Basal Cell Carcinoma • Discus the Differential Diagnosis Jason Stratton MD Pathology Laboratory Associates/ Regional Medical Laboratory, Tulsa Oklahoma

Total Page:16

File Type:pdf, Size:1020Kb

Basal Cell Carcinoma • Discus the Differential Diagnosis Jason Stratton MD Pathology Laboratory Associates/ Regional Medical Laboratory, Tulsa Oklahoma 11/14/2019 Objectives • Introduce BCC Histology • Discuss Histologic Types and Importance. Basal Cell Carcinoma • Discus the Differential Diagnosis Jason Stratton MD Pathology Laboratory Associates/ Regional Medical Laboratory, Tulsa Oklahoma. 12 Duplicate BASAL CELL CARCINOMA Basal Cell Carcinoma (BCC) • first described by Jacob in 1827 • most common human cancer (Lacour, 2002). • Pathologyor • by 1998 roughly one million new cases annually in the • Various growth patterns USA (Miller and Weinstock, 1994) • Often mixed • 4th decade of life and beyond • All proliferation of basaloid cells • Exception with specific genodermatoses or in patients with w/ peripheral palisade immune compromise • All surrounded by fibromucinous • UV light the major etiology : light skin phenotypes stroma • Amyloid deposits – from release particularly predisposed keratin into stroma • Other risk factors: arsenic, coal tar derivatives, • Mitotic figures & apoptotic cells irradiation, scars, draining sinuses, ulcers, burn sites [all • Clefting artifact (retraction) foci of chronic inflammation] between tumor and stroma • Lack of hemidesmosomes 34 BASAL CELL CARCINOMA BASAL CELL CARCINOMA histopathology Distributehistopathology of “undifferentiated” BCC • Indolent- or aggressive-growth types • Originally, BCC was classified into solid/undifferentiated vs • Indolent-growth variants (IGBCC) include those with specific differentiation • superficial – Eccrine • nodular basal cell carcinoma – Sebaceous • Nodulocystic – Keratotic/Pilar • Infundibulocystic – FollicularNot (pilomatricoma like) • Aggressive growth (AGBCC) variants • We now know that the only important histologic • infiltrative basal cell carcinoma prognosticator of biologic behavior is the architectural • micronodular growth pattern. • basosquamous (metatypical) carcinoma Do • morpheiform or sclerosing basal cell carcinoma 56 1 11/14/2019 BASAL CELL CARCINOMA histopathology of “undifferentiated” BCC BCC subtype and sun exposure • In a retrospective series of 1039 consecutive neoplasms: • BCC in sun-protected skin usually of superficial type • 21% were nodular; 6.4%+ve margin (63.2%) vs only 21% nodular and 15.8% infiltrative • 17.4% were superficial; 3.6% +ve margin subtypes • 14.5% were micronodular ; 18.6% +ve margin • BCC in sun-exposed skin infrequently of superficial • 7.4% were infiltrative; 26.5% +ve margin type (14.3%), while 42.9% were nodular type, 33.3% • 1.1% were morpheiform; 33.3% +ve margin were infiltrative, and 3% each were of morpheaform • One-third of all tumors showed mixed patterns and metatypical subtypes (p=0.028) (Crowson et al, Sexton et al, J Am Acad Dermatol,1990 1996) 78 Duplicate Superficial Basal Cell Carcinoma • Epidemiology or • Earlier age • Location • More frequent on trunk • Clinical features • More subtle • Often multiple • Erythematous patch BCC, superficial • Resemble dermatitis, but has pearly border / central superficial erosion w/ h/o of bleeding easily 910 Superficial Basal CellDistribute Carcinoma • Histopathology • Superficial lobules of basaloid cells • Usually confined to papillary dermis • Projecting from epidermis or adnexa • Multifocal Not• Usually connected by stroma & in 3D BCC, superficial Do 11 12 2 11/14/2019 Nodular Basal Cell Carcinoma • Epidemiology • Later age; most common pattern (60-80%) • Location • More frequent on head Superficial basal cell carcinoma : atypical basaloid cells form an axis parallel to the • Clinical features epidermal surface; mitoses and apoptotic cells rare • Elevated pearly nodules • Assoc. w/ telangiectasia 13 14 Duplicate Nodular Basal Cell Carcinoma • Histopathologyor • Large lobules of basaloid cells • Project into reticular dermis / deeper • May have adenoid (cribiform) or organoid pattern • Secondary features • Mucinous degeneration w/ cysts Nodular BCC : courtesy Dr. G. Monks, Tulsa OK 15 16 Distribute Not BCC, Nodular BCC, Nodular Do BCC, Nodular 17 18 3 11/14/2019 Micronodular Basal Cell Carcinoma • Location • Most common site is back • Clinical features • Not specific 19 20 Duplicate Micronodular Basal Cell Carcinoma • Histopathology or • Small lobules of basaloid cells • Project into reticular dermis / deeper • Fibrotic stroma • Prognosis & predictive factors • Worse • Possibly b/c surgical margins often underestimated Micronodular BCC : Plaque like;, poorly demarcated; nests smaller with individual fibrotic stroma; widely dispersed into deep dermis and/or subcutis 21 22 DistributeInfiltrating Basal Cell Carcinoma • Location • Usually on upper back & face • Clinical features • Pale, indurated poorly defined plaque • Paraesthesia / loss of sensation Not • Due perineural extension DoBCC, Micronodular 23 24 4 11/14/2019 Infiltrative basal cell carcinoma clinical correlates • poorly circumscribed • may invade subcutis and adjacent structures • perineural infiltration a distinct risk for recurrence • depressed yellowish or fibrotic plaque lacking rolled border or elevated nodule unless a co- existant nodular component Courtesy Dr. Michael Wilkerson, Galveston TX 25 26 Duplicate Infiltrating Basal Cell Carcinoma • Histopathology or • Infiltrative strands, cords, or columns of basaloid cells • Project into reticular dermis / deeper • Peripheral palisade & retraction usually absent • Frequent perineural invasion • No fibrosis / sclerosis • As seen in sclerosing / morpheiform variant • Prognosis & predictive factors • Worse • Again possibly b/c surgical margins often underestimated BCC, Infiltrative 27 28 Distribute Not Irregular tongues of tumor and stromal fibroplasia in mixed nodular and infiltrative growth BCC mitotic activity and individual Do cell necrosis 29 30 5 11/14/2019 Fibroepithelial Basal Cell Carcinoma (Fibroepithelioma of Pinkus, Pinkus tumor) • Location • Usually on back • Clinical features • Elevated flesh colored / erythematous nodule • DDx: SK, acrochordon Mixed nodular and infiltrative growth BCC 31 32 Duplicate Fibroepithelial Basal Cell Carcinoma • Histopathology or • Arborizing network of cords of basaloid cells • Prognosis & predictive factors • Indolent BCC, (Fibroepithelioma of Pinkus) 33 34 DistributeBasosquamous Carcinoma (Metatypical carcinoma, basosquamous cell carcinoma) • Clinical features • No distinguishing clinical features • Histopathology • More abundant cytoplasm Not • More marked keratinization • Prognosis & predictive factors • More aggressive behavior Fibroepithelioma of Pinkus: fleshy Do lesion above natal cleft 35 36 6 11/14/2019 Basosquamous/metatypical carcinoma : inter- cellular bridge formation, keratinization; admixed nodular or superficial component Basosquamous carcinoma: • Defined as an infiltrative growth BCC with areas of keratinization and/or intercellular bridge formation and a prototypic stromal response • Published recurrence rates 12-50% after surgical excision vs 4% after Mohs surgery Garcia, Poletti + Crowson. J Am Acad Dermatol 2009; 60:137 37 38 Duplicate “Differentiated” basal cell carcinomas Basosquamous (metatypical) carcinoma: differential diagnosis • Basal cell carcinomas show various lineage differentiation features that do not impact prognosis: • keratoticor BCC (de Faria, 1985), • Keratotic/pilar BCC, most often a nodular BCC • infundibulocystic BCC (Walsh and Ackerman, 1990) • follicular BCC (Aloi et al, 1988) [has collision features with with horn cyst formation (primitive attempt at pilomatricoma] hair differentiation) • pleomorphic BCC (Garcia et al, 1995) • mixed [basal cell and squamous cell] carcinoma, • BCC with eccrine differentiation (Kato and Ueno, 1993) • BCC with sebaceous differentiation a collision between two clonally distinctive, • fibroepithelioma of Pinkus (Pinkus, 1953) geographically separate neoplasms in the same • BCC with myoepithelial differentiation (Suster + Cajal, 1991) biopsy or excision • squamous cell carcinoma 39 40 Keratotic Basal CellDistribute Carcinoma • Clinical features • May be studded w/ small keratin cysts (milia) • Histopathology • Nodular architecture • ProminentNot keratin formation (horn cysts) center of tumor nodules follicular BCC : matrical Do differentiation 41 42 7 11/14/2019 Pleomorphic BCC Pleomorphic basal cell carcinoma infiltrative type (“BCC with monster cells” ) • giant nuclei scattered through tumor lobules or clustered suggesting a similar clone • All cases evaluated by static image analysis cytometry have proven to be aneuploid • mitoses present same frequency as in typical nodular BCC; rarely atypical (Elston et al, 1993; Garcia et al, 1995) • pleomorphic cells a form of senescent atypia; impart no prognostic significance 43 44 Duplicate Basal cell carcinoma with eccrine or apocrine differentiation Basal cell carcinoma • seen in roughly 1% of nodular BCC in our experience “rippled pattern” (Kato and Ueno, 1993) or • Characteristic interlobular • centrally disposed in basaloid tumor cell aggregates palisade of nuclei are tubules lined by cuboidal epithelium with an • Remainder of histologic internal eosinophilic cuticle characteristics are similar to nodular BCC • decorate with immunohistochemical stains for • Shares almost identical carcinoembryonic antigen (CEA) and epithelial histology to “rippled type membrane antigen (EMA) sebaceoma” 45 46 DistributeClear Cell BCC (BCC with Trichilemmal Differentiation) • Clear cell change in otherwise typical BCC of any pattern due to glycogen accumulation in cytosol • Differential diagnosis : • sebaceous carcinoma • clear cell squamous cell carcinoma Not • other clear cell carcinomas metastatic to skin (ie renal cell ca or thyroid carcinoma)
Recommended publications
  • P-CRESIDINE for POSSIBLE CARCINOGENICITY
    National Cancer Institute CARCINOGENESIS Technical Report Series No. 142 1979 BIOASSAY OF p-CRESIDINE FOR POSSIBLE CARCINOGENICITY CAS No. 120-71-8 NCI-CG-TR-142 U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service National Institutes of Health BIOASSAY OF p-CRESIDINE FOR POSSIBLE CARCINOGENICITY Carcinogenesis Testing Program Division of Cancer Cause and Prevention National Cancer Institute National Institutes of Health Bethesda, Maryland 20014 U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service National Institutes of Health DHEW Publication No. (NIH) 79-1397 REPORT ON THE BIOASSAY OF p-CRESIDINE FOR POSSIBLE CARCINOGENICITY CARCINOGENESIS TESTING PROGRAM DIVISION OF CANCER CAUSE AND PREVENTION NATIONAL CANCER INSTITUTE, NATIONAL INSTITUTES OF HEALTH FOREWORD: This report presents the results of the bioassay of p-cresidine conducted for the Carcinogenesis Testing Program, Divi­ sion of Cancer Cause and Prevention, National Cancer Institute (NCI), National Institutes of Health, Bethesda, Maryland. This is one of a series of experiments designed to determine whether selected chemicals have the capacity to produce cancer in animals. Negative results, in which the test animals do not have a significantly greater incidence of cancer than control animals, do not necessarily mean the test chem­ ical is not a carcinogen because the experiments are conducted under a limited set of circumstances. Positive results demonstrate that the test chemical is carcinogenic for animals under the conditions of the test and indicate a potential risk to man. The actual determination of the risk to man from animal carcinogens requires a wider analysis. CONTRIBUTORS; This bioassay of p-cresidine was conducted by Mason Research Institute, Worcester, Massachusetts, initially under direct contract to the NCI and currently under a subcontract to Tracor Jitco, Inc., prime contractor for the NCI Carcinogenesis Testing Program.
    [Show full text]
  • Gastrointestinal Stromal Tumor: Clinicopathological Characteristics and Pathologic Prognostic Analysis Chayanit Jumniensuk1 and Mongkon Charoenpitakchai2*
    Jumniensuk and Charoenpitakchai World Journal of Surgical Oncology (2018) 16:231 https://doi.org/10.1186/s12957-018-1532-1 RESEARCH Open Access Gastrointestinal stromal tumor: clinicopathological characteristics and pathologic prognostic analysis Chayanit Jumniensuk1 and Mongkon Charoenpitakchai2* Abstract Objective: This study aimed to understand clinicopathological characteristics of gastrointestinal stromal tumors (GISTs) and correlation between pathologic features and clinical outcome. Methods: We used 76 cases diagnosed as primary GISTs during January 2007 to July 2017 at Army Institute of Pathology, Thailand. Clinical, survival, and pathological data were collected and analyzed. Results: Ages of the patients ranged from 15 to 88 years (M:F = 1:1). The most common presentation was gastrointestinal bleeding (39.7%). The most common site was the stomach (64.5%). Tumor size ranged from 0.6 to 25.5 cm (average 8.78 cm). Histologic types were spindle cell type (75%), mixed spindled-epithelioid type (17.1%), and epithelioid type (7.9%). The majority of histologic subtype was diffuse hypercellularity (67.1%). Tumor necrosis was found in 38.1% and 80% showed low mitotic counts. Most gastrointestinal stromal tumors (27.6%) are low-risk category according to Miettinen and Lasota’s algorithm. Metastasis was found in 27.7%, mostly occurs within 2 years, and is correlated with tumor size > 10 cm (P = 0.023), non-spindle cell histologic type (P = 0.027), mitotic count > 5/5mm2 (P = 0.000), myxoid change (P = 0.011), and mucosal invasion (P = 0.002). Recurrence was found in 8.1%, mostly occurs within 7 years, and correlated with myxoid change (P = 0.045).
    [Show full text]
  • CPT® New Codes 2019: Biopsy, Skin
    Billing and Coding Update Alexander Miller, M.D. AAD Representative to the AMA CPT Advisory Committee New Skin Biopsy CPT® Codes It’s all about the Technique! SPEAKER: Alexander Miller, M.D. AAD Representative to the AMA -CPT Advisory Committee Chair AAD Health Care Finance Committee Arriving on January 1, 2019 New and Restructured Biopsy Codes Tangential biopsy Punch Biopsy Incisional Biopsy How Did We Get Here? CMS CY 2016 Biopsy codes (11100, 11101 identified as potentially mis-valued; high expenditure RUC Survey sent to AAD Members Specialty survey results are the only tool available to support code values Challenging survey results Survey revealed bimodal data distribution; CPT Codes 11100, 11101 referred to CPT for respondents were valuing different procedures restructuring Rationale for New Codes 11100; 11101 • Previous skin biopsy codes did not distinguish between the different biopsy techniques that were being used CPT Recommended technique specification in new biopsy codes • Will also provide for reimbursement commensurate with the technique used How Did We Get Here? • CPT Editorial Panel deleted 11100; 11101 February 2017 • 6 New codes created based on technique utilized • Each technique: primary code and add-on code March 2017 • RUC survey sent to AAD members April 2017 • Survey results presented to the RUC Biopsy Codes Effective Jan., 1, 2019 • Integumentary biopsy codes 11755 Biopsy of nail unit (plate, bed, matrix, hyponychium, proximal and lateral nail folds 11100, 11101 have been deleted 30100 Biopsy, intranasal • New
    [Show full text]
  • Sample Research Poster
    Surgical management and lymph node biopsy of rare malignant cutaneous adnexal carcinomas: a population-based analysis of 7591 patients Amrita Goyal MD, 1 Theodore Marghitu,2 Nikhil Goyal BS,3 Nathan Rubin MS,4 Krishnan Patel MD,6 Kavita Goyal MD,1 Daniel O’Leary MD,5 Kimberly Bohjanen MD, 1 Ian Maher MD 1 1Department of Dermatology, University of Minnesota, Minneapolis, MN 2University of Minnesota Medical School, Minneapolis, MN 3National Institutes of Health/National Cancer Institute, Bethesda, MD 4Biostatistics Core, Masonic Cancer Center, University of Minnesota, Minneapolis MN 5Division of Hematology, Oncology, and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN 6Department of Radiation Oncology, University of Minnesota, Minneapolis, MN Background Overall and Disease-Specific Survival Lymph Node Biopsy and Survival Cutaneous adnexal carcinomas comprise a group of Vital status* All Sweat Hidradenocarc Spiradenocarci Sclerosin Porocarcin Eccrine Sebaceous Lymph Nodes All adnexal tumors adnexal gland inoma noma g sweat oma adenocarci carcinoma Lymph Nodes Examined carcino duct noma Nodes not examined 6592 (91.9) rare cutaneous malignancies that are generally ma tumor Nodes examined 578 (8.1) (MAC) Positive (% of examined) 138 (23.9) considered non-aggressive. Guidelines for the Stage (Derived AJCC N=1863 N=70 N=127 N=46 N=236 N=229 N=187 N=968 Negative (% of examined) 440 (76.1) Stage Group, 6th ed treatment of many of these malignancies are sparse, (2004-2015) Total N=1221 5-year OS 5-year DSS 1,2 I 1221 40 (57.1) 56 (44.1) 14 (30.4) 150 140 (61.1) 103 (55.1) 718 (74.2) Stage I Examined N=112 including guidance on surgical management (65.5) (63.6) Nodes not examined (% of total) 1109 (90.8) 69.7 (66.1-72.4) 99.3 (99.6-100) 3,4 II 440 14 (20.0) 54 (47.5) 28 (60.9) 47 (19.9) 64 (27.9) 51 (27.3) 182 (18.8) Nodes positive (% of examined) 0 (0) -- -- including the utility of lymph node biopsy.
    [Show full text]
  • 第32回日本皮膚病理組織学会学術大会 診断投票結果 口演 1 Drug Eruption 13, うち Erythema Multif
    第32回日本皮膚病理組織学会学術大会 診断投票結果 口演 1 Drug eruption 13, うち erythema multiforme 1, Interface dermatitis 1, GVHD type 1 Cutaneous reaction due to CCR4 3, うち Dysplastic epidermal hyperplasia 2, Adverse reaction 1 Erythema multiforme 3 PLEVA 1 Vacuolar type interface dermatitis 1 口演 2 Syringofibroadenoma 15, うち + amyloid 1 Syringofibroadenoma with BCC 5 Basal cell carcinoma 4, うち Pinkus type of BCC with syringofibroadenoma 2 口演 3 Darier disease 5 Hailey-Hailey disease 4 Pemphigus 3, うち Pemphigus Vegetans 1, Neonatal pemphigus 1 Grover's disease 4 Epidermal nevus 5, うち Acantholytic (dyskeratotic) epidermal nevus 4, Linear epidermal nevus 1 口演 4 Hydradenoma 13, うち Clear cell hidradenoma 12, Nodular hidradenoma 1 Sebaceous adenoma 1 Trichilemmoma 1 Metastatic tumor 8, うち ~ renal carcinoma6, ~ Clear cell carcinoma 2 口演 5 Apocrine carcinoma 3, うち ~with pagetoid spreading 2 Ectopic breast carcinoma(invasive ductal type)with pagetoid phenomenon 2 Extramammary Paget's disease 12, うち Paget carcinoma 3, ~ with Apocrine adenoma 2, ~ with Tubular adenoma 1, Invasive ~ 1, +Skin metastasis 1, With syringoma 1, with Microcystic Adnexal Carcinoma 1 Syringomatous carcinoma 2, うち ~with paget phenomenon 1 Tubular adenocartinoma 1 Tubular (apocrine) adenoma 2 Syringoma 1 口演 6 Dermatofibroma 10, うち Lipidized ~ 3, Hemosiderotic deep cellular ~ 2, Xanthomatous ~ 1, ~ Histiocytoid variant 1 Fibous histiocytoma 8, うち Atypical ~ 3, Malignant ~ 2, Aneurismal ~ 2 Undifferentiated pleomorphic sarcoma 2 Progressive nodular histiocytosis 1 Squamous
    [Show full text]
  • Arxiv:1204.3809V1 [Q-Bio.QM] 17 Apr 2012 Servicio De Oncolog´Iaradioter´Apica.Hospital General Universitario De Ciudad Real, 13005 Ciudad Real, Spain
    Bulletin of Mathematical Biology manuscript No. (will be inserted by the editor) Hypoxic Cell Waves around Necrotic Cores in Glioblastoma: A Biomathematical Model and its Therapeutic Implications Alicia Mart´ınez-Gonz´alez · Gabriel F. Calvo · Luis A. P´erezRomasanta · V´ıctorM. P´erez-Garc´ıa Received: date / Accepted: date Abstract Glioblastoma is a rapidly evolving high-grade astrocytoma that is distinguished pathologically from lower grade gliomas by the presence of necro- sis and microvascular hiperplasia. Necrotic areas are typically surrounded by hypercellular regions known as pseudopalisades originated by local tumor ves- sel occlusions that induce collective cellular migration events. This leads to the formation of waves of tumor cells actively migrating away from central hypoxia. We present a mathematical model that incorporates the interplay among two tumor cell phenotypes, a necrotic core and the oxygen distribution. Our simu- lations reveal the formation of a traveling wave of tumor cells that reproduces the observed histologic patterns of pseudopalisades. Additional simulations of the model equations show that preventing the collapse of tumor microvessels leads to slower glioma invasion, a fact that might be exploited for therapeutic purposes. Keywords Glioblastoma multiforme; tumor hypoxia; pseudopalisades; invasion; mathematical model Mathematics Subject Classification (2010) 92C50 · 35Q80 · 92C17 A. Mart´ınez-Gonz´alez,V. M. P´erez-Garc´ıa Departamento de Matem´aticas,E. T. S. I. Industriales and Instituto de Matem´aticaApli- cada a la Ciencia y la Ingenier´ıa,Universidad de Castilla-La Mancha, 13071 Ciudad Real, Spain. E-mail: [email protected], [email protected] G. F. Calvo Departamento de Matem´aticas,E.
    [Show full text]
  • An Institutional Experience
    Original Research Article Skin Adnexal Tumors- An Institutional Experience 1 2* 3 4 5 6 Rekha M Haravi , Roopa K N , Priya Patil , Rujuta Datar , Meena N Jadhav , Shreekant K Kittur 1,5Associate Professor, 2Post Graduate Student, 3,4Assistant Professor, 6Professor & HOD, Department of Pathology, Belgaum Institute of Medical Sciences Dr B R Ambedkar Road, Belagavi, Karnataka – 590001, INDIA. Email: [email protected] Abstract Background: Skin adnexal tumors are a wide spectrum of benign and malignant tumors that differentiate towards one or more adnexal structures found in normal skin. The adnexal structures of skin are the hair follicles, sebaceous glands, eccrine and apocrine sweat glands. These skin adnexal tumors are often difficult to diagnose clinically. This retrospective study was undertaken to know the various histomorphological patterns of skin adnexal tumors at our institution and to determine the incidence among the genders and age groups along with the site distribution. Materials and methods: A total of 40 specimens received and diagnosed as skin adnexal tumors in the department of Pathology at Belgaum Institute of Medical Sciences, Belagavi for a period of 6 years from January 2014 to December 2019 were taken for the study. Histopathological slides prepared from tissue blocks retrieved from departmental archives were reviewed and classified according to the WHO classification 2017. Results: Out of the total 40 samples, benign tumors were 36 (90%) and malignant were 4 (10%). Largest group was the benign tumors of apocrine and eccrine differentiation (47.5%) followed by benign tumors of hair follicle differentiation (40%). Malignant tumors of sebaceous differentiation were 5%, malignant tumors of eccrine and apocrine differentiation were 2.5% and malignant hair follicle differentiation tumors were 2.5% of the total.
    [Show full text]
  • Diagnostic Quality Control Exam Review of Answers
    Question 1 50-year-old healthy male with a family history of colorectal carcinoma presents with a rapidly growing nodule on the left nasal sidewall. A biopsy was performed, and he was referred for MMS. Review the 1st stage (H&E stain) section, and select the true statement: A. This is a basal cell carcinoma and will stain with BerEP4. B. This is a merkel cell carcinoma and will stain with CK20. C. This is a sebaceous carcinoma and may show loss of staining with MSH2, MSH6 or MLH1. D. This is a squamous cell carcinoma and will stain with cytokeratin stains. Discussion Question 1 Correct Answer: C. This is a sebaceous carcinoma and may show loss of staining with MSH2, MSH6 or MLH1. Fig. 1 – Collection of atypical basaloid cells with prominent nucleoli that exhibit vacuolization within the cytoplasm indicating sebocytic differentiation. Main Histologic Features: Dermally based basaloid tumor that forms a uniformly nested or lobular pattern and does not demonstrate peripheral palisading or clefting On high power, cells demonstrate multivacuolated foamy cytoplasm and scalloped nuclei designating sebocytic differentiation May demonstrate infiltrative features including invasion into the subcutis and native structures such as nerves, vessels, and lymphatics Atypia, mitosis, and necrosis may be seen Pagetoid spread is more commonly observed in periocular tumors Over 60% of tumors are moderately or poorly differentiated, necessitating immunohistochemistry for definitive diagnosis IHC markers that may aid in diagnosis include androgen receptor (AR), adipophilin (ADP), cytokeratin-7, BerEP4, EMA IHC with EMA, CEA or cytokeratin-7 immunopositivity can help to distinguish SC from BCC or SCC.
    [Show full text]
  • A Rare Clinical Presentation of Desmoplastic Trichilemmoma
    Revista5Vol89ingles_Layout 1 8/8/14 10:17 AM Página 796 796 CASE REPORT s A rare clinical presentation of Desmoplastic Trichilemmoma mimicking Invasive Carcinoma* Daniela Tiemi Sano1 Jeane Jeong Hoon Yang1 Antonio José Tebcherani1 Luiz Arthur de Paula Machado Bazzo1 DOI: http://dx.doi.org/10.1590/abd1806-4841.20143095 Abstract: Trichilemmoma is a benign neoplasm from the outer sheath of the pilosebaceous follicle. Desmoplastic trichilemmoma, a rare variant, is histologically characterized by a central area of desmoplasia that can clinically mimic an invasive carcinoma, requiring histopathological examination to define the diagnosis. Keywords: Hair diseases; Hair follicle; Skin neoplasms INTRODUCTION The trichilemmoma is a benign solid tumor ori- ma, without the presence of malignant processes, and ginating from external sheath cells of pilosebaceous associated with nevus sebaceous of Jadassohn in the follicles, and the desmoplastic trichilemmoma is a rare periphery of the lesion (Figures 3, 4, 5 and 6). Patient benign histological variant.1,2,3 Clinically, it may look is still under outpatient follow-up, with good clinical like other cutaneous lesions.2 Among the differential evolution and no relapse of lesion. diagnoses, we can cite basal-cell carcinoma, squamous cell carcinoma and viral lesions; the histopathological DISCUSSION examination is necessary for diagnostic confirmation. The trichilemmoma is a benign tumor origina- We report here a case of desmoplastic trichilemmoma ting from external root sheath cells of pilosebaceous in a
    [Show full text]
  • Pdf 344.65 K
    Differential Diagnosis of Basal Cell Carcinoma and Benign Tumors of Hair Follicles Using CD34 RESEARCH COMMUNICATION Differential Diagnosis of Basal Cell Carcinoma and Benign Tumors of Cutaneous Appendages Originating from Hair Follicles by Using CD34 Demet Sengul1, Ilker Sengul2*, Muzeyyen Hesna Astarci3, Huseyin Ustun3, Gamze Mocan4 Abstract Background and Aims: Differential diagnosis of the group of benign trichoblastomas, trichofolliculomas, trichoadenomas and trichoepitheliomas, and basal cell carcinomas (BCCs) is troublesome for the clinician as well as the pathologist, especially when only small biopsy specimens are available. Here we investigated whether CD34 expression might be of assistance. Methods: Thirty benign tumors of cutaneous appendages originating from hair follicles (BTCOHF) and 30 BCCs were retrieved from our archives and immunohistochemically stained. CD 34 expression was graded from [0] to [2+] and compared among the groups and subgroups. Results: There was no significant difference between the degree of expression between [0] and [1+] and [0] and [2+] for each group. However, [1+] and [2+] immunopositivity of BTCOHFs was significantly stronger than in BCCs (p= 0.014). Conclusions: CD34 may contribute to differential diagnosis of skin lesions. Keywords: Basal cell cancer - hair follicle lesions - CD 34 immunohistochemistry Asian Pacific J Cancer Prev, 11, 1615-1619 Introduction in 1958. TAs occur as a nodular lesion usually on the face and buttocks (Rahbari et al., 1977, Swaroop et al., 2008) Ackerman et al classified benign tumors of cutaneous and have a variant of verrucous TA mimicing seboreic appendages originating from hair follicle (BTCOHF)’s keratosis. using eight textbooks of dermatopathology in 2001 as Trichoepithelioma (TE) is a benign skin tumor with germ tumors of hair follicle and hamartomas, infindubular follicular differentiation determined in the classification and isthmic tumors, tumors of external layer, tumors of WHO as the synonym of TB (Cotton, 1991).
    [Show full text]
  • Mohs Surgery Educational Information for Patients
    DEPARTMENT OF DERMATOLOGY Mohs Surgery Educational information for patients Thank you for choosing the OHSU Department of Dermatology to provide your dermatologic care. Since the 1920s, the Department of Dermatology has been educati ng doctors, researching skin diseases and providing world-class care to pati ents in Oregon and beyond. We thank you for trusti ng us with your care. The surgeons and staff within the department welcome you. We have prepared this educati onal informati on to answer the most common questi ons presented to us by our pati ents. If you have additi onal questi ons aft er reading this material, please let us know. Some of the questi ons addressed include: • What is skin cancer? • What is Mohs surgery? • How do I prepare for Mohs surgery? • What happens the day of surgery? • What type of wound will I have and how will I care for that wound aft er surgery? • What measures can I take to prevent future skin cancer? What is skin cancer? Cancer is the abnormal growth of cells at an uncontrolled and unpredictable rate. The cancer tissue usually grows at the expense of surrounding normal tissue. The abnormal growth (cancer) originates in the uppermost layer of the skin and may grow downward, forming root and fi nger-like projections under the surface of the skin. Unfortunately, these roots may be subtle and unable to be seen without the aid of a microscope. Therefore, what you see on your skin is sometimes only a small portion of the total cancer. The most common types of skin cancer are basal cell carcinoma and squamous cell carcinoma.
    [Show full text]
  • Inherited Skin Tumour Syndromes
    CME GENETICS Clinical Medicine 2017 Vol 17, No 6: 562–7 I n h e r i t e d s k i n t u m o u r s y n d r o m e s A u t h o r s : S a r a h B r o w n , A P a u l B r e n n a n B a n d N e i l R a j a n C This article provides an overview of selected genetic skin con- and upper trunk. 1,2 These lesions are fibrofolliculomas, ditions where multiple inherited cutaneous tumours are a cen- trichodiscomas and acrochordons. Patients are also susceptible tral feature. Skin tumours that arise from skin structures such to the development of renal cell carcinoma, lung cysts and as hair, sweat glands and sebaceous glands are called skin pneumothoraces. 3 appendage tumours. These tumours are uncommon, but can Fibrofolliculomas and trichodiscomas clinically present as ABSTRACT have important implications for patient care. Certain appenda- skin/yellow-white coloured dome shaped papules 2–4 mm in geal tumours, particularly when multiple lesions are seen, may diameter (Fig 1 a and Fig 1 b). 4 These lesions usually develop indicate an underlying genetic condition. These tumours may in the third or fourth decade.4 In the case of fibrofolliculoma, not display clinical features that allow a secure diagnosis to be hair specific differentiation is seen, whereas in the case of made, necessitating biopsy and dermatopathological assess- trichodiscoma, differentiation is to the mesodermal component ment.
    [Show full text]