Abstract
Basal cell carcinoma (BCC) is the most common, accounting for 80–90% of skin cancers. It arises from the basal layer of the epidermis and its appendages. A complex interplay of environmental, phenotypic and genetic variables leads to the development of BCC. Literature has documented several clinical subtypes of BCC, the most common of which are nodular, superficial and morpheaform. Expeditious diagnosis and analysis are essential for improving the outcome of BCC. Preventive measures, particularly when implemented in childhood and adolescence, may play a critical role. Due to its low metastatic potential, treatment for BCC mostly focuses on local management. The standard treatment of basal cell carcinoma involved complete removal of the lesion by excision or Mohs surgery. In special circumstances, basal cell carcinoma can be treated with cryosurgery, electrodesiccation and curettage, topical medications and photodynamic therapy. This review aimed to evaluate the contemporary diagnosis and management of basal cell carcinoma.
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Inspection by a physician and dermoscopy are used to make a preliminary diagnosis of basal cell carcinoma. Biopsy with histopathologic examination confirms the diagnosis. The pathologic diagnosis with classification as low- or high-risk basal cell carcinoma will guide treatment. Low-risk basal cell carcinomas are removed by surgical excision or Mohs surgery, the latter with facial lesions or in areas where conserving normal adjacent tissue is required. Metastatic or unresectable BCC can respond to treatment with Hedgehog pathway inhibitors, and because of its tumor mutation burden, it can respond to immune checkpoint inhibitors. |
Introduction
Basal cell carcinoma (BCC) is the most common type of skin cancer [1]. Due to its low mortality rate, cancer registries in many countries do not include data on BCC; however, according to data from insurance registries and official statistics, the annual incidence of BCC in the USA is estimated to be 4.3 million [2]. The Caucasian population has a much higher prevalence of BCC. The incidence of BCC is inversely proportional to a country's geographic latitude and its inhabitants’ pigment status [3]. Similar rates of incidence have been discovered in Canada, Europe and Asia, with Australia having the highest rate globally. Even though the incidence trend in Australia appears to have reached a plateau, the rate is consistently growing in all other continents, including South America and Asia. A systematic review by Perera et al. [4] reported that Australia has the highest incidence of non-melanoma skin cancer worldwide. The incidence was higher for men than women and higher for BCC than SCC. Incidence was diverse covering the states of Australia, with the highest in Queensland. However, the aggressive slip, slop, slap campaign has made a significant difference revealing substantial benefits for skin cancer prevention interventions [5]. In Europe, the incidence has risen at a rate of 5% per year over the last decade compared to approximately 2% in the USA. Due to improved diagnosis and an aging population with anamnestic ultraviolet (UV) exposure, this epidemiologic trend is projected to continue in the near future [1,2,3]. The incidence of BCC increases dramatically after 40 years of age, although lately, there has been an increase in its incidence among the younger population, particularly women, as a result of increased UV exposure from the sun or artificial sources [6]. The current review aims to evaluate the contemporary methods of detection and integrated treatment of basal cell carcinoma. This article is primarily based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.
Pathogenesis and Risk Factors
The Patched/Hedgehog intracellular signaling pathway controls cell proliferation, and its constant activation contributes to the development of BCC [7]. Inactivating mutations in PTCH1 and activating mutations in SMOm are the most prevalent mutations, resulting in abnormal Hedgehog pathway activation and tumor development. In a small percentage of BCCs, a loss-of-function mutation in SUFU gene, a negative regulator of the Hedgehog pathway, has been discovered [8]. UV-specific abnormalities in the p53 tumor suppressor gene, which are seen in half of BCCs, are another prevalent mutation [8].
Fitzpatrick skin types I and II are more likely to develop BCCs, with a lifetime risk of 30%. Light eye color, freckles and red hair are all associated with a higher risk of BCC [8]. The most significant environmental risk factor is exposure to UV radiation. Childhood sunburns, family history, photosensitizing medicines, ionizing radiation, the use of tanning beds, chronic immunosuppression and exposure to carcinogenic substances, particularly arsenic, are all risk factors [9,10,11,12,13]. The development of BCC is strongly linked to childhood and severe and intermittent sun exposure [10, 14].
Diagnosis of Basal Cell Carcinoma
Inspection is first process for diagnosis of BCC followed by dermoscopy with confirmation by biopsy and histopathologic examination. Photography of the lesion is also important so that the surgeon performing the definitive procedure can locate the site. Wrong site definitive procedures are the biggest error in this process [15, 16]. Skin biopsy is still necessary to verify the clinical interpretation. BCCs are distinguished histologically by the multiplication of propagating homogeneous basaloid cells with a hyperchromatic nucleus and a small quantity of poorly defined cytoplasm, peripheral palisading and retraction artifact [17]. While the basaloid cells are morphologically similar to epidermal basal cells, they behave similarly to follicular germinative cells [18, 19]. BCC has a variety of clinicopathologic forms, including nodular, infiltrative, fibroepithelial, morpheaform and superficial, all of which have specific clinicopathologic characteristics. Micronodular and basosquamous BCCs are the two most histopathologically important subtypes, and the treatment options may vary according to the type of BCC.
Patients with BCC benefit from standardized follow-up because it allows for early diagnosis of local recurrence and secondary malignancies. It should be carried out in a risk-stratified manner: Isolated, surgically treated BCC and low recurrence risk: follow-up after 6 months to rule out local recurrence, then once a year. Multiple BCCs, high recurrence risk, laBCC, mBCC, syndromes: follow-up every 3 months. Follow-up once a year if no new BCC or recurrence has occurred in the previous 2 years. Closer follow-up may be performed in individual cases [20].
Superficial Type
The superficial variety of BCC (sBCC) is usually found on the torso and limbs and accounts for approximately 20% of all BCCs [21]. The lesions are well-circumscribed, light reddish spots or thin plaques, ranging from micrometers to centimeters in width. A thin rolling border or central atrophy are other characteristics, but other lesions show just erythema and slight scale resembling a nummular eczema patch [21, 22]. Structureless hypopigmentation, short fine telangiectasia, multiple erosions, varying chromatism and a pearly crimson backdrop are all typical findings on dermoscopic inspection [16, 23]. Histologically, several minuscule enclaves of neoplastic cells adhere to the substratum of the epidermis and are generally restricted to the papillary dermis. The nests may be surrounded by a thin zone of fibrous stroma [17, 24] (Fig. 1).
Nodular Type
Nodular BCC (nBCC) accounts for 60–80% of all BCCs, often appearing on the head and neck [21, 25]. Usually, this neoplasm manifests as burl growth with thin vascular channels or transparent papules or pearly, and these lesions are often ulcerated and eroded with crusting whether large tumors or small. The nodule is commonly reported to have convoluted perimeters, suggesting that the boundaries are higher than their centers. Ulceration may be observed in larger lesions. Ramified vascular avenues and a pearly crimson backdrop are common findings on dermoscopic inspection [16, 23]. Nodular lesions are distinguished by an abnormal growth of basaloid cells that create enormous tumor nests with peripheral palisading and random central organization. The presence of retraction gaps between tumor nests and the surrounding stroma is frequently observed [17, 24] (Fig. 2).
Infiltrative Type
BCCs of the infiltrative type are frequently found in conjunction with other categories, particularly the nodular form. Clinically, they appear as weakly defined, white or blanched dull rosy plaques that are thick, hardened, depressed or flat. There may also be ulcerations, erosions, crusts and papules on the surface [21]. On histopathology, proliferation of basaloid cells results in tumor nests with a palisading pattern around the edges, which may be seen superficially. On the periphery or base, permeating areas with extended strings of malignant cells without a fencing sequence can be detected [17, 24] (Fig. 3).
Morpheaform (Sclerosing, Desmoplastic) Type
Morpheaform type BCC is seen on the face and neck, accounting for 5–10% of all BCCs [25]. The poorly defined edges of flesh-colored infiltrating plaques resemble cicatrization [21]. Short, thin telangiectasia, structureless and pigment-less pale dull pink plaques are all common findings on dermoscopic examination [23]. Thin protracted filaments and tiny archipelagos of neoplasms are histopathologically surrounded by a sclerotic collagenous stroma [17, 24] (Fig. 4).
Pigmented BCCs
BCCs with pigmented characteristics due to basal cells which produce melanin, leading to a brown clinical coloration, which can be present in all subtypes, are referred to as pigmented BCCs [26]. Asians and Africans are more likely to have pigmented lesions, while Caucasians are less likely to have them. Despite this, dermoscopic inspection reveals that about 30% of BCCs categorized as “non-pigmented BCC” include pigmented structures [27]. The lesions are histologically strongly associated with the dermoscopic findings, resulting in the identification of two brackets. The principal structure appears brown in color, signifying pigmentation at the dermo-epidermal junction. Surface and penetrating BCC are characterized by rosette-shaped areas and coaxial formations. Subsequent structures that appear blue or gray in color indicate pigmentation in the deeper layers of the dermis. Several pigmented variegated areas are diagnostic of this variety [28, 29] (Fig. 5).
Fibroepithelial Type
This unusual variation most commonly affects the lower back. It appears as a soft papule or pedunculated papulonodular lesion with a skin-colored or erythematous appearance, similar to a fibroma or papilloma [21]. Fibroepithelial-type BCC has a prominent loose stroma and is made up of thin anastomosing strands of basaloid cells. The proliferation index of tumor cells is high [17, 24] (Fig. 6).
Management
Surgical Excision
Archetype surgical excision is the treatment of choice for low-risk BCCs [30, 31]. Three- to 4-mm free surgical boundaries are generally acceptable for tumor elimination in small (< 2 cm) BCCs [32, 33]. Clinical practice recommendations have proposed 4-mm clear brims [34]. The reappearance rate of BCCs following standard excision is usually modest, with the 5-year recurrence rates for low-risk lesions ranging from 0.7 to 5% [30, 32, 35,36,37,38]. Since local anatomy is altered as a result of tissue reorganization, linear closure or secondary intention healing should ideally be used to complete the reconstruction. Intra-surgery tumor margin evaluation should be performed to ensure tumor elimination [34]. Nonsurgical therapy may be explored in patients with non-aggressive, low-risk BCCs [34]. Individuals who are not surgical candidates may benefit from radiotherapy (RT); however, it is often reserved for those older than 60 years. Other low-risk approaches are exclusively advised for patients with the superficial variety who are unable to sustain surgery or radiation.
Mohs Surgery
Mohs micrographic surgery (MMS) is a specialized surgical technique for removing locally invasive, high-risk skin cancers [39]. MMS is an accurate, tissue-sparing method of skin cancer removal named after Frederick Mohs, the surgeon who invented it. It is a surgical methodical process for treating a wide spectrum of cutaneous neoplasms, including BCC and SCC, and has a proven high cure rate. The cornerstone benefit of MMS is that it allows for exact microscopic control of the entire tumor margin while preserving as much healthy tissue as possible [39].
Dr. Mohs developed this procedure in the 1930s. Because the approach involves the application of a chemical fixative (zinc chloride) to the in situ tumor, the treatment was originally named “chemosurgery.” The tumor was removed and microscopically inspected after 24 h of in situ fixing. The procedure was repeated until the tumor had been removed completely [40]. Mohs surgery shifted away from zinc chloride fixation in favor of processing fresh tissue that was frozen and sectioned in a cryostat microtome throughout the next few decades. When compared to traditional chemosurgery, this approach provided various benefits, including shorter processing times (15–30 min), reduced patient discomfort and improved tissue preservation [41].
Mohs surgery is used to treat skin malignancies that have a high risk of recurrence and require tissue preservation [42]. A thin margin of tissue is removed circumferentially around and deep to the clinical margins of a skin tumor during this procedure. To facilitate tissue processing, the specimen is usually removed with a 45-degree bevel. The tissue is then rapidly frozen and sectioned in a cryostat microtome, allowing for rapid tissue processing (about 15–30 min). When tissue is sectioned horizontally, practically all of the tissue margin (peripheral and deep margins) can be studied under the microscope. The procedure is repeated until the tumor’s histopathologic margins are negative [39].
Electrodessication and Curettage (EDC)
EDC is usually used for lesions on the trunk, which can be monitored for recurrence by the patient since the cure rate is not as high as other approaches. It is relatively quick and inexpensive and often done following a shave biopsy procedure [43]. EDCs are fast, inexpensive and easy to use [44, 45]. However, the absence of histopathologic margin evaluation and the difficulty in utilizing this procedure in terminal hair bearing regions because of the tumor's potential to extend down follicular units are its disadvantages [44]. To ensure tumor eradication, conversion to standard surgical excision with postoperative margin evaluation (SSEPME) should begin once the subcutaneous layer is reached. In studies with suitable low-risk selection, 5-year EDC cure rates vary from 91 to 97% [35, 45]. Other studies have reported greater recurrence rates (19–27%), most likely due to malignancies with a high risk of recurrence [30, 46,47,48].
Topical Therapies
Topical 5-fluorouracil (5-FU) 5% cream and imiquimod 5% cream have been approved by the US Food and Drug Administration (FDA) for the treatment of sBCC [49,50,51,52]. Six weeks after treatment, an randomized controlled trial of imiquimod administered twice daily for 12 weeks showed 100% histologic remission [53]. At the 5-year follow-up, further studies found clearance rates of 77.9% and 80.4% for sBCC, highlighting the necessity for long-term research to reliably detect tumor recurrence [54, 55]. Topical imiquimod has a 5-year clinical success rate of 82.5% for sBCCs and nBCCs compared to 97.7% for standard surgical excision with postoperative margin evaluation (SSEPME), according to an RCT comparing topical imiquimod and SSEPME for sBCCs and nBCCs. Imiquimod provided substantially better cosmetic outcomes [56]. For a period of 12 weeks, imiquimod was used once a day, and nBCCs showed similar therapeutic effectiveness, with 76% clinical clearance [57]. Imiquimod is also prescribed to patients with necessitated BCC syndrome [58, 59]. Topical 5-FU is a topical therapeutic option for sBCCs and is usually reserved for them [60,61,62]. An RCT found that at the 12-month follow-up, 5-FU and imiquimod were statistically similar in treating sBCC [63]. Various additional topical therapies for BCC have been proposed; however, there is little long-term evidence [64,65,66]. Long-term studies show that imiquimod is better than 5-FU, with a clearance rate of 79.7% after 3 years, compared to 68.2% with 5-FU. The effectiveness of 5-FU for treating nBCC is documented only through case studies and is therefore not widely advised [67, 68]. Several topical therapies and the level of evidence for nodular and superficial BCCs are listed in Table 1.
Immunotherapy
BCC has been successfully treated with immunotherapy and molecular-targeted therapy. For BCCs that are locally advanced or metastatic, there are currently no FDA approvals for first-line or upfront immunotherapy. On the other hand, BCC has one of the greatest tumor mutation burdens, making it a strong candidate for immune checkpoint inhibitor treatment. In the first-line setting, there are currently no pivotal trial data, but several case reports with anti-CTLA-4 therapy and anti-PD-1 agents have reported activity and responses in advanced disease [69,70,71,72]. Pembrolizumab has shown anticancer efficacy against advanced BCC in a recent phase Ib research. Pembrolizumab with vismodegib was administered to seven individuals, while pembrolizumab alone was administered to nine others [73]. For the monotherapy versus combination therapy cohorts, the overall response rates (ORRs) at 18 weeks were 44% and 29%, respectively, and the progression-free survival at 1 year was 62% and 83%, respectively. Pembrolizumab has also been used in the treatment of BCC, according to five case reports with complete and partial responses, as well as a report of worsening of metastatic BCC bone lesions on medication. Cemiplimab and nivolumab have also proved to be effective in the treatment of advanced BCC [70,71,72, 74,75,76,77,78]. Cemiplimab resulted in a partial response (PR) in a patient with HHI-refractory recurrent metastatic BCC [77]. Two patients with metastatic BCC were treated with nivolumab, one of whom had a PR and a progression-free survival (PFS) of 116 weeks, while the other had an SD and a PFS of 22 weeks [70, 79]. Cemiplimab obtained accelerated FDA approval in February 2021 for the treatment of patients with locally advanced or metastatic BCC who suffered disease progression on HHI or who were HHI-therapy intolerant. The approval was based on the findings of a phase II open-label, multicenter, non-randomized experiment (NCT03132636). With the FDA's recent approval of immunotherapy in the HHI refractory scenario, further research and trials (Phase Ib/NCT04323202) in advanced BCC are expected to result in an increase in FDA-approved indications. Several FDA-approved agents for BCCs and tissue-agnostic approvals are presented in Table 2.
Other Options
Intralesional Therapies
The penetration of topical medicines is sometimes limited because of the protective stratum corneum layer. Direct intralesional injection is an alternative treatment option. Several intralesional chemotherapies for BCC therapy have been studied with varying degrees of success such as methotrexate, rituximab and 5-flurouracil. Adverse events (AEs) are uncommon and are typically dose related [80]. However, local effects at the treatment site and flu-like symptoms are common AEs.
Laser Therapy
Preliminary research has investigated laser therapy as both an adjuvant therapy and monotherapy for BCC (OEBM II) [81]. A retrospective study employing superpulsed carbon dioxide laser therapy for sBCC and nBCC has shown 100% histologic eradication and no recurrence during a 3-year follow-up [82]. A retrospective study employing superpulsed carbon dioxide laser therapy for sBCC and nBCC showed 100% histologic eradication and no recurrence during a 3-year follow-up [83]. In 78.6% of patients, sBCC therapy with a pulsed-dye laser resulted in histologic clearance at 6 months [84]. Reactive hyperemia, edema, scarring and discomfort are some of the reported side effects [85]. The laser-assisted administration of PDT photosensitizers has been examined as a novel therapeutic approach. The recurrence rates of aminolevulinic acid PDT with erbium were considerably reduced in two RCTs: (1) compared to PDT and erbium: yttrium aluminum garnet laser pretreatment; (2) monotherapies using erbium: yttrium aluminum garnet [85, 86].
Cryosurgery
The use of vigorous cryosurgery to destroy tumors is another treatment option. Large variations in recurrence rates (1–39%) have been noted in prospective studies, owing to a lack of homogeneity in patient and tumor selection, follow-up period and inter-operator performance approaches (OEBM II) [87,88,89,90]. After 5 years of follow-up, one dermatologist reported a 99% cure rate for 415 BCCs treated with cryosurgery [87]. Over a 30-year period, non-melanoma skin tumors had a 98.6% overall cure rate according to longer-term statistics. Non-melanoma skin malignancies have also shown good 5-year cure rates in other trials [91, 92]. Compared to surgery, cryotherapy has poorer aesthetic results [93]. Therefore, it is not recommended in hair-bearing regions to avoid scarring alopecia and in the lower legs to avoid ulceration [37]. Large tumors, aggressive histologic subtypes, fixation to the underlying bone, recurrences and deep penetration are not indications for cryosurgery.
Radiotherapy (RT)
The objective of RT is to completely eradicate cancer while preserving as much healthy tissue as possible. For the treatment of BCC, two forms of RT have been used: teletherapy (external beam RT) and brachytherapy. The most appropriate form and quality of RT for each patient is determined by the size, depth and anatomic placement of the invasion. In prospective RCTs, RT has been compared with a variety of alternative treatment options for BCC. In one study, cryotherapy was compared with superficial RT; recurrence occurred 2 years after RT in 4% of 93 patients, whereas after cryotherapy, the recurrence rate was 39% [94]. There were no cases of tumor necrosis or severe pain. Telangiectasias were observed in 14% of the patients after RT. Both groups had a “mild” cosmetic effect. Another RCT compared EDC with 5% topical imiquimod for 6 weeks to superficial RT for BCC of the eyelids [95]. Six weeks following therapy, all 27 patients exhibited evidence of pathologic full response, and after 24 months, there were no clinical signs of recurrence in any of the patients. For newly diagnosed BCCs on the face, a landmark RCT compared surgery with RT [96]. Most RT patients (55%) received inpatient low-dose-rate interstitial brachytherapy, whereas only a small percentage (12%) received traditional outpatient teletherapy. Recurrence occurred in 0.7% of the surgery group and 7.5% of the RT group 4 years after therapy. There have been only a few high-quality comparative assessments of the various RT techniques.
Photodynamic Therapy
Another therapeutic option for low-risk BCCs is photodynamic therapy (PDT) (OEBM I). As photosensitizers, aminolevulinic acid and methyl aminolevulinate have equal efficiency [97]. The US FDA has authorized both substances for the treatment of non-hypertrophic actinic keratosis of the face and scalp. A red-light source is optimal for methyl aminolevulinate, whereas a blue light source is better for aminolevulinic acid. In a meta-analysis (n = 1583) of BCCs treated with PDT, 86.4% of the patients showed full clearance compared to 98.2% of surgically treated lesions [98]. PDT provided much better cosmesis than did surgery, but it was less effective. It has been used as an off-label neoadjuvant treatment to reduce the tumor burden and as an adjuvant treatment to reduce the risk of tumor recurrence [99,100,101].
Fractional lasers such erbium:YAG (Er:YAG) are among popular options for facial rejuvenation. Lasers with infrared wavelength ranges such as long pulse Nd:YAG have been used in nonablative rejuvenation of skin with variable outcomes [102]. Laser may be an alternative treatment for BCC cases according to many hypotheses. Vascular laser such as pulsed dye (595, 585 nm) and long-pulse Nd YAG laser (1064 nm) could be used, relying on the selective photothermolysis theory and selectively targeting tumor’s vascular supply [103].
Vismodegib and Sonidegib
Currently, the FDA has approved two treatments that target the Hedgehog pathway for the treatment of recurrent, metastatic or locally advanced BCC that is not responsive to surgery or radiation. Mutations in the PTCH1 or SMO genes frequently cause the Hedgehog signaling pathway to be dysregulated in BCCs. The FDA approved Vismodegib as the first Hedgehog inhibitor (HHI) in 2012, based on the phase II ERIVANCE (NCT00833417) experiment. At 12 months, an ORR of 47.6% for locally advanced BCC and 30% for metastatic BCC was observed [104, 105]. After 39 months of follow-up, updated study findings revealed an ORR of 60.3% for locally advanced BCC and 48.5% for metastatic BCC [104].
Sonidegib was the second oral HHI to be approved by the FDA for the treatment of BCC. It was approved in 2015 for the treatment of locally advanced BCC that recurred after surgery or radiation therapy, or in patients who were considered ineligible for surgery or radiation therapy. The phase II BOLT pivotal study (NCT01327053) indicated a 56.1% ORR, a median duration of response of 26.1 months and a 93.2% 2-year survival rate for locally advanced BCC. For metastatic BCC, an ORR of 7.7% was recorded [106].
Selection of Appropriate Management Plan
It is imperative to decide from the pathology biopsy report whether the BCC is low or high risk. Table 3 shows the differentiating criteria between high- and low-risk BCC [107].
Advanced BCC is either metastatic or locally advanced BCC with one or more high-risk factors where currently available standard treatments are contraindicated. Locally advanced cases also include BCC > 5 cm in size, which would require extensive surgery, multiple coexisting neoplasms, infiltrative tumors with poorly defined margins and multi-time recurrences. Once these categories and staging are firmly established, the treating consultant can follow this flow chart for management [107] (Fig. 7).
Conclusion
Advances in BCC biology have allowed us to better understand the pathways of lesional evolution, prompting clinicians to demand both precision and accuracy in morphologic classification. Since the precise categorization and staging of BCC have such a significant influence on therapy, all practicing surgical pathologists should be familiar with the histologic criteria for diagnosis and the sub-classification of this human malignancy, which is one of the most prevalent. Smoothened inhibitors, which block the activity of the Hedgehog signaling pathway, have recently been approved for the treatment of metastatic or locally advanced tumors, and remarkable tumor shrinkage results have been reported. Although the exact prognosis of metastatic BCC is yet to be determined, it is likely to be poor, given the rarity of the condition. However, emerging molecular targeting agents hold therapeutic promise.
References
Rogers HW, Weinstock MA, Feldman SR, Coldiron BM. Incidence estimate of nonmelanoma skin cancer (keratinocyte carcinomas) in the US population, 2012. JAMA Dermatol. 2015;151:1081. https://doi.org/10.1001/jamadermatol.2015.1187.
The Skin Cancer Foundation. Skin Cancer Facts and statistics. [(accessed on 25 September 2021)]; Available online: http://www.skincancer.org/skin-cancer-information/skin-cancer-facts.
Verkouteren JAC, Ramdas KHR, Wakkee M, Nijsten T. Epidemiology of basal cell carcinoma: scholarly review. Br J Dermatol. 2017;177:359–72.
Perera E, Gnaneswaran N, Staines C, Win AK, Sinclair R. Incidence and prevalence of non-melanoma skin cancer in Australia: a systematic review. Australas J Dermatol. 2015;56:258–67. https://doi.org/10.1111/ajd.12282.
Walker H, Maitland C, Tabbakh T, Preston P, Wakefield M, Sinclair C. Forty years of Slip! Slop! Slap! A call to action on skin cancer prevention for Australia. Public Health Res Pract. 2022;32(1):1–7.
Christenson LJ. Incidence of basal cell and squamous cell carcinomas in a population younger than 40 years. JAMA. 2005;294:681.
Sehgal VN, Chatterjee K, Pandhi D, Khurana A. Basal cell carcinoma: pathophysiology. Skinmed. 2014;12:176–81.
Bonilla X, Parmentier L, King B, Bezrukov F, Kaya G, Zoete V, et al. Genomic analysis identifies new drivers and progression pathways in skin basal cell carcinoma. Nat Genet. 2016;48:398–406.
Lai V, Cranwell W, Sinclair R. Epidemiology of skin cancer in the mature patient. Clin Dermatol. 2018;36:167–76.
Gallagher RP, Hill GB, Bajdik CD, Fincham S, Coldman AJ, McLean DI, et al. Sunlight exposure, pigmentary factors, and risk of nonmelanocytic skin cancer: I. Basal cell carcinoma. Arch Dermatol. 1995;131:157–63.
Robinson SN, Zens MS, Perry AE, Spencer SK, Duell EJ, Karagas MR. Photosensitizing agents and the risk of non-melanoma skin cancer: a population-based case–control study. J Investig Dermatol. 2013;133:1950–5.
Karagas MR, McDonald JA, Greendberg ER, Stukel TA, Weiss JE, Baron JA, et al. Risk of basal cell and squamous cell skin cancers after ionizing radiation therapy. JNCI J Natl Cancer Inst. 1996;88:1848–53.
Martinez VD, Vucic EA, Becker-Santos DD, Gil L, Lam WL. Arsenic exposure and the induction of human cancers. J Toxicol. 2011;2011:1–13.
Kricker A, Armstrong BK, English DR, Heenan PJ. Does intermittent sun exposure cause basal cell carcinoma? A case control study in Western Australia. Int J Cancer. 1995;60:489–94.
Altamura D, Menzies SW, Argenziano G, Zalaudek I, Soyer HP, Sera F, et al. Dermatoscopy of basal cell carcinoma: morphologic variability of global and local features and accuracy of diagnosis. J Am Acad Dermatol. 2010;62:67–75.
Zalaudek I, Kreusch J, Giacomel J, Ferrara G, Catricala C, Argenziano G. How to diagnose nonpigmented skin tumors: a review of vascular structures seen with dermoscopy: part I Melanocytic skin tumors. J Am Acad Dermatol. 2010;63:361–74.
Patterson JW. Weedon’s skin pathology E-book. Amsterdam: Elsevier Health Sciences; 2014.
Tanese K, Fukuma M, Yamada T, Mori T, Yoshikawa T, Watanabe W, et al. G-protein-coupled receptor GPR49 is up-regulated in basal cell carcinoma and promotes cell proliferation and tumor formation. Am J Pathol. 2008;173:835–43.
Sellheyer K, Krahl D. Basal cell (trichoblastic) carcinoma: Common expression pattern for epithelial cell adhesion molecule links basal cell carcinoma to early follicular embryogenesis, secondary hair germ, and outer root sheath of the vellus hair follicle: a clue to the adnex. J Am Acad Dermatol. 2008;58:158–67.
Lang BM, Balermpas P, Bauer A, Blum A, Brölsch GF, Dirschka T, et al. S2k guidelines for cutaneous basal cell carcinoma—part 2: treatment, prevention and follow-up. JDDG Journal der Deutschen Dermatologischen Gesellschaft. 2019;17:214–30. https://doi.org/10.1111/ddg.13755.
Scrivener Y, Grosshans E, Cribier B. Variations of basal cell carcinomas according to gender, age, location and histopathological subtype. Br J Dermatol. 2002;147:41–7.
Mortz CG, Brockow K, Bindslev-Jensen C, Broesby-Olsen S. It looks like childhood eczema but is it? Clin Exp Allergy. 2019;49:744–53. https://doi.org/10.1111/cea.13381.
Popadic M. Dermoscopic features in different morphologic types of basal cell carcinoma. Dermatol Surg LWW. 2014;40:725–32.
Rosai J. Rosai and Ackerman’s surgical pathology, vol. 1. London: Mosby; 2004.
Dourmishev LA, Rusinova D, Botev I. Clinical variants, stages, and management of basal cell carcinoma. Indian Dermatol Online J. 2013;4:12.
Wozniak Rito A, Zalaudek I, Rudnicka L. Dermoscopy of basal cell carcinoma. Clin Exp Dermatol. 2018;43:241–7.
Lallas A, Argenziano G, Kyrgidis A, Apalla Z, Moscarella E, Longo C, et al. Dermoscopy uncovers clinically undetectable pigmentation in basal cell carcinoma. Br J Dermatol. 2014;170:192–5.
Tabanlıoğlu Onan D, Şahin S, Gököz Ö, Erkin G, Çakır B, Elçin G, et al. Correlation between the dermatoscopic and histopathological features of pigmented basal cell carcinoma. J Eur Acad Dermatol Venereol. 2010;24:1317–25.
Peris K, Altobelli E, Ferrari A, Fargnoli MC, Piccolo D, Esposito M, et al. Interobserver agreement on dermoscopic features of pigmented basal cell carcinoma. Dermatol Surg. 2002;28:643–5.
Thissen MRTM, Neumann MHA, Schouten LJ. A systematic review of treatment modalities for primary basal cell carcinomas. Arch Dermatol. 1999;135:1177–83.
Bath-Hextall F, Bong J, Perkins W, Williams H. Interventions for basal cell carcinoma of the skin: systematic review. BMJ Br Med J. 2004;329:705.
Gulleth Y, Goldberg N, Silverman RP, Gastman BR. What is the best surgical margin for a basal cell carcinoma: a meta-analysis of the literature. Plast Reconstr Surg LWW. 2010;126:1222–31.
Wolf DJ. Surgical margins for basal cell carcinoma. Arch Dermatol. 1987;123:340.
NCCN. NCCN clinical practice guidelines in oncology (NCCN guidelines). Cent Nervous Syst Cancers Version. 2011;2:19–21.
Rowe DE, Carroll RJ, Day CL Jr. Long-Term recurrence rates in previously untreated (primary) basal cell carcinoma: implications for patient follow-up. J Dermatol Surg Oncol. 1989;15:315–28.
Silverman MK, Kopf AW, Bart RS, Grin CM, Levenstein MS. Recurrence rates of treated basal cell carcinomas: part 3: surgical excision. J Dermatol Surg Oncol. 1992;18:471–6.
Kuijpers DIM, Thissen MRTM, Berretty PJM, Ideler FHLB, Nelemans PJ, Neumann MHAM. Surgical excision versus curettage plus cryosurgery in the treatment of basal cell carcinoma. Dermatol Surg. 2007;33:579–87.
Rhodes LE, de Rie MA, Leifsdottir R, Raymond CY, Bachmann I, Goulden V, et al. Five-year follow-up of a randomized, prospective trial of topical methyl aminolevulinate photodynamic therapy vs surgery for nodular basal cell carcinoma. Arch Dermatol. 2007;143:1131–6.
Prickett KA, Ramsey ML. Mohs micrographic surgery. Treasure Island: StatPearls, StatPearls Publishing; 2021.
Mohs FE. Chemosurgery. Clin Plast Surg. 1980;7:349–60.
Tromovitch TA, Stegman SJ. Microscopic-controlled excision of cutaneous tumors. Chemosurgery, fresh tissue technique. Cancer. 1978;41:653–8. https://doi.org/10.1002/1097-0142(197802)41:2%3c653::AID-CNCR2820410232%3e3.0.CO;2-X.
Connolly SM, Baker DR, Coldiron BM, Fazio MJ, Storrs PA, Vidimos AT, et al. AAD/ACMS/ASDSA/ASMS 2012 appropriate use criteria for Mohs micrographic surgery: a report of the American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery Association, and the American Society for Mohs Su. J Am Acad Dermatol. 2012;67:531–50. https://doi.org/10.1016/j.jaad.2012.06.009.
Ferry AM, Sarrami SM, Hollier PC, Gerich CF, Thornton JF. Treatment of non-melanoma skin cancers in the absence of Mohs micrographic surgery. Plast Reconstr Surg Glo Open. 2020;8: e3300. https://doi.org/10.1097/GOX.0000000000003300.
Bichakjian CK, Olencki T, Aasi SZ, Alam M, Andersen JS, Berg D, et al. Basal cell skin cancer, version 1.2016, NCCN clinical practice guidelines in oncology. J Natl Compr Cancer Netw. 2016;14:574–97.
Barlow JO, Zalla MJ, Kyle A, DiCaudo DJ, Lim KK, Yiannias JA. Treatment of basal cell carcinoma with curettage alone. J Am Acad Dermatol. 2006;54:1039–45.
Blixt E, Nelsen D, Stratman E. Recurrence rates of aggressive histologic types of basal cell carcinoma after treatment with electrodesiccation and curettage alone. Dermatol Surg. 2013;39:719–25.
Rodriguez-Vigil T, Vázquez-López F, Perez-Oliva N. Recurrence rates of primary basal cell carcinoma in facial risk areas treated with curettage and electrodesiccation. J Am Acad Dermatol. 2007;56:91–5.
Julian C, Bowers PW, Pritchard C. A comparative study of the effects of disposable and Volkmann spoon curettes in the treatment of basal cell carcinoma. Br J Dermatol. 2009;161:1407–9.
Geisse J, Caro I, Lindholm J, Golitz L, Stampone P, Owens M. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, randomized, vehicle-controlled studies. J Am Acad Dermatol. 2004;50:722–33.
Schulze HJ, Cribier B, Requena L, Reifenberger J, Ferrandiz C, Garcia Diez A, et al. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from a randomized vehicle controlled phase III study in Europe. Br J Dermatol. 2005;152:939–47.
Micali G, Lacarrubba F, Nasca MR, Ferraro S, Schwartz RA. Topical pharmacotherapy for skin cancer: part II. Clinical applications. J Am Acad Dermatol. 2014;70:979-e1.
Roozeboom MH, Arits A, Nelemans PJ, Kelleners Smeets NWJ. Overall treatment success after treatment of primary superficial basal cell carcinoma: a systematic review and meta analysis of randomized and nonrandomized trials. Br J Dermatol. 2012;167:733–56.
Geisse JK, Rich P, Pandya A, Gross K, Andres K, Ginkel A, et al. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: a double-blind, randomized, vehicle-controlled study. J Am Acad Dermatol. 2002;47:390–8.
Gollnick H, Barona CG, Frank RGJ, Ruzicka T, Megahed M, Maus J, et al. Recurrence rate of superficial basal cell carcinoma following treatment with imiquimod 5% cream: conclusion of a 5-year long-term follow-up study in Europe. Eur J Dermatol. 2008;18:677–82.
Quirk C, Gebauer K, De’Ambrosis B, Slade HB, Meng T-C. Sustained clearance of superficial basal cell carcinomas treated with imiquimod cream 5%: results of a prospective 5-year study. Cutis. 2010;85:318–24.
Bath-Hextall F, Ozolins M, Armstrong SJ, Colver GB, Perkins W, Miller PSJ, et al. Surgical excision versus imiquimod 5% cream for nodular and superficial basal-cell carcinoma (SINS): a multicentre, non-inferiority, randomised controlled trial. Lancet Oncol. 2014;15:96–105.
Shumack S, Robinson J, Kossard S, Golitz L, Greenway H, Schroeter A, et al. Efficacy of topical 5% imiquimod cream for the treatment of nodular basal cell carcinoma: comparison of dosing regimens. Arch Dermatol. 2002;138:1165–71.
Micali G, De PR, Caltabiano R, Impallomeni R, Lacarrubba F. Topical imiquimod treatment of superficial and nodular basal cell carcinomas in patients affected by basal cell nevus syndrome: a preliminary report. J Dermatol Treat. 2002;13:123–7.
Micali G, Lacarrubba F, Nasca MR, De Pasquale R. The use of imiquimod 5% cream for the treatment of basal cell carcinoma as observed in Gorlin’s syndrome. Clin Exp Dermatol. 2003;28:19–23.
Mohs FE, Jones DL, Bloom RF. Tendency of fluorouracil to conceal deep foci of invasive basal cell carcinoma. Arch Dermatol. 1978;114:1021–2.
Klostermann GF. Effects of 5-fluorouracil (5-FU) ointment on normal and diseased skin histological findings and deep action. Dermatology. 1970;140:47–54.
Reymann F. Treatment of basal cell carcinoma of the skin with 5-fluorouracil ointment. Dermatology. 1979;158:368–72.
Arits AHMM, Mosterd K, Essers BAB, Spoorenberg E, Sommer A, De Rooij MJM, et al. Photodynamic therapy versus topical imiquimod versus topical fluorouracil for treatment of superficial basal-cell carcinoma: a single blind, non-inferiority, randomised controlled trial. Lancet Oncol. 2013;14:647–54.
Siller G, Rosen R, Freeman M, Welburn P, Katsamas J, Ogbourne SM. PEP005 (ingenol mebutate) gel for the topical treatment of superficial basal cell carcinoma: results of a randomized phase IIa trial. Australas J Dermatol. 2010;51:99–105.
Cuevas P, Angulo J, Cuevas-Bourdier A, Salguero I, Gimenez-Gallego G. Treatment of infiltrative basal cell carcinomas by inhibiting the fibroblast growth factor (FGF)-signal transducer and activator of transcription (STAT)-3 signalling pathways. J Cancer Sci Ther. 2011;3:3.
Punjabi S, Cook LJ, Kersey P, Marks R, Cerio R. Solasodine glycoalkaloids: a novel topical therapy for basal cell carcinoma. A double blind, randomized, placebo controlled, parallel group, multicenter study. Int J Dermatol. 2008;47:78–82.
Shelley WB, Wood MG. Nodular superficial pigmented basal cell epitheliomas: long-term fluorouracil treatment. Arch Dermatol. 1982;118:928–30.
Eovi R, Smolkovi N, Pasi A, Kostovi K, Hrsan D. Multiple basal cell carcinomas of lower legs with stasis dermatitis: a therapeutic challenge. Acta Dermatovenerol Croat. 2012;20:191–6.
Mohan SV, Kuo KY, Chang ALS. Incidental regression of an advanced basal cell carcinoma after ipilimumab exposure for metastatic melanoma. JAAD Case Rep. 2016;2:13–5. https://doi.org/10.1016/j.jdcr.2015.11.007.
Ikeda S, Goodman AM, Cohen PR, Jensen TJ, Ellison CK, Frampton G, et al. Metastatic basal cell carcinoma with amplification of PD-L1: exceptional response to anti-PD1 therapy. npj Genom Med. 2016;1:16037. https://doi.org/10.1038/npjgenmed.2016.37.
Lipson EJ, Lilo MT, Ogurtsova A, Esandrio J, Xu H, Brothers P, et al. Basal cell carcinoma: PD-L1/PD-1 checkpoint expression and tumor regression after PD-1 blockade. J Immunother Cancer. 2017;5:23. https://doi.org/10.1186/s40425-017-0228-3.
Cannon JGD, Russell JS, Kim J, Chang ALS. A case of metastatic basal cell carcinoma treated with continuous PD-1 inhibitor exposure even after subsequent initiation of radiotherapy and surgery. JAAD Case Rep. 2018;4:248–50. https://doi.org/10.1016/j.jdcr.2018.01.015.
Chang ALS, Tran DC, Cannon JGD, Li S, Jeng M, Patel R, et al. Pembrolizumab for advanced basal cell carcinoma: an investigator-initiated, proof-of-concept study. J Am Acad Dermatol. 2019;80:564–6. https://doi.org/10.1016/j.jaad.2018.08.017.
Moreira A, Kirchberger MC, Toussaint F, Erdmann M, Schuler G, Heinzerling L. Effective anti-programmed death-1 therapy in a SUFU -mutated patient with Gorlin–Goltz syndrome. Br J Dermatol. 2018;179:747–9. https://doi.org/10.1111/bjd.16607.
Winkler JK, Schneiderbauer R, Bender C, Sedlaczek O, Fröhling S, Penzel R, et al. Anti-programmed cell death-1 therapy in nonmelanoma skin cancer. Br J Dermatol. 2017;176:498–502. https://doi.org/10.1111/bjd.14664.
Fischer S, Ali OH, Jochum W, Kluckert T, Flatz L, Siano M. Anti-PD-1 therapy leads to near-complete remission in a patient with metastatic basal cell carcinoma. Oncol Res Treat. 2018;41:391–4. https://doi.org/10.1159/000487084.
Falchook GS, Leidner R, Stankevich E, Piening B, Bifulco C, Lowy I, et al. Responses of metastatic basal cell and cutaneous squamous cell carcinomas to anti-PD1 monoclonal antibody REGN2810. J Immunother Cancer. 2016;4:70. https://doi.org/10.1186/s40425-016-0176-3.
Cohen P, Kato S, Goodman A, Ikeda S, Kurzrock R. Appearance of new cutaneous superficial basal cell carcinomas during successful nivolumab treatment of refractory metastatic disease: implications for immunotherapy in early versus late disease. Int J Mol Sci. 2017;18:1663. https://doi.org/10.3390/ijms18081663.
Borradori L, Sutton B, Shayesteh P, Daniels GA. Rescue therapy with anti-programmed cell death protein 1 inhibitors of advanced cutaneous squamous cell carcinoma and basosquamous carcinoma: preliminary experience in five cases. Br J Dermatol. 2016;175:1382–6. https://doi.org/10.1111/bjd.14642.
Good LM, Miller MD, High WA. Intralesional agents in the management of cutaneous malignancy: a review. J Am Acad Dermatol. 2011;64:413–22.
Lanoue J, Goldenberg G. Basal cell carcinoma: a comprehensive review of existing and emerging nonsurgical therapies. J Clin Aesthet Dermatol. 2016;9:26.
Campolmi P, Brazzini B, Urso C, Ghersetich I, Mavilia L, Hercogova J, et al. Superpulsed CO2 laser treatment of basal cell carcinoma with intraoperatory histopathologic and cytologic examination. Dermatol Surg. 2002;28:909–12.
Moskalik K, Kozlov A, Demin E, Boiko E. The efficacy of facial skin cancer treatment with high-energy pulsed neodymium and Nd: YAG lasers. Photomed Laser Surg. 2009;27:345–9.
Karsai S, Friedl H, Buhck H, Junger M, Podda M. The role of the 595 nm pulsed dye laser in treating superficial basal cell carcinoma: outcome of a double blind randomized placebo controlled trial. Br J Dermatol. 2015;172:677–83.
Smucler R, Vlk M. Combination of Er: YAG laser and photodynamic therapy in the treatment of nodular basal cell carcinoma. Lasers Surg Med. 2008;40:153–8.
Choi SH, Kim KH, Song KH. Er: YAG ablative fractional laser primed photodynamic therapy with methyl aminolevulinate as an alternative treatment option for patients with thin nodular basal cell carcinoma: 12 month follow up results of a randomized, prospective, comparative trial. J Eur Acad Dermatol Venereol. 2016;30:783–8.
Kuflik EG. Cryosurgery for skin cancer: 30 year experience and cure rates. Dermatol Surg. 2004;30:297–300.
Mallon E, Dawber R. Cryosurgery in the treatment of basal cell carcinoma: assessment of one and two freeze thaw cycle schedules. Dermatol Surg. 1996;22:854–8.
Wang I, Bendsoe N, Klinteberg CA, Enejder AMK, Andersson-Engels S, Svanberg S, et al. Photodynamic therapy vs. cryosurgery of basal cell carcinomas: results of a phase III clinical trial. Br J Dermatol. 2001;144:832–40.
Basset-Seguin N, Ibbotson SH, Emtestam L, Tarstedt M, Morton C, Maroti M, et al. Topical methyl aminolaevulinate photodynamic therapy versus cryotherapy for superficial basal cell carcinoma: a 5 year randomized trial. Eur J Dermatol. 2008;18:547–53.
Nordin P, Stenquist B. Five-year results of curettage-cryosurgery for 100 consecutive auricular non-melanoma skin cancers. J Laryngol Otol. 2002;116:893–8.
Nordin P, Larke O, Stenquist B. Five-year results of curettage-cryosurgery of selected large primary basal cell carcinomas on the nose: an alternative treatment in a geographical area underserved by Mohs’ surgery. Br J Dermatol. 1997;136:180–3.
Thissen MRTM, Nieman FHM, Ideler AHLB, Berretty PJM, Neumann HAM. Cosmetic results of cryosurgery versus surgical excision for primary uncomplicated basal cell carcinomas of the head and neck. Dermatol Surg. 2000;26:759–64.
Hall VL, Leppard BJ, McGill J, Kesseler ME, White JE, Goodwin P. Treatment of basal-cell carcinoma: comparison of radiotherapy and cryotherapy. Clin Radiol. 1986;37:33–4.
Garcia-Martin E, Gil-Arribas LM, Idoipe M, Alfaro J, Pueyo V, Pablo LE, et al. Comparison of imiquimod 5% cream versus radiotherapy as treatment for eyelid basal cell carcinoma. Br J Ophthalmol. 2011;95:1393–6.
Avril MF, Auperin A, Margulis A, Gerbaulet A, Duvillard P, Benhamou E, et al. Basal cell carcinoma of the face: surgery or radiotherapy? Results of a randomized study. Br J Cancer. 1997;76:100–6.
Tarstedt M, Gillstedt M, Wennberg Larko AM, Paoli J. Aminolevulinic acid and methyl aminolevulinate equally effective in topical photodynamic therapy for non melanoma skin cancers. J Eur Acad Dermatol Venereol. 2016;30:420–3.
Wang H, Xu Y, Shi J, Gao X, Geng L. Photodynamic therapy in the treatment of basal cell carcinoma: a systematic review and meta analysis. Photodermatol Photoimmunol Photomed. 2015;31:44–53.
Jeremic G, Brandt MG, Jordan K, Doyle PC, Yu E, Moore CC. Using photodynamic therapy as a neoadjuvant treatment in the surgical excision of nonmelanotic skin cancers: prospective study. J Otolaryngol Head Neck Surg. 2011;40:S82-9.
Torres T, Fernandes I, Costa V, Selores M. Photodynamic therapy as adjunctive therapy for morpheaform basal cell carcinoma. Acta Dermatovenerologica Alpina Panonica et Adriatica. 2011;20:23–5.
Lu Y, Wang Y, Yang Y, Zhang X, Gao Y, Yang Y, et al. Efficacy of topical ALA-PDT combined with excision in the treatment of skin malignant tumor. Photodiagn Photodyn Ther. 2014;11:122–6.
Dadkhahfar S, Fadakar K, Robati RM. Efficacy and safety of long pulse Nd:YAG laser versus fractional erbium:YAG laser in the treatment of facial skin wrinkles. Lasers Med Sci. 2019;34:457–64. https://doi.org/10.1007/s10103-018-2614-6.
Soleymani T, Abrouk M, Kelly KM. An analysis of laser therapy for the treatment of nonmelanoma skin cancer. Dermatol Surg. 2017;43:615–24. https://doi.org/10.1097/DSS.0000000000001048.
Sekulic A, Migden MR, Basset-Seguin N, Garbe C, Gesierich A, Lao CD, et al. Long-term safety and efficacy of vismodegib in patients with advanced basal cell carcinoma: final update of the pivotal ERIVANCE BCC study. BMC Cancer. 2017;17:332. https://doi.org/10.1186/s12885-017-3286-5.
Sekulic A, Migden MR, Lewis K, Hainsworth JD, Solomon JA, Yoo S, et al. Pivotal ERIVANCE basal cell carcinoma (BCC) study: 12-month update of efficacy and safety of vismodegib in advanced BCC. J Am Acad Dermatol. 2015;72:1021-1026.e8. https://doi.org/10.1016/j.jaad.2015.03.021.
Lear JT, Migden MR, Lewis KD, Chang ALS, Guminski A, Gutzmer R, et al. Long-term efficacy and safety of sonidegib in patients with locally advanced and metastatic basal cell carcinoma: 30-month analysis of the randomized phase 2 BOLT study. J Eur Acad Dermatol Venereol. 2018;32:372–81. https://doi.org/10.1111/jdv.14542.
Nasr I, McGrath EJ, Harwood CA, Botting J, Buckley P, Budny PG, et al. British Association of Dermatologists guidelines for the management of adults with basal cell carcinoma 2021*. Br J Dermatol. 2021;185:899–920. https://doi.org/10.1111/bjd.20524.
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Naik, P.P., Desai, M.B. Basal Cell Carcinoma: A Narrative Review on Contemporary Diagnosis and Management. Oncol Ther 10, 317–335 (2022). https://doi.org/10.1007/s40487-022-00201-8
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DOI: https://doi.org/10.1007/s40487-022-00201-8