferable to use either an excisional or punch biopsy in order to determine the depth of the lesion [4].

Laboratory Tests

There are no laboratory tests that play a role in the diagnosis of non-melanoma skin cancers [2,3,5].

Imaging

Imaging is seldom used in the diagnosis of non-melanoma skin cancers. In rare cases when the lesions are large and it is difficult to determine the lesion’s depth an ultrasound, CT or MRI can be ordered [4,5]. Imaging may also be used to determine the stage of disease (see Staging).

References:

[1] Stern, R.S. (2012). Epidemiology and clinical features of basal cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[2] Lim, J.L., & Asgari M. (2012). Epidemiology and risk factors for cutaneous squamous cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate

[3] Basal cell carcinoma, squamous cell carcinoma (and related lesions) – a guide to clinical management in Australia. Cancer Council Australia and Australian Cancer Network, Sydney, 2008.[/restab]
[restab title=”Staging”]

Staging

TNM

The current standard for staging non-melanoma skin cancers is the TNM classification system. This classification is only applicable to malignant disease and cannot be applied to precursor lesions. The 2007 guidelines are as follows [1]:

TNM staging

Stages

In the aforementioned TNM system, imaging is necessary to establish the “N” and “M” stages. However, imaging is not performed on the majority of patients with BCCs or cSCCs because only 1-5% of cSCCs and <0.1% of BCCs metastasize [2,3]. That being said, it is important to note that despite the low rate of mortality incurred by these cancers, there can be significant morbidity. BCCs can be extremely locally destructive to tissues and bones despite being low grade [4].

There is no definitive consensus as to how to determine which patients should be imaged. Experts agree that the TNM system is inadequate, as the vast majority patients have T1N0M0 disease and they do not all have the same prognosis [2,5,6]. As such, most guidelines suggest that tumours should be classified as either “high risk” or “low risk” according to their potential for metastasis [2,5,6]. These defining features are not standardized, however, the high-risk features typically increase the 5-year recurrence rate and/or metastatic rate over 15% [3].

High-Risk Features of Basal Cell Carcinoma [2,3,4]

Clinical features

  • >2 cm in size
  • High risk locations: nose, eyelid, temple, preauricular, postauricular, lower legs
  • Inadequate margins for excision
  • Poorly circumscribed
  • Recurrent tumour
  • Incomplete excision

Histologic features

  • Morpheaform/sclerosing subtype
  • Perineural spread
  • Poor prognostic features
High-Risk Features of Cutaneous Squamous Cell Carcinoma [2,3,5,6,7]

Clinical features

  • >2 cm in size
  • High risk locations: ear, lip, genitals
  • Rapid growth
  • Immunosupressed patient
  • Arisen from within a trauma site
  • Recurrent disease
  • Incomplete excision

Histologic features

  • Depth >4 mm
  • Close margins (<2mm)
  • Primary mucosal SCC
  • Poorly differentiated
  • Perineural spread
  • Intravascular invasion

Imaging

Basal Cell Carcinoma

As it is exceedingly rare for BCCs to metastasize, there is no standardized approach for imaging high risk BCCs. BCCs that do metastasize most commonly spread to the local lymph nodes, lung and bone [3].

Cutaneous Squamous Cell Carcinoma

The protocol for imaging cSCCs is much more established than that for BCCs because of their higher rate of nodal spread and metastasis. cSCCs most commonly spread to regional lymph nodes, however they can also metastasize to the lung, liver, bone and brain [3].

A suggested approach for investigating invasive cSCC is depicted in the image below [modified from reference 3]:

Staging

Patients with palpable lymphadenopathy must undergo a lymph node biopsy to establish whether there is evidence of disease in the palpable node. The biopsy is typically conducted using a fine needle aspiration technique. If the cytology confirms that the node is positive for disease, the patient should undergo imaging tests to characterize the extent of nodal involvement. If the cytology does not indicate that there is disease in the palpable lymph node, the physician should consider whether the tumour is “high-risk”. Physicians may decide to send patients with sufficient high-risk features, with or without palpable lymphadenopathy, for imaging of the regional lymph nodes. The most common imaging modality used for staging nodal involvement is CT. Other imaging techniques that may be considered are MRI, PET and ultrasound [2,3].

Patients with confirmed nodal involvement and/or extremely high-risk disease may undergo full-body imaging for distant metastases. The options for full-body imaging include CT, PET and PET-CT. The gold standard is currently unknown [3].

Prognosis

The prognosis for nonmelanoma skin cancers is extremely good in most cases with a greater than 95% disease free survival at 5 years for low stage disease [2]. However, this prognosis changes considerably for high-risk lesions with rates dropping down below 50% for T4 lesions [3]. This underscores the importance of properly staging nonmelanoma skin cancers.

References:

[1] UiCC International Union against Cancer. (2010). Skin Tumours. In: Sobin, L., Gospodarowicz, M., & Wittekind, C. (Eds.). TNM Classification of Malignant Tumours (pp. 162-168). West Sussex, UK: Wiley-Blackwell.

[2] Basal cell carcinoma, squamous cell carcinoma (and related lesions) – a guide to clinical management in Australia. Cancer Council Australia and Australian Cancer Network, Sydney, 2008.

[3] Vidimos, A., & Stultz, T. (2011). Evaluation for locoregional and distant metastases in cutaneous squamous cell and basal cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate

[4] Stern, R.S. (2012). Epidemiology and clinical features of basal cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[5] Brantsch, K.D, Mesiner, C., Schonfisch, B., Trilling, B., Whener-Caroli, J., Rocken, M., & Breuninger, H. (2008). Analysis of risk factors determining prognosis of cutaneous squamous-cell carcinoma: a prospective study. Lancet Oncology, 9, 713-20. DOI: 10.1016/S1470-2045(08)70178-5

[6] Weinberg, A.S., Ogle, C.A., & Shin, E.K. (2007). Metastatic Cutaneous Squamous Cell Carcinoma: An Update. Dermatologic Surgery, 33, 885-899. DOI: 10.1111/j.1524-4725.2007.33190.x

[7] Lim, J.L, & Asgari, M. (2011). Clinical features and diagnosis of cutaneous squamous cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.[/restab]
[restab title=”Treatment”]

Treatment

Treatment Modalities [1,2,3,4]

treatment modalities

Treatment Modality Algorithm

The most commonly used therapy for both BCCs and cSCCs is surgical excision. Radiation therapy is the second most common therapy. The following flow chart outlines an approach for what therapies are appropriate in which cases:

treatment algorithim

1) E&D, cryotherapy and topical therapy are used in select cases when lesions are of low risk (including low metastatic potential) and slow growing. These treatments typically slow disease progression but may not be fully curative and lesions may recur.

2) Watchful waiting may be suitable for lesions which are slowly growing or in cases where patients have multiple comorbidities exceeding the risk of their cancer.

References:

[1] Chartier, T.K., & Stern, R.S. (2012). Treatment and prognosis of cutaneous squamous cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[2] Chartier, T.K., & Asai, S.Z. (2011). Treatment and prognosis of basal cell carcinoma. In: Basow, D.S. (Ed.), UptoDate. Waltham, MA: UptoDate.

[3] Basal cell carcinoma, squamous cell carcinoma (and related lesions) – a guide to clinical management in Australia. Cancer Council Australia and Australian Cancer Network, Sydney, 2008.

[4] Clarke, P. (2012). Nonmelanoma Skin Cancer: Treatment Options. Australian Family Physician, 41(7), 476-80. Retrieved from: http://www.racgp.org.au/afp/201207/47498.[/restab]
[restab title=”Follow-up”]

Follow-up

Follow-up of non-melanoma skin cancers is essential in order to monitor for disease recurrence, metastasis and the presence of new skin cancers. The protocol for follow-up, as laid out by the BC Cancer Agency, differs according to the type of cancer [1]. Any patient with disease recurrence should be referred to a dermatologist or to the cancer agency for further treatment.

Basal Cell Carcinoma

It is very common for patients with one BCC to develop a second BCC. As such, careful follow-up is critical. The following is a suggested approach:

1st Follow-up Visit – 6-8 weeks after treatment

1st Year – Follow-up every 6 months

After 1st Year – Annual follow up, this should be more frequent if the patient develops new BCCs

Squamous Cell Carcinoma

The follow-up for patients with a cSCC depends on whether the tumour was high or low risk. For low-risk disease it is suggested that patients undergo a full body skin examination and a regional lymph node assessment annually for at least 5 years. It is suggested that this approach is continued past the first 5 years as well.

Patients with high-risk disease should be examined more frequently. The following is a suggested approach:

1st Year – Follow-up every 2-3 months with careful examination of the treatment site and regional lymph nodes as well as a full body skin examination

Year 2-5 – Decrease frequency of follow-up in stages

Year 5+ – Annual follow-up

References:

[1] BC Cancer Agency. Non-melanoma skin cancer management policies: Follow-up. Retrieved from: http://www.bccancer.bc.ca/HPI/CancerManagementGuidelines/Skin/NonMelanoma/ManagementPolicies/Followup.htm. Accessed July 30th, 2012.[/restab]
[restab title=”Virtual Patient Case”]

Virtual Patient Case

This case study was designed to supplement your knowledge on the workup of non-melanoma skin cancer and test what you have learned after going through module. Use your mouse to click through the slides and answer each question in the text box provided.

Note: This case can be completed on an Ipad. To do this download the (free) Articulate Mobile Player for the Ipad by clicking here.

Click here to start the Non-Melanoma Skin Cancer Virtual Patient Case[/restab]
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Evaluation

Thank you for using Learn Oncology. This website was designed to supplement teaching in oncology. While the material is targeted to medical students it is our hope that a variety of health care professionals can use this site. Feedback on your experience will help us to improve the resources. Responses are anonymous. Thank you.

Click here to fill out the Skin Cancer Module Survey[/restab]
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Major Contributors:

Elana Thau – Medical Student
Dr. Paris Ann Ingledew – MD, FRCP Radiation Oncologist[/restab][/restabs]


Last Updated: August 2014