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81515454.Pdf CORE Metadata, citation and similar papers at core.ac.uk Provided by Springer - Publisher Connector Rare Cancers Ther (2015) 3:133–145 DOI 10.1007/s40487-015-0012-9 REVIEW Reviewing Challenges in the Diagnosis and Treatment of Lentigo Maligna and Lentigo-Maligna Melanoma Margit L. W. Juha´sz . Ellen S. Marmur To view enhanced content go to www.rarecancers-open.com Received: May 10, 2015 / Published online: October 15, 2015 Ó The Author(s) 2015. This article is published with open access at Springerlink.com ABSTRACT non-uniform pigmentation/distribution of melanocytes, and increased melanocyte Lentigo maligna (LM) and lentigo-maligna density in a background of extensive melanoma (LMM) are pigmented skin lesions photodamage. Advancements in that may exist on a continuous clinical and immunohistochemical staining techniques, pathological spectrum of melanocytic skin including soluble adenylyl cyclase (antibody cancer. LM is often described as a ‘‘benign’’ R21), makes diagnosis easier and allows the lesion and is accepted as a melanoma in situ; definition of borders down to a single cell. After LM can undergo malignant transformation to a pathologic diagnosis, there are a variety of particularly aggressive melanoma. LMM is an treatment options, both surgical and invasive melanoma that shares properties of non-surgical. Although surgical removal with a LM, as well as exhibiting the metastatic wide excision border is the preferred treatment potential of malignant melanoma. due to decreased recurrence rates, experimental Unfortunately, LM/LMM diagnosis based on combination therapies are gaining popularity. dermoscopy is rather ambiguous, and these However, no matter the treatment, LM/LMM lesions are often mistaken for junctional carries a high recurrence rate, and patients must dysplastic nevi over sun-damaged skin, be monitored rigorously for recurrence as well pigmented actinic keratosis, solar lentigo, or as the appearance of additional skin seborrheic keratosis. Diagnosis must be made lesions/cancers. on biopsy using distinct dermatopathologic features. These include a pagetoid appearance of melanocytes, melanocyte atypia, Keywords: Lentigo maligna; Lentigo-maligna melanoma; Pigmented actinic keratosis; M. L. W. Juha´sz (&) Dermoscopy; Histopathology; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY, USA Immunohistochemistry; Surgical excision; e-mail: [email protected] Non-surgical techniques E. S. Marmur Marmur Medical, New York, NY, USA 134 Rare Cancers Ther (2015) 3:133–145 INTRODUCTION surface area, increasing border irregularity, and/or development of elevated areas [1, 3–5]. Lentigo maligna (LM) is a pigmented skin lesion LMM, on the other hand, is a subset of that is often mistaken for a ‘‘benign-type’’ lesion. melanoma that accounts for 4–15% of However, to date, no longitudinal studies have melanoma diagnoses [1, 3–5]. Early studies proven this assumption. In fact, recent research suggested a lifetime risk of developing LMM is pointing to a continuous clinical and from LM of 5% [6]; however, more recent work pathological spectrum of skin cancer spanning suggests that this number may be as high as lentigo, LM, and lentigo-maligna melanoma 20% [7–9]. Ultraviolet radiation-induced (LMM) in the same fashion as benign nevus, mutation of the hair follicle has been melanoma in situ, and invasive melanoma. LM suggested as the cause of LMM, producing a is currently considered to be ‘‘melanoma fairly aggressive and deep skin cancer [3, 4]. in situ’’, with a 5–20% lifetime risk of LMM is so named because it demonstrates progression to LMM [1], and represents 4–15% features of LM in its in situ component, while of all invasive melanomas [2], with properties of also displaying features typical of invasive LM plus the metastatic potential of malignant melanoma [1, 3–5]. Risk factors that predispose melanoma [1, 3–5]. At this point, it is the a patient to either LM or LMM include light skin dermatologist’s and dermatopathologist’s that freckles, a history of non-melanoma skin challenge to assess the risk of invasive cancer, and a history of sun damage/burn. potential of each pigmented lesion and to However, the development of LM/LMM has no prevent further morbidity and mortality from reported dose–effect relationship with respect to melanoma transformation. This article is based an individual’s cumulative sun damage or an on previously conducted studies and does not association with the genetic propensity of an involve any new studies of human or animal individual to form nevi [10, 11] (Fig. 1). subjects performed by any of the authors. LM and LMM have similar clinical presentation. The lesions are both found in LM and LMM chronically sun-exposed areas, often of the nose, cheeks, and ears (not often on the upper LM, formerly known as a Hutchinson melanotic freckle, is defined as ‘‘melanoma in situ’’ occurring at a site of chronic sun exposure. In 5–20% of patients, it will develop into an invasive melanoma, most often of the aggressive desmoplastic melanoma subtype [1]. This progression can take anywhere from less than 10 years to more than 50 years, and any time in between. Confusing as these statistics may seem, these data come from studies completed 30 years ago and have not yet been Fig. 1 Pigmented lesion of the cheek in an elderly man. Biopsy showed atypical intraepidermal melanocytic refuted [1, 3–5]. The probability that LM proliferation extending to the lateral margins. With transforms into a melanoma increases if the anti-melan-A staining, a final diagnosis of melanoma LM exhibits variation in color, expanding in situ was made Rare Cancers Ther (2015) 3:133–145 135 back, forearms, or legs). The peak incidence for pigmented AK is not believed to be due to both lesions is 65–80 years of age, but in recent changes in the quality or quantity of years there has been increasing incidence in melanocytes, as in a melanoma [19]. younger age groups (40–65 years), as witnessed Histologically, a pigmented AK will show signs in a cohort from northern California [1, 3, 12]. of apoptotic keratinocytes in the epidermis and Characteristically, an LM/LMM will present as upper dermis, hyperkeratosis/parakeratosis, an atypical, non-scaly pigmented patch with melanophages in the papillary dermis, and ill-defined borders and variable size, shape, or increased melanin deposition [20, 21]. shade (from tan to black to the rare amelanotic). These skin lesions grow radially and may grow/ Dermoscopy of LM/LMM Versus regress in a pattern that makes the LM/LMM Pigmented AK appear to ‘‘move across’’ the skin [1, 3]. The skin surrounding the LM/LMM may also show signs Under the dermatoscope, a pigmented AK will of chronic solar damage [solar elastosis, solar have characteristics such as asymmetric lentigines, actinic keratosis (AK)]. If an LM pigmented follicular openings, develops dark pigmentation, sharp borders, or hyperpigmentation of the follicle rim, light elevated areas, these changes may suggest a brown pseudo-networks, light rhomboidal clinical progression to LMM [1, 3, 13]. structures, light streaks, and peripheral grey dots. Though these features are very similar to Differential Diagnoses of LM/LMM those found with LM/LMM dermoscopy, the lighter color pigment differentiates pigmented The differential diagnosis of LM/LMM includes AK from LM/LMM [13]. myriad other pigmented skin lesions, including There are three dermoscopic criteria that solar lentigo, seborrheic keratosis, lichen significantly differentiate a pigmented AK from planus-like keratosis, junctional dysplastic nevus a malignant LM/LMM: dark rhomboidal over sun damage, and pigmented AK [14–16]. structures, dark streaks, and black blotches. However, there are distinct differences that can be Dark streaks and blotches are specific for LM/ used to distinguish between these differential LMM at a rate of 97% and 100%, respectively [13]. diagnoses and the diagnosis of LM/LMM. LM skin lesions show characteristic black One of the most under-recognized blotches, asymmetric hyperpigmented rims differential diagnosis for LM/LMM is the around follicular openings, dark rhomboidal pigmented AK [14]. Pigmented AKs are areas of structures (pigmented lines surrounding skin that are damaged with ultraviolet radiation appendageal openings), asymmetric peripheral and are considered ‘‘pre-cancerous’’. Without dark grey dots (indicative of superficial treatment, they may progress to either a melanotic lesions, with a greater asymmetry squamous cell carcinoma (SCC) within 2 years proportional to greater malignancy), and or a basal cell carcinoma (BCC) [17, 18]. Based annular-granular structures [13]. LMM skin on reporting as of 2012, it is thought that lesions demonstrate features such as a pigmented AKs arise as a collision between a target-like pattern (there is no definitive non-pigmented AK and a separate but pathological correlate to date, but it is believed coexistent pigmented lesion such as a solar to be related to pilar infundibulum invasion), lentigo. Therefore, the pigmentation within a increased vascular density, dark streaks, and 136 Rare Cancers Ther (2015) 3:133–145 Table 1 Summary of dermoscopic and histological findings of pigmented AK, LM, and LMM [1, 10, 13, 16, 19–26] Pigmented AK LM/LMM LM LMM Dermoscopy Precancerous Dark streaks (97% Melanoma ‘‘in situ’’ Melanoma Lighter color pigment (collision specific) Asymmetric hyperpigmented rims Target-like pattern lesion) Dark blotches around follicular openings Increased vascular (100% specific) Dark rhomboidal
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