ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Microcystic adnexal carcinoma

Microcystic adnexal carcinoma
Literature review current through: Jan 2024.
This topic last updated: Apr 05, 2023.

INTRODUCTION — Microcystic adnexal carcinoma (MAC) is an infiltrative cutaneous tumor that most often presents as a scar-like papule or plaque on sun-exposed skin [1]. Historical terms that have been used to refer to this tumor include "sclerosing sweat duct carcinoma," "malignant syringoma," and "syringoid carcinoma." Tissue invasion by MAC frequently extends far beyond the clinical margins of the tumor. In addition, perineural involvement is common.

Although metastasis and death from MAC are rare events, significant morbidity can occur as a result of deep local tissue invasion, and treatment of MAC is recommended. Surgery that results in complete removal of the tumor is the treatment of choice for MAC.

The epidemiology, diagnosis, and management of MAC will be discussed in this topic review.

EPIDEMIOLOGY — Microcystic adnexal carcinoma (MAC) is a rare tumor that was first described in 1982 [2]. In retrospect, earlier reports documented this tumor prior to its recognition as a distinct entity [3].

The vast majority of reported cases of MAC have been in White individuals; however, MAC can also occur in other populations [4-9]. An analysis of data from the Surveillance, Epidemiology, and End Results (SEER) database collected between 1973 and 2004 found an incidence rate of 6.5 per 10 million White individuals [10]. The incidence rates for Black persons and Asian/Pacific Islanders were significantly lower, at 1.9 and 1.6 per 10 million individuals, respectively [10].

The sex distribution in studies of patients with MAC has varied from fairly equivalent proportions to a slight female predominance [7,9-12]. In the SEER database analysis, which represents the largest reported series of patients with MAC (n = 223), 57 percent of patients were female and 43 percent were male [10].

MAC most commonly affects middle-aged and older adults [7,10]. The median age for the development of MAC in the SEER database analysis was 68 years [10]. Rarely, the tumor occurs in children [13-15]. Congenital MAC has been described in a few neonates [16,17].

RISK FACTORS — The rarity of microcystic adnexal carcinoma (MAC) makes it difficult to draw definitive conclusions on risk factors for the disease. Ultraviolet radiation, ionizing radiation, and immunosuppression have been proposed as potential contributory factors:

Ultraviolet radiation – The common localization of tumors to the head and neck and the elevated frequency in White individuals suggest that exposure to ultraviolet radiation may contribute to the development of MAC [10]. Also in support of a role for ultraviolet radiation, a series of 48 patients with MAC in the United States (where drivers sit in the left side of the vehicle) found a predominance of left-sided lesions (52 percent on left, 25 percent on right, and 23 percent in midline or unspecified) [11], whereas a series of 14 patients in Australia (where drivers sit in the right side of the vehicle) found that more lesions occurred on the right side (56 versus 38 percent) [18]. However, ultraviolet light-induced p53 mutations, which have been associated with the development of other cutaneous carcinomas, lack a strong association with MAC [19].

Ionizing radiation – The development of tumors in sites of previous radiation therapy has been reported in multiple patients [7,20-25]. These case reports raise the question of whether ionizing radiation increases risk for MAC.

Immunosuppression – Although immunosuppression increases risk for cutaneous squamous cell carcinoma and basal cell carcinoma, the effect of immunosuppression on the risk for development of MAC is unclear. However, four cases of MAC have been reported in transplant patients [26] (see "Epidemiology and risk factors for skin cancer in solid organ transplant recipients"). Aggressive tumor behavior has been reported in a few immunosuppressed patients [27,28].

Other – MAC has appeared to arise within a nevus sebaceous in at least four patients [29-32] and in association with multiple benign syringomas in at least two patients [33]. (See "Nevus sebaceus and nevus sebaceus syndromes".)

HISTOGENESIS — Histologic studies strongly suggest that microcystic adnexal carcinoma (MAC) derives from pluripotent cells that exhibit differentiation towards both eccrine structures and hair follicles [2,34-38]. Immunohistochemical stains that demonstrate hard keratins in the superficial cystic component of MAC support the presence of follicular differentiation [34,35,39], and the often positive stains for carcinoembryonic antigen in MAC tumors indicate the presence of eccrine differentiation (table 1) [30,35,37,40]. Of note, sebaceous differentiation has also been detected in at least two cases of MAC [41] and germinative follicular differentiation detected in another case (supporting apocrine differentiation) [42], findings that lend additional support to the status of pluripotent cells as the cells of tumor origin. In a rare case of MAC occurring in the tongue, the cell of origin appeared to be derived from the salivary gland [43].

Few data are available on the cytogenetic analysis of MAC [44,45]. One study found a clonal chromosome 6q deletion similar to that seen in salivary tumors, suggesting a histogenetic relationship between these tumors [44]. There is a single case report of a metastatic MAC with DNA sequencing that demonstrated a mutation of TP53 and chromosomal losses in the cyclin-dependant kinase inhibitor 2A (CDKN2A) and cyclin-dependant kinase inhibitor 2B (CDKN2B) genes [46]. Hedgehog signaling (HH) expression was not associated with MAC in one small study, differentiating it from basal cell carcinoma [47].

CLINICAL FEATURES — Microcystic adnexal carcinoma (MAC) most frequently manifests as a fairly unremarkable, white or yellowish papule or plaque with or without overlying telangiectasias (picture 1A-D). Individuals with dark skin may present with only an ill-defined papule or nodule that lacks surface or pigmentary changes. The tumor margins are often indistinct, a feature consistent with the common discrepancy between the clinical size of the tumor and the more extensive tumor invasion regularly detected on histologic examination. MAC usually presents as a solitary tumor. However, multiple primary tumors have occurred in at least one patient [4].

Tumor development is usually characterized by slow, gradual growth; periods of stability and more rapid growth may be observed [48]. Early tumors are often only slightly elevated; a more nodular quality tends to develop over time. Tumors that seem fixed to underlying tissues may have invaded underlying structures, such as muscle, cartilage, and bone. Ulceration and necrosis are rare findings.

The vast majority of tumors occur on the head and neck, many of which can be found on the central face [48]. In an analysis of Surveillance, Epidemiology, and End Results (SEER) data on 223 patients with MAC, tumors were located on the head and neck in 74 percent of patients [10]. However, tumors may develop in any cutaneous site. Examples of additional reported sites of MAC include the trunk and extremities, breast, nipple, vulva, auditory canal, axilla, perineum, hands, feet, and scalp [4,5,7,9,15,39,49-51]. Rarely, MAC develops in extracutaneous locations. MAC involving the tongue, oral cavity, or maxillary sinus has been documented in a few patients [10,52]. Most patients with MAC do not experience associated symptoms. Occasionally, symptoms related to perineural invasion, such as burning, pain, hyperesthesia, or paresthesia, are present [53].

DIAGNOSIS — The assessment of skin biopsy findings is usually sufficient for the diagnosis of microcystic adnexal carcinoma (MAC). The use of dermoscopy may also provide clues to diagnosis, particularly the presence of scar-like, white, structureless areas [54,55]. However, it does not provide a consistent pattern, and at least one author found dermoscopy not helpful [56]. Confocal microscopy and optical coherence tomography have been used in single case reports to assist in the clinical diagnosis [57,58].

Despite the relative ease of skin biopsy procedures, the undramatic clinical appearance and insidious growth of MAC can lead to a delay in biopsy and diagnosis for several years [20,30,53].

Biopsy — Superficial shave biopsies are not recommended for the diagnosis of MAC, since the recognition of the architecture of this deeply infiltrative tumor and the detection of perineural invasion are useful for diagnosis. The depth of the biopsy should extend into the deep dermis and subcutis. Thus, punch biopsies, incisional or excisional biopsies, or deep (saucerization) shave biopsies are preferred. (See "Skin biopsy techniques", section on 'Biopsy techniques'.)

The use of fine-needle aspiration for the diagnosis of MAC has been reported [59]. However, in such cases, a subsequent, larger tissue specimen is necessary to confirm the diagnosis.

Pathology — The pathology findings of MAC consist of a deeply infiltrative tumor composed of small nests and cords of bland-appearing cells. The common histologic features of MAC are listed below [60]:

Small, keratin-filled cysts in the upper dermis (picture 2).

Nests and cords of epithelial cells within a hyalinized stroma that seem to form ductal structures; these structures decrease in size at greater depths (picture 3A-B).

Little, if any, cytologic atypia and few mitoses.

Perineural invasion (picture 4).

Deep infiltration within the dermis (infiltration into the subcutaneous tissue, muscle, or deeper structures may also be present) (picture 5).

When MAC encounters bone or cartilage, the tumor may grow laterally along the periosteal or perichondrial plane or may directly invade these structures [53]. Although not typically seen, amyloid deposition [38] and an inflammatory infiltrate with eosinophils [34,61] have been detected in specimens of MAC. There are reports of sebaceous or follicular differentiation or xanthomatous reaction [36,41,42,62,63]. Findings of necrosis and ulceration are uncommon.

Histologic differential diagnosis — Several other cutaneous tumors share pathologic features with MAC. Careful assessment of the histologic features is essential for obtaining the correct diagnosis (table 2) [11,34,64].

The histologic differential diagnosis for MAC primarily consists of benign or malignant cutaneous tumors. The recognition of ductal features in MAC distinguishes it from desmoplastic trichoepithelioma and trichoadenoma [65], which are adnexal tumors of follicular origin. The asymmetrical architecture, single-cell strands, and the perineural and deep invasion of MAC differentiate MAC from syringoma, a benign eccrine tumor [65]. Other disorders to consider in the histologic differential diagnosis include morpheaform basal cell carcinoma, desmoplastic squamous cell carcinoma, and metastatic breast carcinoma.

Immunohistochemistry — Tests beyond routine hematoxylin and eosin staining of pathology specimens are not typically needed for the diagnosis of MAC [48]. However, immunohistochemical studies are occasionally utilized to support the diagnosis and rule out other disorders when the diagnosis is uncertain [19,35,66-71]. In particular, the carcinoembryonic antigen stain, which is positive in half of specimens from MAC, is useful for distinguishing MAC from basal cell carcinoma and squamous cell carcinoma (picture 6) [48]. The addition of androgen receptor stain will help distinguish MAC from infiltrating basal cell carcinoma and desmoplastic trichoepithelioma [72]. The immunohistochemical characteristics of MAC and several disorders that may be mistaken for MAC are provided in a table (table 1).

DIFFERENTIAL DIAGNOSIS — The indurated papules, plaques, or nodules of microcystic adnexal carcinoma (MAC) may clinically resemble scars, morpheaform basal cell carcinoma (picture 7), squamous cell carcinoma, syringomas (picture 8), and cysts (table 3). Histopathologic examination distinguishes MAC from these disorders. (See 'Pathology' above and 'Histologic differential diagnosis' above.)

EVALUATION AND STAGING — Patients diagnosed with microcystic adnexal carcinoma (MAC) should receive a full skin examination that includes careful inspection of the tumor site to assess the clinical extent of the tumor. While nodal spread is rare, palpation of the regional lymph nodes should also be performed to assess for enlarged lymph nodes that may indicate regional metastasis. If enlarged lymph nodes are detected, lymph node biopsy via fine-needle aspiration or surgical removal of the enlarged lymph node is indicated [73].

Radiologic studies are not necessary in most patients diagnosed with MAC. However, if the physical examination suggests that the tumor is fixed to the underlying structures, is large (≥2 cm), or is in the periorbital area or if there is evidence of node involvement, then computed tomography (CT) or magnetic resonance imaging (MRI) of the site is useful. It can confirm bone invasion, involvement of deep structures, deep orbit involvement, or node involvement [60,74-77]. Radiologic imaging of other body sites is not indicated in the absence of signs or symptoms suggestive of distant disease.

The staging of MAC correlates with the staging system for cutaneous squamous cell carcinoma outlined by the American Joint Committee on Cancer Staging (table 4) [78].

TREATMENT — Surgery is the primary treatment modality utilized for the management of microcystic adnexal carcinoma (MAC). Radiation therapy has been employed in select cases; however, the indications for radiation therapy remain uncertain.

Local disease

Approach to treatment — Surgery that results in complete removal of the tumor is the treatment of choice for locally invasive MAC [10]. The surgical techniques most commonly utilized for MAC include Mohs micrographic surgery (MMS), a procedure that involves histologic assessment of the complete tissue margin, and conventional surgical excision with postoperative margin assessment. (See "Mohs surgery".)

We suggest Mohs surgery, rather than conventional surgical excision with postoperative margin assessment, for the treatment of MAC [1,57,79]. This is because the infiltrative quality and often extensive subclinical extension of this tumor can make complete removal by other surgical procedures challenging [11,12,80].

No high-quality trials have evaluated Mohs surgery or conventional surgical excision for the treatment of MAC, and the relative efficacy of these procedures for improving patient outcomes remains uncertain. A systematic review of small case series and single case reports suggests that tumors treated with Mohs surgery are less likely to have positive margin and recur compared with those treated with wide local excision [81]. A 10-year review of periocular tumors highlights the high incidence of perineural tumor, concluding that MMS is the treatment of choice in this location [82]. Mohs surgery may result in defect sizes that may be up to six times larger than the size of the clinically apparent tumor, due to the subclinical extent of the tumor [12].

When Mohs surgery is not an option (eg, tumor size or patient comorbidities prohibit treatment in an outpatient setting, or the procedure is unavailable), conventional surgical excision with postoperative pathologic margin assessment can be utilized for treatment. Intraoperative frozen sections are useful for guiding the extent of excision in these cases.

Mohs surgery — Mohs surgery is an outpatient procedure that allows for intraoperative assessment of 100 percent of the excised tumor margin. This enables the surgeon to confirm complete removal of the tumor on the day of surgery prior to wound closure and allows for the sparing of the maximum amount of healthy tissue. (See "Mohs surgery", section on 'Surgical technique' and "Mohs surgery", section on 'Advantages'.)

In comparison with conventional surgical excision, Mohs surgery may reduce the need for subsequent surgical procedures. In a retrospective study of 69 patients with MAC, 21 of 35 patients (60 percent) treated with conventional surgical excision had positive margins after the procedure [80]. In contrast, clear margins were achieved within a single treatment session in all 34 patients who were treated with Mohs surgery. In another retrospective study of 67 patients treated with Mohs surgery, the mean number of stages was two for primary MAC and increased to four for recurrent tumors [79].

MAC has recurred after Mohs surgery, a finding that reflects the difficulty in achieving complete removal of the tumor [65]. A prospective study found that MAC recurred in 1 of 20 patients who were followed for at least five years after Mohs surgery for primary or recurrent tumors [64]. Retrospective studies with more than 10 patients have found recurrence rates after Mohs surgery between 0 and 12 percent [11,12,27,64,79,83].

Disadvantages of Mohs surgery include its status as a potentially lengthy procedure and as a specialized surgical technique that is not available in all clinical settings. (See "Mohs surgery", section on 'Advantages and disadvantages'.)

Several authors have suggested alterations to the standard Mohs surgery procedure in attempts to improve surgical outcomes. One example is the use of a toluidine blue stain, which may facilitate the identification of isolated tumor nests and perineural invasion [84]. In addition, because the histologic detection of small islands or strands of tumor cells may be easier in permanent sections than in the frozen sections typically utilized in Mohs surgery, techniques utilizing permanent sections have been proposed as methods that may reduce the risk for treatment failure. These include the obtainment of an additional layer of tissue for permanent sections after apparent tumor clearance via Mohs surgery and the performance of a staged Mohs surgery-like procedure utilizing permanent rather than frozen sections ("slow Mohs") [53,85,86]. The effects of these procedures on patient outcomes have not been evaluated in formal studies.

Conventional surgical excision — Conventional surgical excision has been successfully used for the treatment of MAC. A major challenge with conventional surgical excision is the often extensive subclinical extension of MAC, a feature that makes it difficult to identify the true clinical margin that is likely to result in complete removal of the tumor. Surgical margins are determined on an individual basis, with reported margins ranging from a few millimeters to 5 cm [48]. Re-excision is performed if postoperative histologic examination reveals that a tumor is not completely removed [11].

Although the impact of the addition of intraoperative frozen sections to traditional surgical excision in MAC has not been specifically studied, our experience suggests that this intervention may help surgeons to more closely approximate the amount of tissue removal necessary for complete tumor excision during surgery. Frozen sections may be particularly useful in sites on the head and neck where tissue sparing is a significant concern. We suggest the use of intraoperative frozen sections to guide the extent of excision when feasible.

Another challenge of conventional surgical excision is the fact that less than 1 percent of the tissue margin is typically evaluated during histologic examination of the excised tissue. Due to the infiltrative and often asymmetric architecture of MAC, this could lead to a failure to detect residual tumor. Data are limited on the frequency with which tumor recurrence develops following conventional surgical excision. The likelihood of recurrence was high in a retrospective study in which 15 patients were followed for 3 to 25 years; tumors recurred in seven patients (47 percent) [87].

Radiation therapy — The role radiation therapy should play in the treatment of MAC is uncertain. Case reports suggest that radiation therapy alone is capable of achieving clinical clearance of tumors [88,89]; however, tumors may recur [88,90] or fail to respond to therapy [52]. Of note, the recurrence of MAC in a histologically more aggressive form after radiation therapy has been reported in one patient [91]. This finding has not been documented elsewhere.

The use of radiation therapy as an adjuvant to surgical intervention was evaluated in a retrospective study of 14 patients with MAC (11 of whom had positive surgical margins) who were followed for a median of five years [18]. In the study, 13 of 14 patients achieved local control, prompting the authors to suggest that conventional surgical excision plus radiation therapy could yield success rates similar to those observed with Mohs surgery.

Data are insufficient to support a routine recommendation for the use of radiation therapy in patients with MAC. Complete surgical excision remains our treatment of choice for MAC; we reserve radiation therapy for the infrequent cases in which complete surgical removal is not possible and for adjuvant treatment following the complete excision of recurrent tumors in critical locations, such as the periorbital area. Additional studies are necessary to determine the efficacy, safety, indications, and optimal treatment regimen.

Metastatic disease — Locoregional or distant metastasis of MAC is a rare event, and standards for the approach to such patients are lacking. Data on the management of metastatic disease are limited to case reports.

A patient with a 4 cm tumor in the axilla, for whom excision of the tumor and axillary lymph nodes revealed two positive lymph nodes, exhibited no signs of tumor recurrence for 31 months after surgery [51]. A separate patient with MAC on the scalp and biopsy-confirmed cervical lymph node involvement who was treated with a modified radical neck dissection and radiation therapy had no signs of recurrence at one year [73]. In another report, a patient with recurrent tumor on the hand with nodal disease was disease free eight years after original excision after hand amputation and node dissection followed by radiation [92].

Chemoradiation has been used in several patients with MAC. One patient who had a 12-year history of a MAC on the nasal philtrum developed nodal disease. He refused surgery but accepted radiation 70 Gy combined with four cycles of carboplatin and paclitaxel (used as a radiosensitizer). He remained asymptomatic and progression free at six years [93]. A second patient with disease recurrence after surgery was treated with docetaxel plus cisplatin followed by 66 Gy of radiation and was disease free at 18 months [94].

Other case reports document failures of chemotherapy (eg, cisplatinum and fluorouracil, carboplatin and paclitaxel) for metastatic disease. An immunocompromised patient with intransit metastases failed to achieve a lasting response with radiation therapy [28,46,74,90].

PROGNOSIS — Microcystic adnexal carcinoma (MAC) is primarily a locally aggressive tumor. Metastasis to the lymph nodes or other sites is uncommon. As of 2011, fewer than 10 cases of regional lymph node or distant metastasis had been reported in the literature [88]. The rarity of metastasis is supported by Surveillance, Epidemiology, and End Results (SEER) data; among 223 patients with MAC, regional lymph node involvement was present in three patients (1 percent), and distant metastases occurred in one patient [10]. Deep local invasion occurred more frequently; extension into the subcutaneous tissue was noted in 7 percent of patients, and invasion of the underlying soft tissue, muscle, or bone was documented in 9 percent of patients.

Tumor recurrence is the major prognostic concern in MAC (picture 9). The time to tumor recurrence varies widely. Most cases recur within two to three years [48]. However, recurrence up to 29 years after surgery has been reported [7].

Risk factors for tumor recurrence have not been definitively established. In one series of 67 patients with MAC, the risk of recurrence increased by 11 percent for every 1 cm2 increase in tumor size, and tumors >5 cm2 had a 13-fold higher recurrence rate [79]. Some authors propose that tumors that demonstrate perineural invasion may be more likely to recur after Mohs surgery [86]. This may be due to tumor "skip" areas along involved nerves that lead to failures to detect residual perineural tumor.

There are multiple reports of MAC extending into the orbit, leading to tumor invasion into the brain through the optic nerve or the nerves superior to the orbit [60,76,86,90,95]. This suggests that this location is associated with increased risk for morbidity and that treatment should be followed with close long-term monitoring.

A few cases of death related to local tumor extension into vital areas (eg, intracranial invasion) have been reported [75,86,96]. Only one death directly attributable to metastatic MAC has been documented [96].

FOLLOW-UP — Guidelines for the follow-up of patients with microcystic adnexal carcinoma (MAC) have not been established. The potential for delayed recurrence after years indicates that long-term follow-up is necessary. We typically follow patients every 6 to 12 months and perform a full skin examination and lymph node palpation at each visit. Patients with histories of tumors that invade into deep, vital, or conduit structures (such as the orbit) likely need to be followed more closely. The optimal frequency of follow-up of these patients depends on the individual clinical scenario.

We usually perform radiologic imaging only if signs or symptoms suggestive of extracutaneous involvement are present. Occasionally radiologic studies (computed tomography [CT] or magnetic resonance imaging [MRI]) are used to follow patients with deeply invasive tumors in which physical examination is not adequate for assessing signs of tumor recurrence.

SUMMARY AND RECOMMENDATIONS

Epidemiology – Microcystic adnexal carcinoma (MAC) is a rare, infiltrative cutaneous tumor that is often found on the head and neck. White, middle-aged and older adults are most commonly affected. The risk factors for MAC are poorly defined. Exposure to ultraviolet or ionizing radiation may play a role in the development of some tumors. (See 'Epidemiology' above and 'Risk factors' above.)

Clinical presentation – MAC most commonly presents as a nonulcerated, white or yellow papule, plaque, or nodule on the skin. The head and neck are frequent sites for involvement. Tumors usually grow slowly over the course of years. (See 'Clinical features' above.)

Diagnosis – The diagnosis of MAC is based upon the detection of consistent pathologic findings. Characteristic features include small, keratin-filled cysts; nest and cords of cells that resemble ductal structures; and an infiltrative growth pattern. Perineural invasion is common. Immunohistochemical studies are occasionally used to distinguish MAC from other disorders (table 1). (See 'Diagnosis' above.)

Evaluation and staging – The evaluation of the patient with MAC should include a complete skin examination with careful attention to the tumor site and lymph node palpation. Most patients do not require radiologic studies. (See 'Evaluation and staging' above.)

Treatment – For patients with MAC, we suggest treatment with Mohs surgery (Grade 2C). If Mohs surgery cannot be performed, patients may be treated with conventional surgical excision with pathologic margin assessment. Intraoperative frozen sections are useful for guiding the extent of conventional surgical excision (see 'Mohs surgery' above). We typically reserve radiation therapy for tumors for which complete excision is not possible and as postoperative adjuvant therapy for recurrent tumors in critical locations (eg, periorbital area). The optimal treatment regimen for radiation therapy has not been determined. Chemoradiation has been used successfully in a few instances of metastatic tumor. (See 'Radiation therapy' above.)

Prognosis – MAC is primarily a locally aggressive tumor. Local recurrence is the major prognostic concern. As recurrence of MAC may occur after many years, patients should be routinely followed for signs of disease recurrence every 6 to 12 months and have a full skin examination and lymph node palpation at each visit. (See 'Prognosis' above and 'Follow-up' above.)

  1. Gordon S, Fischer C, Martin A, et al. Microcystic Adnexal Carcinoma: A Review of the Literature. Dermatol Surg 2017; 43:1012.
  2. Goldstein DJ, Barr RJ, Santa Cruz DJ. Microcystic adnexal carcinoma: a distinct clinicopathologic entity. Cancer 1982; 50:566.
  3. Stern JB, Stout DA. Trichofolliculoma showing perineural invasion. Trichofolliculocarcinoma? Arch Dermatol 1979; 115:1003.
  4. Page RN, Hanggi MC, King R, Googe PB. Multiple microcystic adnexal carcinomas. Cutis 2007; 79:299.
  5. Buhl A, Landow S, Lee YC, et al. Microcystic adnexal carcinoma of the vulva. Gynecol Oncol 2001; 82:571.
  6. Nadiminti H, Nadiminti U, Washington C. Microcystic adnexal carcinoma in African-Americans. Dermatol Surg 2007; 33:1384.
  7. Ohtsuka H, Nagamatsu S. Microcystic adnexal carcinoma: review of 51 Japanese patients. Dermatology 2002; 204:190.
  8. Sabhikhi AK, Rao CR, Kumar RV, Hazarika D. Microcystic adnexal carcinoma. Int J Dermatol 1997; 36:134.
  9. Avraham JB, Villines D, Maker VK, et al. Survival after resection of cutaneous adnexal carcinomas with eccrine differentiation: risk factors and trends in outcomes. J Surg Oncol 2013; 108:57.
  10. Yu JB, Blitzblau RC, Patel SC, et al. Surveillance, Epidemiology, and End Results (SEER) database analysis of microcystic adnexal carcinoma (sclerosing sweat duct carcinoma) of the skin. Am J Clin Oncol 2010; 33:125.
  11. Chiller K, Passaro D, Scheuller M, et al. Microcystic adnexal carcinoma: forty-eight cases, their treatment, and their outcome. Arch Dermatol 2000; 136:1355.
  12. Thomas CJ, Wood GC, Marks VJ. Mohs micrographic surgery in the treatment of rare aggressive cutaneous tumors: the Geisinger experience. Dermatol Surg 2007; 33:333.
  13. McAlvany JP, Stonecipher MR, Leshin B, et al. Sclerosing sweat duct carcinoma in an 11-year-old boy. J Dermatol Surg Oncol 1994; 20:767.
  14. Nelson PS, Bourgeois KM, Nicotri T Jr, et al. Sclerosing sweat duct carcinoma in a 6-year-old African American child. Pediatr Dermatol 2008; 25:38.
  15. Wong LK, Kereke AR, Wright AE, Vyas KS. Microcystic Adnexal Carcinoma of the Nipple. Wounds 2018; 30:E65.
  16. Smart DR, Taintor AR, Kelly ME, et al. Microcystic adnexal carcinoma: the first reported congenital case. Pediatr Dermatol 2011; 28:35.
  17. Fu T, Clark FL, Lorenz HP, Bruckner AL. Congenital microcystic adnexal carcinoma. Arch Dermatol 2011; 147:256.
  18. Baxi S, Deb S, Weedon D, et al. Microcystic adnexal carcinoma of the skin: the role of adjuvant radiotherapy. J Med Imaging Radiat Oncol 2010; 54:477.
  19. Smith KJ, Williams J, Corbett D, Skelton H. Microcystic adnexal carcinoma: an immunohistochemical study including markers of proliferation and apoptosis. Am J Surg Pathol 2001; 25:464.
  20. Borenstein A, Seidman DS, Trau H, Tsur H. Microcystic adnexal carcinoma following radiotherapy in childhood. Am J Med Sci 1991; 301:259.
  21. Beer KT, Bühler SS, Mullis P, et al. A microcystic adnexal carcinoma in the auditory canal 15 years after radiotherapy of a 12-year-old boy with nasopharynx carcinoma. Strahlenther Onkol 2005; 181:405.
  22. Antley CA, Carney M, Smoller BR. Microcystic adnexal carcinoma arising in the setting of previous radiation therapy. J Cutan Pathol 1999; 26:48.
  23. Abbate M, Zeitouni NC, Seyler M, et al. Clinical course, risk factors, and treatment of microcystic adnexal carcinoma: a short series report. Dermatol Surg 2003; 29:1035.
  24. Lober CW, Larbig GG. Microcystic adnexal carcinoma (sclerosing sweat duct carcinoma). South Med J 1994; 87:259.
  25. Schwarze HP, Loche F, Lamant L, et al. Microcystic adnexal carcinoma induced by multiple radiation therapy. Int J Dermatol 2000; 39:369.
  26. Stamey CR, Colegio OR, Book SE. Microcystic adnexal carcinoma of the glabella in a liver transplant recipient. JAAD Case Rep 2021; 10:126.
  27. Snow S, Madjar DD, Hardy S, et al. Microcystic adnexal carcinoma: report of 13 cases and review of the literature. Dermatol Surg 2001; 27:401.
  28. Carroll P, Goldstein GD, Brown CW Jr. Metastatic microcystic adnexal carcinoma in an immunocompromised patient. Dermatol Surg 2000; 26:531.
  29. Lountzis N, Junkins-Hopkins J, Uberti-Benz M, Elenitsas R. Microcystic adnexal carcinoma arising within a nevus sebaceus. Cutis 2007; 80:352.
  30. Ongenae KC, Verhaegh ME, Vermeulen AH, Naeyaert JM. Microcystic adnexal carcinoma: an uncommon tumor with debatable origin. Dermatol Surg 2001; 27:979.
  31. Sakanoue M, Matsushita S, Kawai K, Kanekura T. Microcystic adnexal carcinoma arising in a nevus sebaceous. Indian J Dermatol 2013; 58:247.
  32. Hashem R, Tynngård N, Lundmark K, Falk L. Microcystic Adnexal Carcinoma Originating in a Nevus Sebaceous: A Case Report of a 16-year-old Boy. Acta Derm Venereol 2019; 99:1182.
  33. Liang CA, Busam KJ, Nehal KS. Microcystic adnexal carcinoma associated with multiple benign syringomatous proliferations: a report of two cases. Dermatol Surg 2011; 37:1515.
  34. LeBoit PE, Sexton M. Microcystic adnexal carcinoma of the skin. A reappraisal of the differentiation and differential diagnosis of an underrecognized neoplasm. J Am Acad Dermatol 1993; 29:609.
  35. Wick MR, Cooper PH, Swanson PE, et al. Microcystic adnexal carcinoma. An immunohistochemical comparison with other cutaneous appendage tumors. Arch Dermatol 1990; 126:189.
  36. Kazakov DV, Kacerovska D, Michal M. Microcystic adnexal carcinoma with multiple areas of follicular differentiation toward germinative cells and specific follicular stroma (trichoblastomatous areas). Am J Dermatopathol 2011; 33:e47.
  37. Nickoloff BJ, Fleischmann HE, Carmel J, et al. Microcystic adnexal carcinoma. Immunohistologic observations suggesting dual (pilar and eccrine) differentiation. Arch Dermatol 1986; 122:290.
  38. Kato H, Mizuno N, Nakagawa K, et al. Microcystic adnexal carcinoma: a light microscopic, immunohistochemical and ultrastructural study. J Cutan Pathol 1990; 17:87.
  39. Callahan EF, Vidimos AT, Bergfeld WF. Microcystic adnexal carcinoma (MAC) of the scalp with extensive pilar differentiation. Dermatol Surg 2002; 28:536.
  40. Requena L, Marquina A, Alegre V, et al. Sclerosing-sweat-duct (microcystic adnexal) carcinoma--a tumor from a single eccrine origin. Clin Exp Dermatol 1990; 15:222.
  41. Pujol RM, LeBoit PE, Su WP. Microcystic adnexal carcinoma with extensive sebaceous differentiation. Am J Dermatopathol 1997; 19:358.
  42. Moya-Martínez C, Torre-Castro J, Mendoza-Cembranos D, et al. Microcystic adnexal carcinoma with germinative follicular differentiation. J Cutan Pathol 2021; 48:123.
  43. Zhang L, Huang X, Zhou T, Cao H. Microcystic adnexal carcinoma: report of rare cases. Biosci Rep 2020; 40.
  44. Wohlfahrt C, Ternesten A, Sahlin P, et al. Cytogenetic and fluorescence in situ hybridization analyses of a microcystic adnexal carcinoma with del(6)(q23q25). Cancer Genet Cytogenet 1997; 98:106.
  45. Vogelbruch M, Böcking A, Rütten A, et al. DNA image cytometry in malignant and benign sweat gland tumours. Br J Dermatol 2000; 142:688.
  46. Chen MB, Laber DA. Metastatic Microcystic Adnexal Carcinoma with DNA Sequencing Results and Response to Systemic Antineoplastic Chemotherapy. Anticancer Res 2017; 37:5109.
  47. Gambichler T, Hartenstein I, Dreißigacker M, et al. Expression of Hedgehog signalling molecules in microcystic adnexal carcinoma. Clin Exp Dermatol 2021; 46:1052.
  48. Wetter R, Goldstein GD. Microcystic adnexal carcinoma: a diagnostic and therapeutic challenge. Dermatol Ther 2008; 21:452.
  49. Yavuzer R, Boyaci M, Sari A, Ataoğlu O. Microcystic adnexal carcinoma of the breast: a very rare breast skin tumor. Dermatol Surg 2002; 28:1092.
  50. Chi J, Jung YG, Rho YS, Lim HJ. Microcystic adnexal carcinoma of external auditory canal: report of a case. Otolaryngol Head Neck Surg 2002; 127:241.
  51. Ban M, Sugie S, Kamiya H, Kitajima Y. Microcystic adnexal carcinoma with lymph node metastasis. Dermatology 2003; 207:395.
  52. Schipper JH, Holecek BU, Sievers KW. A tumour derived from Ebner's glands: microcystic adnexal carcinoma of the tongue. J Laryngol Otol 1995; 109:1211.
  53. Sebastien TS, Nelson BR, Lowe L, et al. Microcystic adnexal carcinoma. J Am Acad Dermatol 1993; 29:840.
  54. Shinohara R, Ansai S, Ogita A, et al. Dermoscopic findings of microcystic adnexal carcinoma. Eur J Dermatol 2015; 25:516.
  55. Calderón-Castrat X, Román-Curto C, Santos-Briz A, Fernández-López E. Microcystic adnexal carcinoma mimicking basal cell carcinoma. JAAD Case Rep 2017; 3:492.
  56. Gupta V, Kakkar A, Agarwal S, et al. Dermoscopic pitfall: Microcystic adnexal carcinoma mimicking basal cell carcinoma. Indian J Dermatol Venereol Leprol 2020; 86:202.
  57. Giambrone D, Salvaggio C, Victor FC, Rao BK. Microcystic Adnexal Carcinoma Detected by Reflectance Confocal Microscopy. Dermatol Surg 2016; 42:126.
  58. Alawi SA, Batz S, Röwert-Huber J, et al. Correlation of optical coherence tomography and histology in microcystic adnexal carcinoma: a case report. Skin Res Technol 2015; 21:15.
  59. Sirikanjanapong S, Seymour AW, Amin B. Cytologic features of microcystic adnexal carcinoma. Cytojournal 2011; 8:5.
  60. Cooper PH, Mills SE. Microcystic adnexal carcinoma. J Am Acad Dermatol 1984; 10:908.
  61. McCalmont TH, Ye J. Eosinophils as a clue to the diagnosis of microcystic adnexal carcinoma. J Cutan Pathol 2011; 38:849, 850.
  62. Fujii K, Arimura A, Ibusuki A, et al. Microcystic Adnexal Carcinoma with Xanthomatous Reaction. Acta Derm Venereol 2021; 101:adv00436.
  63. Fernandez-Flores A, Llamas-Velasco M, Saus C, et al. Microcystic adnexal carcinoma with sebaceous differentiation: Three cases. J Cutan Pathol 2018; 45:290.
  64. Leibovitch I, Huilgol SC, Selva D, et al. Microcystic adnexal carcinoma: treatment with Mohs micrographic surgery. J Am Acad Dermatol 2005; 52:295.
  65. Diamantis SA, Marks VJ. Mohs micrographic surgery in the treatment of microcystic adnexal carcinoma. Dermatol Clin 2011; 29:185.
  66. Krahl D, Sellheyer K. Monoclonal antibody Ber-EP4 reliably discriminates between microcystic adnexal carcinoma and basal cell carcinoma. J Cutan Pathol 2007; 34:782.
  67. Hoang MP, Dresser KA, Kapur P, et al. Microcystic adnexal carcinoma: an immunohistochemical reappraisal. Mod Pathol 2008; 21:178.
  68. Abesamis-Cubillan E, El-Shabrawi-Caelen L, LeBoit PE. Merked cells and sclerosing epithelial neoplasms. Am J Dermatopathol 2000; 22:311.
  69. Vidal CI, Goldberg M, Burstein DE, et al. p63 Immunohistochemistry is a useful adjunct in distinguishing sclerosing cutaneous tumors. Am J Dermatopathol 2010; 32:257.
  70. Plaza JA, Ortega PF, Stockman DL, Suster S. Value of p63 and podoplanin (D2-40) immunoreactivity in the distinction between primary cutaneous tumors and adenocarcinomas metastatic to the skin: a clinicopathologic and immunohistochemical study of 79 cases. J Cutan Pathol 2010; 37:403.
  71. Rollins-Raval M, Chivukula M, Tseng GC, et al. An immunohistochemical panel to differentiate metastatic breast carcinoma to skin from primary sweat gland carcinomas with a review of the literature. Arch Pathol Lab Med 2011; 135:975.
  72. Evangelista MT, North JP. Comparative analysis of cytokeratin 15, TDAG51, cytokeratin 20 and androgen receptor in sclerosing adnexal neoplasms and variants of basal cell carcinoma. J Cutan Pathol 2015; 42:824.
  73. Rotter N, Wagner H, Fuchshuber S, Issing WJ. Cervical metastases of microcystic adnexal carcinoma in an otherwise healthy woman. Eur Arch Otorhinolaryngol 2003; 260:254.
  74. Gabillot-Carré M, Weill F, Mamelle G, et al. Microcystic adnexal carcinoma: report of seven cases including one with lung metastasis. Dermatology 2006; 212:221.
  75. Gomez-Maestra MJ, España-Gregori E, Aviñó-Martinez JA, et al. Brainstem and cavernous sinus metastases arising from a microcystic adnexal carcinoma of the eyebrow by perineural spreading. Can J Ophthalmol 2009; 44:e17.
  76. Birkby CS, Argenyi ZB, Whitaker DC. Microcystic adnexal carcinoma with mandibular invasion and bone marrow replacement. J Dermatol Surg Oncol 1989; 15:308.
  77. Nagatsuka H, Rivera RS, Gunduz M, et al. Microcystic adnexal carcinoma with mandibular bone marrow involvement: a case report with immunohistochemistry. Am J Dermatopathol 2006; 28:518.
  78. Edge SF, Byrd DR, Compton CC, et al. AJCC cancer staging manual, 7th ed, Springer, 2010.
  79. King BJ, Tolkachjov SN, Winchester DS, et al. Demographics and outcomes of microcystic adnexal carcinoma. J Am Acad Dermatol 2018; 79:756.
  80. Yerneni S, Murad F, Schmults CD, Ruiz ES. Improved Margin Control of Microcystic Adnexal Carcinoma After Mohs Micrographic Surgery Compared With Wide Local Excision. Dermatol Surg 2023; 49:317.
  81. Chaudhari SP, Mortazie MB, Blattner CM, et al. Treatments for microcystic adnexal carcinoma--A review. J Dermatolog Treat 2016; 27:278.
  82. Mestre T, Oliphant T, Lawrence CM, et al. Mohs micrographic surgery is the required treatment for periocular microcystic adnexal carcinoma to maximize the possibility of tumour clearance. Br J Dermatol 2016; 175:119.
  83. Friedman PM, Friedman RH, Jiang SB, et al. Microcystic adnexal carcinoma: collaborative series review and update. J Am Acad Dermatol 1999; 41:225.
  84. Wang SQ, Goldberg LH, Nemeth A. The merits of adding toluidine blue-stained slides in Mohs surgery in the treatment of a microcystic adnexal carcinoma. J Am Acad Dermatol 2007; 56:1067.
  85. Khachemoune A, Olbricht SM, Johnson DS. Microcystic adnexal carcinoma: report of four cases treated with Mohs' micrographic surgical technique. Int J Dermatol 2005; 44:507.
  86. Palamaras I, McKenna JD, Robson A, Barlow RJ. Microcystic adnexal carcinoma: a case series treated with mohs micrographic surgery and identification of patients in whom paraffin sections may be preferable. Dermatol Surg 2010; 36:446.
  87. Cooper PH, Mills SE, Leonard DD, et al. Sclerosing sweat duct (syringomatous) carcinoma. Am J Surg Pathol 1985; 9:422.
  88. Pugh TJ, Lee NY, Pacheco T, Raben D. Microcystic adnexal carcinoma of the face treated with radiation therapy: a case report and review of the literature. Head Neck 2012; 34:1045.
  89. Gulmen S, Pullon PA. Sweat gland carcinoma of the lips. Oral Surg Oral Med Oral Pathol 1976; 41:643.
  90. Bier-Laning CM, Hom DB, Gapany M, et al. Microcystic adnexal carcinoma: management options based on long-term follow-up. Laryngoscope 1995; 105:1197.
  91. Stein JM, Ormsby A, Esclamado R, Bailin P. The effect of radiation therapy on microcystic adnexal carcinoma: a case report. Head Neck 2003; 25:251.
  92. Chakrapan Na Ayudhya K, Chakrapan Na Ayudhya V, Tipsuwannakul P, et al. Axillary and elbow lymph node metastasis arising after complete excision of microcystic adnexal carcinoma of a hand: A rare presentation. Int J Surg Case Rep 2019; 64:154.
  93. Kim DW, Lee G, Lam MB, et al. Microcystic Adnexal Carcinoma of the Face Treated With Definitive Chemoradiation: A Case Report and Review of the Literature. Adv Radiat Oncol 2020; 5:301.
  94. Al-Wassia RK, Al-Qathmi MS. Microcystic adnexal carcinoma of the scalp treated with surgical resection along with chemoradiation: A case report and review of the literature. Saudi J Biol Sci 2021; 28:7117.
  95. Ohta M, Hiramoto M, Ohtsuka H. Metastatic microcystic adnexal carcinoma: an autopsy case. Dermatol Surg 2004; 30:957.
  96. Yugueros P, Kane WJ, Goellner JR. Sweat gland carcinoma: a clinicopathologic analysis of an expanded series in a single institution. Plast Reconstr Surg 1998; 102:705.
Topic 13719 Version 13.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟