View Item 

Show simple item record

Molecular pathology of skin adnexal tumours
dc.contributor.authorPlotzke, Jaclyn M
dc.contributor.authorAdams, David J
dc.contributor.authorHarms, Paul W
dc.date.accessioned2022-01-06T15:50:49Z
dc.date.available2023-02-06 10:50:46en
dc.date.available2022-01-06T15:50:49Z
dc.date.issued2022-01
dc.identifier.citationPlotzke, Jaclyn M; Adams, David J; Harms, Paul W (2022). "Molecular pathology of skin adnexal tumours." Histopathology (1): 166-183.
dc.identifier.issn0309-0167
dc.identifier.issn1365-2559
dc.identifier.urihttps://hdl.handle.net/2027.42/171211
dc.publisherLippincott Williams and Wilkins
dc.publisherWiley Periodicals, Inc.
dc.subject.othercutaneous adnexal
dc.subject.othertumor syndrome
dc.subject.othersweat gland
dc.subject.othersebaceous
dc.subject.othermutation
dc.subject.othermolecular pathology
dc.subject.otherhair follicle
dc.titleMolecular pathology of skin adnexal tumours
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelMicrobiology and Immunology
dc.subject.hlbtoplevelHealth Sciences
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/171211/1/his14441.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/171211/2/his14441_am.pdf
dc.identifier.doi10.1111/his.14441
dc.identifier.sourceHistopathology
dc.identifier.citedreferencePanagopoulos I, Gorunova L, Lund‐Iversen M, Bassarova A, Heim S. Fusion of the genes PHF1 and TFE3 in malignant chondroid syringoma. Cancer Genomics Proteomics 2019; 16; 345 – 351.
dc.identifier.citedreferenceSekine S, Kiyono T, Ryo E et al. Recurrent YAP1‐MAML2 and YAP1‐NUTM1 fusions in poroma and porocarcinoma. J. Clin. Invest. 2019; 129; 3827 – 3832.
dc.identifier.citedreferenceMacagno N, Kervarrec T, Sohier P et al. NUT Is a specific immunohistochemical marker for the diagnosis of YAP1‐NUTM1‐rearranged cutaneous poroid neoplasms. Am. J. Surg. Pathol. 2021; 45; 1221 – 1227.
dc.identifier.citedreferenceParra O, Kerr DA, Bridge JA, Loehrer AP, Linos K. A case of YAP1 and NUTM1 rearranged porocarcinoma with corresponding immunohistochemical expression: review of recent advances in poroma and porocarcinoma pathogenesis with potential diagnostic utility. J. Cutan. Pathol. 2021; 48; 95 – 101.
dc.identifier.citedreferenceVarelas X. The Hippo pathway effectors TAZ and YAP in development, homeostasis and disease. Development 2014; 141; 1614 – 1626.
dc.identifier.citedreferenceHarvey KF, Zhang X, Thomas DM. The Hippo pathway and human cancer. Nat. Rev. Cancer 2013; 13; 246 – 257.
dc.identifier.citedreferencePrieto‐Granada C, Morlote D, Pavlidakey P et al. Poroid adnexal skin tumors with YAP1 fusions exhibit similar histopathologic features: A series of six YAP1‐rearranged adnexal skin tumors. J. Cutan. Pathol. 2021; 48; 1139 – 1149.
dc.identifier.citedreferenceRussell‐Goldman E, Hornick JL, Hanna J. Utility of YAP1 and NUT immunohistochemistry in the diagnosis of porocarcinoma. J. Cutan. Pathol. 2021; 48; 403 – 410.
dc.identifier.citedreferenceAntonescu CR, Zhang L, Chang NE et al. EWSR1‐POU5F1 fusion in soft tissue myoepithelial tumors. A molecular analysis of sixty‐six cases, including soft tissue, bone, and visceral lesions, showing common involvement of the EWSR1 gene. Genes Chromosomes Cancer 2010; 49; 1114 – 1124.
dc.identifier.citedreferenceZahn J, Chan MP, Wang G et al. Altered Rb, p16, and p53 expression is specific for porocarcinoma relative to poroma. J. Cutan. Pathol. 2019; 46; 659 – 664.
dc.identifier.citedreferenceWatanabe Y, Shido K, Niihori T et al. Somatic BRAF c.1799T>A p. V600E Mosaicism syndrome characterized by a linear syringocystadenoma papilliferum, anaplastic astrocytoma, and ocular abnormalities. Am. J. Med. Genet A. 2016; 170A; 189 – 194.
dc.identifier.citedreferenceKim JT, Newsom KJ, Shon W. Detection of somatic mutations in secondary tumors associated with nevus sebaceus by targeted next generation sequencing. Comment on Kitamura et al. Int. J. Dermatol. 2018; 57; 120 – 122.
dc.identifier.citedreferenceLevinsohn JL, Tian LC, Boyden LM et al. Whole‐exome sequencing reveals somatic mutations in HRAS and KRAS, which cause nevus sebaceus. J. Invest. Dermatol. 2013; 133; 827 – 830.
dc.identifier.citedreferenceFriedman BJ, Sahu J, Solomides CC, Connolly DM, Lee JB. Contiguous verrucous proliferations in syringocystadenoma papilliferum: a retrospective analysis with additional evaluation via mutation‐specific BRAFV600E immunohistochemistry. J. Cutan. Pathol. 2018; 45; 212 – 216.
dc.identifier.citedreferenceAlegria‐Landa V, Jo‐Velasco M, Santonja C et al. Syringocystadenoma papilliferum associated with verrucous carcinoma of the skin in the same lesion: report of four cases. J. Cutan. Pathol. 2020; 47; 12 – 16.
dc.identifier.citedreferenceAltunel E, Perepletchikov A, Kozyreva O. Metastatic syringocystadenocarcinoma papilliferum: a case report, tumor genomic profiling, and literature review. Case Rep. Oncol. Med. 2020; 2020; 9056209.
dc.identifier.citedreferencePfarr N, Allgauer M, Steiger K et al. Several genotypes, one phenotype: PIK3CA/AKT1 mutation‐negative hidradenoma papilliferum show genetic lesions in other components of the signalling network. Pathology 2019; 51; 362 – 368.
dc.identifier.citedreferencePfarr N, Sinn HP, Klauschen F et al. Mutations in genes encoding PI3K‐AKT and MAPK signaling define anogenital papillary hidradenoma. Genes Chromosomes Cancer 2016; 55; 113 – 119.
dc.identifier.citedreferenceWu WM, Lee YS. Autosomal dominant multiple syringomas linked to chromosome 16q22. Br. J. Dermatol. 2010; 162; 1083 – 1087.
dc.identifier.citedreferenceLiau JY, Tsai JH, Huang WC, Lan J, Hong JB, Yuan CT. BRAF and KRAS mutations in tubular apocrine adenoma and papillary eccrine adenoma of the skin. Hum. Pathol. 2018; 73; 59 – 65.
dc.identifier.citedreferenceGoto K, Kukita Y, Honma K et al. Signet‐ring cell/histiocytoid carcinoma of the axilla: a clinicopathologic and genetic analysis of 11 cases, review of the literature, and comparison with potentially related tumours. Histopathology 2021. https://doi.org/10.1111/his.14436
dc.identifier.citedreferenceBahrami A, Dalton JD, Krane JF, Fletcher CDM. A subset of cutaneous and soft tissue mixed tumors are genetically linked to their salivary gland counterpart. Genes Chromosom. Cancer 2012; 51; 140 – 148.
dc.identifier.citedreferencePanagopoulos I, Gorunova L, Andersen K et al. NDRG1‐PLAG1 and TRPS1‐PLAG1 fusion genes in chondroid syringoma. Cancer Genomics Proteomics 2020; 17; 237 – 248.
dc.identifier.citedreferenceMatsuyama A, Hisaoka M, Hashimoto H. PLAG1 expression in cutaneous mixed tumors: an immunohistochemical and molecular genetic study. Virchows. Arch. 2011; 459; 539 – 545.
dc.identifier.citedreferenceRussell‐Goldman E, Dubuc A, Hanna J. Differential expression of PLAG1 in apocrine and eccrine cutaneous mixed tumors: evidence for distinct molecular pathogenesis. Am. J. Dermatopathol. 2020; 42; 251 – 257.
dc.identifier.citedreferenceKazakov D, McKee P, Michal M, Kacerovska D. Cutaneous adnexal tumors. Philadelphia, United States: Lippincott Williams and Wilkins, 2012.
dc.identifier.citedreferenceBignell GR, Warren W, Seal S et al. Identification of the familial cylindromatosis tumour‐suppressor gene. Nat. Genet. 2000; 25; 160 – 165.
dc.identifier.citedreferenceElder DE, Massi D, Scolyer RA, Willemze R, eds. WHO classification of skin tumors. 4th ed. Lyon, France: International Agency for Research on Cancer, 2018.
dc.identifier.citedreferenceHile G, Harms PW. Update on molecular genetic alterations of cutaneous adnexal neoplasms. Surg. Pathol. Clin. 2021; 14; 251 – 272.
dc.identifier.citedreferenceBolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. China: Elsevier, 2018.
dc.identifier.citedreferenceNorth JP. Molecular genetics of sebaceous neoplasia. Surg. Pathol. Clin. 2021; 14; 273 – 284.
dc.identifier.citedreferenceRoberts ME, Riegert‐Johnson DL, Thomas BC et al. Screening for Muir‐Torre syndrome using mismatch repair protein immunohistochemistry of sebaceous neoplasms. J. Genet. Couns. 2013; 22; 393 – 405.
dc.identifier.citedreferencePonti G, Ponz de Leon M, Maffei S et al. Attenuated familial adenomatous polyposis and Muir‐Torre syndrome linked to compound biallelic constitutional MYH gene mutations. Clin. Genet. 2005; 68; 442 – 447.
dc.identifier.citedreferenceNorth JP, Golovato J, Vaske CJ et al. Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma. Nat. Commun. 2018; 9; 1894.
dc.identifier.citedreferenceHarvey NT, Tabone T, Erber W, Wood BA. Circumscribed sebaceous neoplasms: a morphological, immunohistochemical and molecular analysis. Pathology 2016; 48; 454 – 462.
dc.identifier.citedreferenceTetzlaff MT, Curry JL, Ning J et al. Distinct biological types of ocular adnexal sebaceous carcinoma: HPV‐driven and virus‐negative tumors arise through nonoverlapping molecular‐genetic alterations. Clin. Cancer Res. 2019; 25; 1280 – 1290.
dc.identifier.citedreferenceTetzlaff MT, Singh RR, Seviour EG et al. Next‐generation sequencing identifies high frequency of mutations in potentially clinically actionable genes in sebaceous carcinoma. J. Pathol. 2016; 240; 84 – 95.
dc.identifier.citedreferenceGeorgeson P, Walsh MD, Clendenning M et al. Tumor mutational signatures in sebaceous skin lesions from individuals with Lynch syndrome. Mol. Genet. Genomic. Med. 2019; 7; e00781.
dc.identifier.citedreferenceKutzner H, Requena L, Rutten A, Mentzel T. Spindle cell predominant trichodiscoma: a fibrofolliculoma/trichodiscoma variant considered formerly to be a neurofollicular hamartoma: a clinicopathological and immunohistochemical analysis of 17 cases. Am. J. Dermatopathol. 2006; 28; 1 – 8.
dc.identifier.citedreferenceMichalova K, Kutzner H, Steiner P et al. Spindle cell predominant trichodiscoma or spindle cell lipoma with adnexal induction? a study of 25 cases, revealing a subset of cases with RB1 heterozygous deletion in the spindle cell stroma. Am. J. Dermatopathol. 2019; 41; 637 – 643.
dc.identifier.citedreferenceChan EF, Gat U, McNiff JM, Fuchs E. A common human skin tumour is caused by activating mutations in beta‐catenin. Nat. Genet. 1999; 21; 410 – 413.
dc.identifier.citedreferenceTumminello K, Hosler GA. CDX2 and LEF‐1 expression in pilomatrical tumors and their utility in the diagnosis of pilomatrical carcinoma. J. Cutan. Pathol. 2018; 45; 318 – 324.
dc.identifier.citedreferenceLazar AJ, Calonje E, Grayson W et al. Pilomatrix carcinomas contain mutations in CTNNB1, the gene encoding beta‐catenin. J. Cutan. Pathol. 2005; 32; 148 – 157.
dc.identifier.citedreferenceAgoston AT, Liang C, Richkind KE, Fletcher JA, Vargas SO. Trisomy 18 is a consistent cytogenetic feature in pilomatricoma. Mod. Pathol. 2010; 23; 1147.
dc.identifier.citedreferenceLiu K, Luo J, Ma T et al. Germline mutation of PLCD1 contributes to human multiple pilomatricomas through protein kinase D/extracellular signal‐regulated kinase1/2 cascade and TRPV6. J. Invest. Dermatol. 2021; 141; 533 – 544.
dc.identifier.citedreferenceTrufant J, Kurz W, Frankel A et al. Familial multiple pilomatrixomas as a presentation of attenuated adenomatosis polyposis coli. J. Cutan. Pathol. 2012; 39; 440 – 443.
dc.identifier.citedreferenceChmara M, Wernstedt A, Wasag B et al. Multiple pilomatricomas with somatic CTNNB1 mutations in children with constitutive mismatch repair deficiency. Genes Chromosomes Cancer 2013; 52; 656 – 664.
dc.identifier.citedreferenceRubben A, Wahl RU, Eggermann T, Dahl E, Ortiz‐Bruchle N, Cacchi C. Mutation analysis of multiple pilomatricomas in a patient with myotonic dystrophy type 1 suggests a DM1‐associated hypermutation phenotype. PLoS One 2020; 15; e0230003.
dc.identifier.citedreferenceLuong TMH, Akazawa Y, Mussazhanova Z et al. Cutaneous pilomatrical carcinosarcoma: a case report with molecular analysis and literature review. Diagn. Pathol. 2020; 15; 7.
dc.identifier.citedreferenceShen AS, Peterhof E, Kind P et al. Activating mutations in the RAS/mitogen‐activated protein kinase signaling pathway in sporadic trichoblastoma and syringocystadenoma papilliferum. Hum. Pathol. 2015; 46; 272 – 276.
dc.identifier.citedreferenceHafner C, Schmiemann V, Ruetten A et al. PTCH mutations are not mainly involved in the pathogenesis of sporadic trichoblastomas. Hum. Pathol. 2007; 38; 1496 – 1500.
dc.identifier.citedreferenceHu G, Onder M, Gill M et al. A novel missense mutation in CYLD in a family with Brooke‐Spiegler syndrome. J. Invest. Dermatol. 2003; 121; 732 – 734.
dc.identifier.citedreferenceSalhi A, Bornholdt D, Oeffner F et al. Multiple familial trichoepithelioma caused by mutations in the cylindromatosis tumor suppressor gene. Cancer Res. 2004; 64; 5113 – 5117.
dc.identifier.citedreferenceZhang XJ, Liang YH, He PP et al. Identification of the cylindromatosis tumor‐suppressor gene responsible for multiple familial trichoepithelioma. J. Invest. Dermatol. 2004; 122; 658 – 664.
dc.identifier.citedreferenceBrummelkamp TR, Nijman SM, Dirac AM, Bernards R. Loss of the cylindromatosis tumour suppressor inhibits apoptosis by activating NF‐kappaB. Nature 2003; 424; 797 – 801.
dc.identifier.citedreferenceFewings E, Ziemer M, Hortnagel K et al. Malta (MYH9 associated elastin aggregation) syndrome: germline variants in MYH9 cause rare sweat duct proliferations and irregular elastin aggregations. J. Invest. Dermatol. 2019; 139 ( 2238–2241 ); e6.
dc.identifier.citedreferencePark HS, Papanastasi E, Blanchard G et al. ARP‐T1‐associated Bazex‐Dupre‐Christol syndrome is an inherited basal cell cancer with ciliary defects characteristic of ciliopathies. Commun. Biol. 2021; 4; 544.
dc.identifier.citedreferenceVorechovsky I, Unden AB, Sandstedt B, Toftgard R, Stahle‐Backdahl M. Trichoepitheliomas contain somatic mutations in the overexpressed PTCH gene: support for a gatekeeper mechanism in skin tumorigenesis. Cancer Res. 1997; 57; 4677 – 4681.
dc.identifier.citedreferenceKazakov DV, Sima R, Vanecek T et al. Mutations in exon 3 of the CTNNB1 gene (beta‐catenin gene) in cutaneous adnexal tumors. Am. J. Dermatopathol. 2009; 31; 248 – 255.
dc.identifier.citedreferenceKim C, Brown A, Osipov V. Trichoblastic carcinosarcoma in a 34‐year‐old woman with histopathologic and molecular analysis, including re‐demonstration of a CDKN2A p.(R58*) mutation. J. Cutan. Pathol. 2021; 48: 334 – 339.
dc.identifier.citedreferenceGiang J, Biswas A, Mooyaart AL, Groenendijk FH, Dikrama P, Damman J. Trichoblastic carcinosarcoma with panfollicular differentiation (panfollicular carcinosarcoma) and CTNNB1 (beta‐catenin) mutation. J. Cutan. Pathol. 2021; 48; 309 – 313.
dc.identifier.citedreferenceZhuang SM, Zhang GH, Chen WK et al. Survival study and clinicopathological evaluation of trichilemmal carcinoma. Mol. Clin. Oncol. 2013; 1; 499 – 502.
dc.identifier.citedreferenceTsai JH, Huang WC, Jhuang JY et al. Frequent activating HRAS mutations in trichilemmoma. Br. J. Dermatol. 2014; 171; 1073 – 1077.
dc.identifier.citedreferenceAl‐Zaid T, Ditelberg JS, Prieto VG et al. Trichilemmomas show loss of PTEN in Cowden syndrome but only rarely in sporadic tumors. J. Cutan. Pathol. 2012; 39; 493 – 499.
dc.identifier.citedreferenceHa JH, Lee C, Lee KS et al. The molecular pathogenesis of Trichilemmal carcinoma. BMC Cancer 2020; 20; 516.
dc.identifier.citedreferencePickering CR, Zhou JH, Lee JJ et al. Mutational landscape of aggressive cutaneous squamous cell carcinoma. Clin. Cancer Res. 2014; 20; 6582 – 6592.
dc.identifier.citedreferenceHorer S, Marrakchi S, Radner FPW et al. A monoallelic two‐hit mechanism in PLCD1 explains the genetic pathogenesis of hereditary trichilemmal cyst formation. J. Invest. Dermatol. 2019; 139 ( 2154–2163 ); e5.
dc.identifier.citedreferenceGallant JN, Sewell A, Almodovar K et al. Genomic landscape of a metastatic malignant proliferating tricholemmal tumor and its response to PI3K inhibition. NPJ Precis. Oncol. 2019; 3; 5.
dc.identifier.citedreferenceBesagni F, Dika E, Ricci C et al. Basaloid follicular hamartomas in pediatric basal cell nevus syndrome: a diagnostic challenge. J. Dermatol. 2021; 48; 1101 – 1105.
dc.identifier.citedreferenceSeo SH, Lee SE, Kim SC. Happle‐Tinschert syndrome: a case report of unilateral segmentally arranged basaloid follicular hamartoma with scoliosis and review of literature. Ann. Dermatol. 2020; 32; 159 – 163.
dc.identifier.citedreferenceShevchenko A, Durkin JR, Moon AT. Generalized basaloid follicular hamartoma syndrome versus Gorlin syndrome: a diagnostic challenge. Pediatr. Dermatol. 2018; 35; e396 – e397.
dc.identifier.citedreferenceGrachtchouk V, Grachtchouk M, Lowe L et al. The magnitude of hedgehog signaling activity defines skin tumor phenotype. EMBO J. 2003; 22; 2741 – 2751.
dc.identifier.citedreferenceRashid M, van der Horst M, Mentzel T et al. ALPK1 hotspot mutation as a driver of human spiradenoma and spiradenocarcinoma. Nat. Commun. 2019; 10; 2213.
dc.identifier.citedreferencevan der Horst MP, Marusic Z, Hornick JL, Luzar B, Brenn T. Morphologically low‐grade spiradenocarcinoma: a clinicopathologic study of 19 cases with emphasis on outcome and MYB expression. Mod. Pathol. 2015; 28; 944 – 953.
dc.identifier.citedreferenceVerhoef S, Schrander‐Stumpel CT, Vuzevski VD et al. Familial cylindromatosis mimicking tuberous sclerosis complex and confirmation of the cylindromatosis locus, CYLD1, in a large family. J. Med. Genet. 1998; 35; 841 – 845.
dc.identifier.citedreferenceFehr A, Kovacs A, Loning T, Frierson H Jr, van den Oord J, Stenman G. The MYB‐NFIB gene fusion‐a novel genetic link between adenoid cystic carcinoma and dermal cylindroma. J. Pathol. 2011; 224; 322 – 327.
dc.identifier.citedreferenceRamsay RG, Gonda TJ. MYB function in normal and cancer cells. Nat. Rev. Cancer 2008; 8; 523 – 534.
dc.identifier.citedreferenceRajan N, Andersson MK, Sinclair N et al. Overexpression of MYB drives proliferation of CYLD‐defective cylindroma cells. J. Pathol. 2016; 239; 197 – 205.
dc.identifier.citedreferenceCorda G, Sala A. Cutaneous cylindroma: it’s all about MYB. J. Pathol. 2016; 239; 391 – 393.
dc.identifier.citedreferenceDavies HR, Hodgson K, Schwalbe E et al. Epigenetic modifiers DNMT3A and BCOR are recurrently mutated in CYLD cutaneous syndrome. Nat. Commun. 2019; 10; 4717.
dc.identifier.citedreferenceLe LP, Dias‐Santagata D, Pawlak AC et al. Apocrine‐eccrine carcinomas: molecular and immunohistochemical analyses. PLoS One 2012; 7; e47290.
dc.identifier.citedreferenceKazakov DV, Grossmann P, Spagnolo DV et al. Expression of p53 and TP53 mutational analysis in malignant neoplasms arising in preexisting spiradenoma, cylindroma, and spiradenocylindroma, sporadic or associated with Brooke‐Spiegler syndrome. Am. J. Dermatopathol. 2010; 32; 215 – 221.
dc.identifier.citedreferenceBiernat W, Peraud A, Wozniak L, Ohgaki H. p53 mutations in sweat gland carcinomas. Int. J. Cancer 1998; 76; 317 – 320.
dc.identifier.citedreferenceSuchak R, Wang WL, Prieto VG et al. Cutaneous digital papillary adenocarcinoma: a clinicopathologic study of 31 cases of a rare neoplasm with new observations. Am. J. Surg. Pathol. 2012; 36; 1883 – 1891.
dc.identifier.citedreferenceTrager MH, Jurkiewicz M, Khan S, Niedt GW, Geskin LJ, Carvajal RD. A case report of papillary digital adenocarcinoma with BRAFV600E mutation and quantified mutational burden. Am. J. Dermatopathol. 2021; 43; 57 – 59.
dc.identifier.citedreferenceBell D, Aung P, Prieto VG, Ivan D. Next‐generation sequencing reveals rare genomic alterations in aggressive digital papillary adenocarcinoma. Ann. Diagn. Pathol. 2015; 19; 381 – 384.
dc.identifier.citedreferenceDias‐Santagata D, Lam Q, Bergethon K et al. A potential role for targeted therapy in a subset of metastasizing adnexal carcinomas. Mod. Pathol. 2011; 24; 974 – 982.
dc.identifier.citedreferenceEmanuel PO, de Vinck D, Waldorf HA, Phelps RG. Recurrent endocrine mucin‐producing sweat gland carcinoma. Ann. Diagn. Pathol. 2007; 11; 448 – 452.
dc.identifier.citedreferenceAgni M, Raven ML, Bowen RC et al. An update on endocrine mucin‐producing sweat gland carcinoma: clinicopathologic study of 63 cases and comparative analysis. Am. J. Surg. Pathol. 2020; 44; 1005 – 1016.
dc.identifier.citedreferenceMathew JG, Bowman AS, Saab J, Busam KJ, Nehal K, Pulitzer M. Next generation sequencing analysis suggests varied multistep mutational pathogenesis for endocrine mucin producing sweat gland carcinoma with comments on INSM1 and MUC2 suggesting a conjunctival origin. J. Am. Acad. Dermatol. 2021. https://doi.org/10.1016/j.jaad.2020.11.073
dc.identifier.citedreferenceQin H, Moore RF, Ho CY, Eshleman J, Eberhart CG, Cuda J. Endocrine mucin‐producing sweat gland carcinoma: a study of 11 cases with molecular analysis. J. Cutan. Pathol. 2018; 45; 681 – 687.
dc.identifier.citedreferenceHeld L, Ruetten A, Kutzner H, Palmedo G, John R, Mentzel T. Endocrine mucin‐producing sweat gland carcinoma: clinicopathologic, immunohistochemical, and molecular analysis of 11 cases with emphasis on MYB immunoexpression. J. Cutan. Pathol. 2018; 45; 674 – 680.
dc.identifier.citedreferenceCornejo KM, Hutchinson L, Meng X, O’Donnell P, Deng A. Endocrine mucin‐producing sweat gland carcinoma of the eyelid: a report of a case with molecular analysis. Am. J. Dermatopathol. 2016; 38; 636 – 638.
dc.identifier.citedreferenceBehboudi A, Winnes M, Gorunova L et al. Clear cell hidradenoma of the skin‐a third tumor type with a t(11;19)–associated TORC1‐MAML2 gene fusion. Genes Chromosomes Cancer 2005; 43; 202 – 205.
dc.identifier.citedreferenceWinnes M, Molne L, Suurkula M et al. Frequent fusion of the CRTC1 and MAML2 genes in clear cell variants of cutaneous hidradenomas. Genes Chromosomes Cancer 2007; 46; 559 – 563.
dc.identifier.citedreferenceKuma Y, Yamada Y, Yamamoto H et al. A novel fusion gene CRTC3‐MAML2 in hidradenoma: histopathological significance. Hum. Pathol. 2017; 70; 55 – 61.
dc.identifier.citedreferenceMoller E, Stenman G, Mandahl N et al. POU5F1, encoding a key regulator of stem cell pluripotency, is fused to EWSR1 in hidradenoma of the skin and mucoepidermoid carcinoma of the salivary glands. J. Pathol. 2008; 215; 78 – 86.
dc.identifier.citedreferenceKazakov DV, Ivan D, Kutzner H et al. Cutaneous hidradenocarcinoma: a clinicopathological, immunohistochemical, and molecular biologic study of 14 cases, including Her2/neu gene expression/amplification, TP53 gene mutation analysis, and t(11;19) translocation. Am. J. Dermatopathol. 2009; 31; 236 – 247.
dc.identifier.citedreferenceCavalieri S, Busico A, Capone I et al. Identification of potentially druggable molecular alterations in skin adnexal malignancies. J. Dermatol. 2019; 46; 507 – 514.
dc.identifier.citedreferenceChan MP, Plouffe KR, Liu CJ et al. Next‐generation sequencing implicates oncogenic roles for p53 and JAK/STAT signaling in microcystic adnexal carcinomas. Mod. Pathol. 2020; 33; 1092 – 1103.
dc.identifier.citedreferenceChen MB, Laber DA. Metastatic microcystic adnexal carcinoma with DNA sequencing results and response to systemic antineoplastic chemotherapy. Anticancer Res. 2017; 37; 5109 – 5111.
dc.identifier.citedreferenceWohlfahrt C, Ternesten A, Sahlin P, Islam Q, Stenman G. Cytogenetic and fluorescence in situ hybridization analyses of a microcystic adnexal carcinoma with del(6)(q23q25). Cancer Genet. Cytogenet. 1997; 98; 106 – 110.
dc.identifier.citedreferenceSchaller J, Rytina E, Rutten A, Hendricks C, Ha T, Requena L. Sweat duct proliferation associated with aggregates of elastic tissue and atrophodermia vermiculata: a simulator of microcystic adnexal carcinoma. Report of two cases. J. Cutan. Pathol. 2010; 37; 1002 – 1009.
dc.identifier.citedreferenceRobson A, Greene J, Ansari N et al. Eccrine porocarcinoma (malignant eccrine poroma): a clinicopathologic study of 69 cases. Am. J. Surg. Pathol. 2001; 25; 710 – 720.
dc.identifier.citedreferenceNazemi A, Higgins S, Swift R et al. Eccrine porocarcinoma: new insights and a systematic review of the literature. Dermatol. Surg. 2018; 44; 1247 – 1261.
dc.identifier.citedreferenceHarms PW, Hovelson DH, Cani AK et al. Porocarcinomas harbor recurrent HRAS‐activating mutations and tumor suppressor inactivating mutations. Hum. Pathol. 2016; 51; 25 – 31.
dc.identifier.citedreferenceBosic M, Kirchner M, Brasanac D et al. Targeted molecular profiling reveals genetic heterogeneity of poromas and porocarcinomas. Pathology 2018; 50; 327 – 332.
dc.working.doiNOen
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Name:
his14441.pdf
Size:
14.74MB
Format:
PDF
View/Open
Name:
his14441_am.pdf
Size:
1.065MB
Format:
PDF
View/Open

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.