Desmoid tumor differential diagnosis: Difference between revisions

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**Gardner [[fibroma]]<ref name="pmid11342777">{{cite journal| author=Wehrli BM, Weiss SW, Yandow S, Coffin CM| title=Gardner-associated fibromas (GAF) in young patients: a distinct fibrous lesion that identifies unsuspected Gardner syndrome and risk for fibromatosis. | journal=Am J Surg Pathol | year= 2001 | volume= 25 | issue= 5 | pages= 645-51 | pmid=11342777 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11342777  }} </ref>
**Gardner [[fibroma]]<ref name="pmid11342777">{{cite journal| author=Wehrli BM, Weiss SW, Yandow S, Coffin CM| title=Gardner-associated fibromas (GAF) in young patients: a distinct fibrous lesion that identifies unsuspected Gardner syndrome and risk for fibromatosis. | journal=Am J Surg Pathol | year= 2001 | volume= 25 | issue= 5 | pages= 645-51 | pmid=11342777 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11342777  }} </ref>
*'''Intra-[[abdominal]] [[fibromatosis]]''' must be differentiated from:<ref name="pmid17414097">{{cite journal| author=Coffin CM, Hornick JL, Fletcher CD| title=Inflammatory myofibroblastic tumor: comparison of clinicopathologic, histologic, and immunohistochemical features including ALK expression in atypical and aggressive cases. | journal=Am J Surg Pathol | year= 2007 | volume= 31 | issue= 4 | pages= 509-20 | pmid=17414097 | doi=10.1097/01.pas.0000213393.57322.c7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17414097  }} </ref>
*'''Intra-[[abdominal]] [[fibromatosis]]''' must be differentiated from:<ref name="pmid17414097">{{cite journal| author=Coffin CM, Hornick JL, Fletcher CD| title=Inflammatory myofibroblastic tumor: comparison of clinicopathologic, histologic, and immunohistochemical features including ALK expression in atypical and aggressive cases. | journal=Am J Surg Pathol | year= 2007 | volume= 31 | issue= 4 | pages= 509-20 | pmid=17414097 | doi=10.1097/01.pas.0000213393.57322.c7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17414097  }} </ref>
**[[Gastrointestinal stromal tumor]] (GIST)
**[[Gastrointestinal stromal tumor]] ([[GIST]])
**[[Benign]] [[fibrous]] [[tumor]]/[[Solitary fibrous tumor of the pleura|Solitary fibrous tumor]] (SFT)
**[[Benign]] [[fibrous]] [[tumor]]/[[Solitary fibrous tumor of the pleura|Solitary fibrous tumor]] (SFT)
**[[Inflammatory]] myofibroblastic [[tumor]] (IMT)
**[[Inflammatory]] myofibroblastic [[tumor]] (IMT)
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* [[Precursor]] [[lesion]] for [[Colon|colonic]] [[adenomas]] in [[asymptomatic]] [[FAP]] [[patients]]
* [[Precursor]] [[lesion]] for [[Colon|colonic]] [[adenomas]] in [[asymptomatic]] [[FAP]] [[patients]]
|-
|-
|'''[[Gastrointestinal stromal tumor]] (GIST)'''<ref name="pmid26055339">{{cite journal| author=Zarkavelis G, Petrakis D, Pavlidis N| title=Gastrointestinal stromal tumors during pregnancy: a systematic review of an uncommon but treatable malignancy. | journal=Clin Transl Oncol | year= 2015 | volume= 17 | issue= 10 | pages= 757-62 | pmid=26055339 | doi=10.1007/s12094-015-1315-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26055339  }} </ref><ref name="pmid27384431">{{cite journal| author=Navarrete A, Momblán D, Almenara R, Lacy A| title=Giant Gastric Gastrointestinal Stromal Tumor (GIST). | journal=J Gastrointest Surg | year= 2017 | volume= 21 | issue= 1 | pages= 202-204 | pmid=27384431 | doi=10.1007/s11605-016-3196-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27384431  }} </ref><ref name="pmid19763238">{{cite journal| author=Scherjon S, Lam WF, Gelderblom H, Jansen FW| title=Gastrointestinal stromal tumor in pregnancy: a case report. | journal=Case Rep Med | year= 2009 | volume= 2009 | issue=  | pages= 456402 | pmid=19763238 | doi=10.1155/2009/456402 | pmc=2745024 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19763238  }} </ref><ref name="pmid22472152">{{cite journal| author=Acín-Gándara D, Pereira-Pérez F, Castaño-Pascual A, Durán-Poveda M, Antequera-Pérez A, Miliani-Molina C| title=Gastrointestinal stromal tumors: diagnosis and treatment. | journal=Cir Cir | year= 2012 | volume= 80 | issue= 1 | pages= 44-51 | pmid=22472152 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22472152  }} </ref><ref name="pmid16413690">{{cite journal| author=Lanzafame S, Minutolo V, Caltabiano R, Minutolo O, Marino B, Gagliano G et al.| title=About a case of GIST occurring during pregnancy with immunohistochemical expression of epidermal growth factor receptor and progesterone receptor. | journal=Pathol Res Pract | year= 2006 | volume= 202 | issue= 2 | pages= 119-23 | pmid=16413690 | doi=10.1016/j.prp.2005.08.013 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16413690  }} </ref>
|'''[[Gastrointestinal stromal tumor]] ([[GIST]])'''<ref name="pmid26055339">{{cite journal| author=Zarkavelis G, Petrakis D, Pavlidis N| title=Gastrointestinal stromal tumors during pregnancy: a systematic review of an uncommon but treatable malignancy. | journal=Clin Transl Oncol | year= 2015 | volume= 17 | issue= 10 | pages= 757-62 | pmid=26055339 | doi=10.1007/s12094-015-1315-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26055339  }} </ref><ref name="pmid27384431">{{cite journal| author=Navarrete A, Momblán D, Almenara R, Lacy A| title=Giant Gastric Gastrointestinal Stromal Tumor (GIST). | journal=J Gastrointest Surg | year= 2017 | volume= 21 | issue= 1 | pages= 202-204 | pmid=27384431 | doi=10.1007/s11605-016-3196-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27384431  }} </ref><ref name="pmid19763238">{{cite journal| author=Scherjon S, Lam WF, Gelderblom H, Jansen FW| title=Gastrointestinal stromal tumor in pregnancy: a case report. | journal=Case Rep Med | year= 2009 | volume= 2009 | issue=  | pages= 456402 | pmid=19763238 | doi=10.1155/2009/456402 | pmc=2745024 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19763238  }} </ref><ref name="pmid22472152">{{cite journal| author=Acín-Gándara D, Pereira-Pérez F, Castaño-Pascual A, Durán-Poveda M, Antequera-Pérez A, Miliani-Molina C| title=Gastrointestinal stromal tumors: diagnosis and treatment. | journal=Cir Cir | year= 2012 | volume= 80 | issue= 1 | pages= 44-51 | pmid=22472152 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22472152  }} </ref><ref name="pmid16413690">{{cite journal| author=Lanzafame S, Minutolo V, Caltabiano R, Minutolo O, Marino B, Gagliano G et al.| title=About a case of GIST occurring during pregnancy with immunohistochemical expression of epidermal growth factor receptor and progesterone receptor. | journal=Pathol Res Pract | year= 2006 | volume= 202 | issue= 2 | pages= 119-23 | pmid=16413690 | doi=10.1016/j.prp.2005.08.013 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16413690  }} </ref>
|Activating mutation of:
|[[Activating group|Activating]] [[mutation]] of:
* ''C-KIT'' ( [[tyrosine kinase]] growth factor [[receptor]]) gene (Exon 9,13 & 17)
* ''[[C-KIT]]'' ( [[tyrosine kinase|tyrosine kinase growth factor receptor]]) [[gene]] ([[Exon]] 9,13 & 17)
* [[Platelet-activating factor receptor|Platelet-derived growth factor receptor alpha]] (''PDGFRA on [[Chromosome 4|chromosome]] 4q11-12)'' gene (Exon 18)
* [[Platelet-activating factor receptor|Platelet-derived growth factor receptor alpha]] (''[[PDGFR]]A on [[Chromosome 4|chromosome]] 4q11-12)'' [[gene]] ([[Exon]] 18)
* ''[[BRAF]]'' kinase (rare)
* ''[[BRAF]]'' [[kinase]] (rare)
* [[Protein kinase C]] (rare)
* [[Protein kinase C]] (rare)
Pediatric GISTs (SDH-deficient) have mutations of one of the:
[[Pediatric]] [[GIST|GISTs]] ([[Succinate dehydrogenase|SDH]]-[[deficient]]) have [[mutations]] of one of the:
* ''SDH'' (succinate dehydrogenase)gene subunits
* ''[[Succinate dehydrogenase|SDH]]'' ([[succinate dehydrogenase]])[[gene]] [[subunits]]
GIST as a part of Carney triad has following mutation:
[[GIST]] as a part of [[Carney triad]] has following [[mutation]]:
* Hypermethylation of the SDHC promoter causing epigenetic inactivation of the ''SDHC'' gene  
* Hypermethylation of the [[SDHC (gene)|SDHC]] [[promoter]] causing [[epigenetic]] inactivation of the [[SDHC (gene)|''SDHC'' gene]]
Wild-type GISTs have following three molecular subtypes:
[[Wild-type]] GISTs have following three [[molecular]] subtypes:
* ''DHX'' mutations (66%)
* ''[[DHX15|DHX]]'' [[mutations]] (66%)
* SDHC promoter hypermethylation (22%)
* [[SDHC]] [[promoter]] hypermethylation (22%)
* SDH competent (12%) which can further be broken into:
* [[SDH]] [[competent]] (12%) which can further be broken into:
** ''NF1'' mutations
** ''[[NF1]]'' [[mutations]]
**''BRAF'' V600E mutations
**[[BRAF (gene)|''BRAF'' V600E]] [[mutations]]
** Other rare mutations or fusions
** Other rare [[mutations]] or fusions
**No identified abnormality
**No identified [[Abnormality (behavior)|abnormality]]


|GIST cells basically arise from interstitial cells of Cajal (ICCs) and appear as follows on histology:
|[[GIST]] [[cells]] basically arise from [[Interstitial cells of Cajal|interstitial cells of Cajal (ICCs)]] and appear as follows on [[histology]]:
* Spindle cells (60%-80%):
* [[Spindle cells]] (60%-80%):
** Fascicular or whorled like appearance
** [[Fascicular block|Fascicular]] or whorled like [[appearance]]
** Multiple compact cells with minimal stroma
** Multiple compact [[Cells (biology)|cells]] with minimal [[stroma]]
** Eosinophilic, basophilic or amphophilic cytoplasm
** [[Eosinophilic]], [[basophilic]] or amphophilic [[cytoplasm]]
* Epithelioid cells (20%-30%)
* [[Epithelioid cell|Epithelioid cells]] (20%-30%)
** Clearly defined with an abundant amphophilic[[cytoplasm]]  
** Clearly defined with an abundant amphophilic[[cytoplasm]]  
* Pleomorphic/mixed cells (occasionally, 10%)
* [[Pleomorphic]]/mixed [[Cells (biology)|cells]] (occasionally, 10%)
** Both spindle or epitheloid cells
** Both [[Spindle cells|spindle]] or epitheloid [[Cells (biology)|cells]]
|Positive for:
|Positive for:
* [[CD117]] (overexpression of the receptor tyrosine kinase KIT is the most prominent diagnostic test)
* [[CD117]] ([[overexpression]] of the [[receptor tyrosine kinase]] KIT is the most prominent [[diagnostic test]])
* CD34
* [[CD34]]
* DOG-1
* DOG-1
* PKC-theta (protein kinase C theta)  
* [[Protein kinase C|PKC-theta (protein kinase C theta)]]
Consistently negative for:
Consistently negative for:
* Beta-catenin
* [[Beta-catenin]]
|
|
* Malignant potential (esophageal and colonal GIST)
* [[Malignant]] [[potential]] ([[esophageal]] and [[Colon (anatomy)|colonal]] [[GIST]])
* Metastasis (to liver, lungs, bones, subcutis, spleen)  
* [[Metastasis]] (to [[liver]], [[lungs]], [[bones]], [[subcutis]], [[spleen]])  
|
|
* Age group of 50-80years
* Age group of 50-80years
* Primary familial GIST syndrome
* Primary [[familial]] [[Gastrointestinal stromal tumor|GIST]] [[syndrome]]
* Neurofibromatosis type 1 (NF1)
* [[Neurofibromatosis type 1]] ([[NF1]])
* Carney-Stratakis syndrome (dyad of GISTs and paragangliomas)
* Carney-Stratakis [[syndrome]] (dyad of [[Gastrointestinal stromal tumor|GISTs]] and [[paragangliomas]])
* Carney triad (GIST, paraganglioma, and pulmonary chondromas)
* Carney triad ([[GIST]], [[paraganglioma]], and [[pulmonary]] [[chondromas]])
* [[Urticaria pigmentosa]]
* [[Urticaria pigmentosa]]
|Can involve any part of GIT:
|Can involve any part of [[Gastrointestinal tract|GIT]]:
* Stomach (most common)
* [[Stomach]] (most common)
* Duodenum
* [[Duodenum]]
* Omentum
* [[Omentum]]
* Mesentery
* [[Mesentery]]
* Esophagus
* [[Esophagus]]
* Colon
* [[Colon]]
* Peritoneum
* [[Peritoneum]]
|Depending on tumor size and localization in GIT:
|Depending on [[tumor]] size and localization in [[Gastrointestinal tract|GIT]]:
* Pain
* [[Pain]]
* Nausea
* [[Nausea]]
* Vomiting
* [[Vomiting]]
* Bleeding
* [[Bleeding]]
* Obstruction
* [[Obstruction]]
* Anemia
* [[Anemia]]
* Melena
* [[Melena]]
* Abdominal distension
* [[Abdominal distension]]
* Abdominal perforation
* [[Abdominal]] [[perforation]]
* [[Peritonitis]]
* [[Peritonitis]]
* [[Volvulus]]
* [[Volvulus]]
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**[[Small bowel obstruction|Small-bowel obstruction]]
**[[Small bowel obstruction|Small-bowel obstruction]]
**[[Deep vein thrombosis|Deep venous thrombosis]]
**[[Deep vein thrombosis|Deep venous thrombosis]]
|
|_
|-
|-
|'''[[Inflammatory]] myofibroblastic [[tumor]] (IMT)'''<ref name="pmid7611533">{{cite journal| author=Coffin CM, Watterson J, Priest JR, Dehner LP| title=Extrapulmonary inflammatory myofibroblastic tumor (inflammatory pseudotumor). A clinicopathologic and immunohistochemical study of 84 cases. | journal=Am J Surg Pathol | year= 1995 | volume= 19 | issue= 8 | pages= 859-72 | pmid=7611533 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7611533  }} </ref><ref name="pmid8635024">{{cite journal| author=Wenig BM, Devaney K, Bisceglia M| title=Inflammatory myofibroblastic tumor of the larynx. A clinicopathologic study of eight cases simulating a malignant spindle cell neoplasm. | journal=Cancer | year= 1995 | volume= 76 | issue= 11 | pages= 2217-29 | pmid=8635024 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8635024  }} </ref><ref name="pmid8847061">{{cite journal| author=Ramachandra S, Hollowood K, Bisceglia M, Fletcher CD| title=Inflammatory pseudotumour of soft tissues: a clinicopathological and immunohistochemical analysis of 18 cases. | journal=Histopathology | year= 1995 | volume= 27 | issue= 4 | pages= 313-23 | pmid=8847061 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8847061  }} </ref><ref name="pmid12673560">{{cite journal| author=Häusler M, Schaade L, Ramaekers VT, Doenges M, Heimann G, Sellhaus B| title=Inflammatory pseudotumors of the central nervous system: report of 3 cases and a literature review. | journal=Hum Pathol | year= 2003 | volume= 34 | issue= 3 | pages= 253-62 | pmid=12673560 | doi=10.1053/hupa.2003.35 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12673560  }} </ref><ref name="pmid16160478">{{cite journal| author=Rabban JT, Zaloudek CJ, Shekitka KM, Tavassoli FA| title=Inflammatory myofibroblastic tumor of the uterus: a clinicopathologic study of 6 cases emphasizing distinction from aggressive mesenchymal tumors. | journal=Am J Surg Pathol | year= 2005 | volume= 29 | issue= 10 | pages= 1348-55 | pmid=16160478 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16160478  }} </ref><ref name="pmid16967468">{{cite journal| author=Kovach SJ, Fischer AC, Katzman PJ, Salloum RM, Ettinghausen SE, Madeb R et al.| title=Inflammatory myofibroblastic tumors. | journal=J Surg Oncol | year= 2006 | volume= 94 | issue= 5 | pages= 385-91 | pmid=16967468 | doi=10.1002/jso.20516 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16967468  }} </ref><ref name="pmid9606802">{{cite journal| author=Coffin CM, Dehner LP, Meis-Kindblom JM| title=Inflammatory myofibroblastic tumor, inflammatory fibrosarcoma, and related lesions: an historical review with differential diagnostic considerations. | journal=Semin Diagn Pathol | year= 1998 | volume= 15 | issue= 2 | pages= 102-10 | pmid=9606802 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9606802  }} </ref><ref name="pmid6336632">{{cite journal| author=Berardi RS, Lee SS, Chen HP, Stines GJ| title=Inflammatory pseudotumors of the lung. | journal=Surg Gynecol Obstet | year= 1983 | volume= 156 | issue= 1 | pages= 89-96 | pmid=6336632 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6336632  }} </ref><ref name="pmid8635024">{{cite journal| author=Wenig BM, Devaney K, Bisceglia M| title=Inflammatory myofibroblastic tumor of the larynx. A clinicopathologic study of eight cases simulating a malignant spindle cell neoplasm. | journal=Cancer | year= 1995 | volume= 76 | issue= 11 | pages= 2217-29 | pmid=8635024 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8635024  }} </ref><ref name="pmid16160478">{{cite journal| author=Rabban JT, Zaloudek CJ, Shekitka KM, Tavassoli FA| title=Inflammatory myofibroblastic tumor of the uterus: a clinicopathologic study of 6 cases emphasizing distinction from aggressive mesenchymal tumors. | journal=Am J Surg Pathol | year= 2005 | volume= 29 | issue= 10 | pages= 1348-55 | pmid=16160478 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16160478  }} </ref><ref name="pmid17414097">{{cite journal| author=Coffin CM, Hornick JL, Fletcher CD| title=Inflammatory myofibroblastic tumor: comparison of clinicopathologic, histologic, and immunohistochemical features including ALK expression in atypical and aggressive cases. | journal=Am J Surg Pathol | year= 2007 | volume= 31 | issue= 4 | pages= 509-20 | pmid=17414097 | doi=10.1097/01.pas.0000213393.57322.c7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17414097  }} </ref>
|'''[[Inflammatory]] myofibroblastic [[tumor]] (IMT)'''<ref name="pmid7611533">{{cite journal| author=Coffin CM, Watterson J, Priest JR, Dehner LP| title=Extrapulmonary inflammatory myofibroblastic tumor (inflammatory pseudotumor). A clinicopathologic and immunohistochemical study of 84 cases. | journal=Am J Surg Pathol | year= 1995 | volume= 19 | issue= 8 | pages= 859-72 | pmid=7611533 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7611533  }} </ref><ref name="pmid8635024">{{cite journal| author=Wenig BM, Devaney K, Bisceglia M| title=Inflammatory myofibroblastic tumor of the larynx. A clinicopathologic study of eight cases simulating a malignant spindle cell neoplasm. | journal=Cancer | year= 1995 | volume= 76 | issue= 11 | pages= 2217-29 | pmid=8635024 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8635024  }} </ref><ref name="pmid8847061">{{cite journal| author=Ramachandra S, Hollowood K, Bisceglia M, Fletcher CD| title=Inflammatory pseudotumour of soft tissues: a clinicopathological and immunohistochemical analysis of 18 cases. | journal=Histopathology | year= 1995 | volume= 27 | issue= 4 | pages= 313-23 | pmid=8847061 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8847061  }} </ref><ref name="pmid12673560">{{cite journal| author=Häusler M, Schaade L, Ramaekers VT, Doenges M, Heimann G, Sellhaus B| title=Inflammatory pseudotumors of the central nervous system: report of 3 cases and a literature review. | journal=Hum Pathol | year= 2003 | volume= 34 | issue= 3 | pages= 253-62 | pmid=12673560 | doi=10.1053/hupa.2003.35 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12673560  }} </ref><ref name="pmid16160478">{{cite journal| author=Rabban JT, Zaloudek CJ, Shekitka KM, Tavassoli FA| title=Inflammatory myofibroblastic tumor of the uterus: a clinicopathologic study of 6 cases emphasizing distinction from aggressive mesenchymal tumors. | journal=Am J Surg Pathol | year= 2005 | volume= 29 | issue= 10 | pages= 1348-55 | pmid=16160478 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16160478  }} </ref><ref name="pmid16967468">{{cite journal| author=Kovach SJ, Fischer AC, Katzman PJ, Salloum RM, Ettinghausen SE, Madeb R et al.| title=Inflammatory myofibroblastic tumors. | journal=J Surg Oncol | year= 2006 | volume= 94 | issue= 5 | pages= 385-91 | pmid=16967468 | doi=10.1002/jso.20516 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16967468  }} </ref><ref name="pmid9606802">{{cite journal| author=Coffin CM, Dehner LP, Meis-Kindblom JM| title=Inflammatory myofibroblastic tumor, inflammatory fibrosarcoma, and related lesions: an historical review with differential diagnostic considerations. | journal=Semin Diagn Pathol | year= 1998 | volume= 15 | issue= 2 | pages= 102-10 | pmid=9606802 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9606802  }} </ref><ref name="pmid6336632">{{cite journal| author=Berardi RS, Lee SS, Chen HP, Stines GJ| title=Inflammatory pseudotumors of the lung. | journal=Surg Gynecol Obstet | year= 1983 | volume= 156 | issue= 1 | pages= 89-96 | pmid=6336632 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6336632  }} </ref><ref name="pmid8635024">{{cite journal| author=Wenig BM, Devaney K, Bisceglia M| title=Inflammatory myofibroblastic tumor of the larynx. A clinicopathologic study of eight cases simulating a malignant spindle cell neoplasm. | journal=Cancer | year= 1995 | volume= 76 | issue= 11 | pages= 2217-29 | pmid=8635024 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8635024  }} </ref><ref name="pmid16160478">{{cite journal| author=Rabban JT, Zaloudek CJ, Shekitka KM, Tavassoli FA| title=Inflammatory myofibroblastic tumor of the uterus: a clinicopathologic study of 6 cases emphasizing distinction from aggressive mesenchymal tumors. | journal=Am J Surg Pathol | year= 2005 | volume= 29 | issue= 10 | pages= 1348-55 | pmid=16160478 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16160478  }} </ref><ref name="pmid17414097">{{cite journal| author=Coffin CM, Hornick JL, Fletcher CD| title=Inflammatory myofibroblastic tumor: comparison of clinicopathologic, histologic, and immunohistochemical features including ALK expression in atypical and aggressive cases. | journal=Am J Surg Pathol | year= 2007 | volume= 31 | issue= 4 | pages= 509-20 | pmid=17414097 | doi=10.1097/01.pas.0000213393.57322.c7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17414097  }} </ref>

Revision as of 17:21, 14 March 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]

Overview

Extra-abdominal desmoid tumor must be differentiated from fibrosarcoma, low-grade fibromyxoid sarcoma and Gardner fibroma. Intra-abdominal desmoid tumor must be differentiated from gastrointestinal stromal tumor (GIST), benign fibrous tumor/solitary fibrous tumor (SFT), inflammatory myofibroblastic tumor (IMT), sclerosing mesenteritis and retroperitoneal fibrosis. Furthermore, generally all desmoid tumors must be differentiated from acute hematoma, lymphoma, rhabdomyosarcoma, liposarcoma, leiomyosarcoma, neurofibroma, nodular fasciitis, hypertrophic scars,keloids and primitive neuroectodermal tumor.

Differentiating Desmoid tumor from other Diseases

Differentiating desmoid tumor from other diseases
Disease entity Etiology (Genetic or others) Histopathological findings Immunohistochemical staining Benign/Malignant Risk factors Common site of involvement Clinical manifestations Other associated features
Desmoid tumor Sporadic desmoids are associated with following mutations:

Familial desmoids/Hereditary desmoid disease is associated with:

Pediatric desmoids have following additional mutations involving:

Histologically, desmoid tumors consist of: Positive for:

Negative for:

Desmoids may be associated with following:
Fibrosarcoma/Fibroblastic sarcoma Strongly positive for:

Negative for:

Primary bone malignancy involving end of long bones:
Low-grade fibromyxoid sarcoma[4][5][9][10][11][12][13][14] Translocation:
  • t(7;18;16) or
  • t(7;16) (q34:p11)

Fusion gene:

Positive for:
  • MUC4 (highly specific and sensitive)

Occasionally positive for:

Negative for:

_
Majority occurring in subfascial location and rarely involving subcutis or dermis in following sites:
  • Painless, slow-growing well-circumscribed mass
  • Average size-5cm (ranges from 1-20cm)
_
Benign fibrous tumor/Solitary fibrous tumor (SFT) [15][16][17][18][19][20][21][22][23] Intra-chromosomal inversion at:

TERT promoter mutations responsible for:

Positive for:

In few cases, positive for:

Negative for:

_ Paraneoplastic syndromes associated with SFTs include:
Gardner fibroma/Gardner-associated fibroma (GAF)[24][25][6][26] Positive for: Any part of body:
Gastrointestinal stromal tumor (GIST)[27][28][29][30][31] Activating mutation of:

Pediatric GISTs (SDH-deficient) have mutations of one of the:

GIST as a part of Carney triad has following mutation:

Wild-type GISTs have following three molecular subtypes:

GIST cells basically arise from interstitial cells of Cajal (ICCs) and appear as follows on histology: Positive for:

Consistently negative for:

Can involve any part of GIT: Depending on tumor size and localization in GIT: _
Inflammatory myofibroblastic tumor (IMT)[32][33][34][35][36][37][38][39][33][36][7] Unknown underlying etiology, may be due to inflammatory reaction to:
  • Infection
  • Underlying low grade malignancy

Mutations such as:

  • ALK (anaplastic lymphoma kinase) gene mutations in the tyrosine kinase locus at band 2p23
  • Spindle to stellate-shaped cells
  • Spindle cells arranged in short fascicles with a focal storiform (whorled or cartwheel-like) architecture
  • Spindle cells show features of fibroblasts and myofibroblasts
  • Variably dense, chronic, mixed polymorphic infiltrate of mononuclear inflammatory (plasma cells and lymphocytes, histiocytes, neutrophils, and occasional eosinophils)
  • Histiocytes have multinucleated forms with finely vacuolated cytoplasmic lipid droplets
  • Plasma cells with cytoplasmic Russell bodies (globular cytoplasmic inclusions of immunoglobulin) and polyclonal pattern of light chain expression
  • Absent hyperchromasia and atypical mitoses
Positive for:
  • IG+ (plasma cells)
  • IL-1
  • IL-6
  • Smooth muscle actin
  • Desmin
  • Calponin
  • Activin-like kinase 1

Negative for:

  • Beta-catenin
  • Metastatic
  • Multiorgan disease in association with chronic persistent Eikenella corrodens infection
  • Epstein Barr virus infection
  • Human herpes virus (HHV)-8 infection (Kaposi's sarcoma, multicentric Castleman's disease)
  • Lungs
  • Gastrointestinal system
  • Pelvic region
    • Bladder
    • Uterus
  • Retroperitoneum
  • Skin
  • Bone (femur, temporal bone, jaw bone)
  • CNS
  • Soft tissues
  • Larynx
  • Heart (right ventricle is most commonly involved)
  • Pancreas (rarely)
  • Asymptomatic (70%)
  • Painless asymptomatic mass/lump/swelling
  • Pulmonary IMT presents as:
    • Chest pain
    • Cough
    • Dyspnea
    • Hemoptysis (recurrent)
    • Fever
    • Fatigue
    • Weight loss
    • Appetite loss
  • Bone IMT presents with:
    • Mild bone pain
    • Easy fractures
    • Headache
    • Dizziness
    • Numbness at tumor site
    • Bone marrow involvement in some cases
  • Heart IMT presents with:
    • Chest pain
    • Difficulty breathing
    • Palpitations
    • Fainting
    • Obstruction of blood flow in the heart (large tumors)
  • Bladder IMT presents with:
    • Painless hematuria
    • Chronic pelvic pain
    • Difficulty in urinating
    • Presence of burning sensation
  • CNS IMT presents with:
    • Presence of solitary or multiple tumors at various locations in the brain
    • Recurrent headaches
    • Headache
    • Nausea and vomiting
    • Blurred vision
    • Double vision
    • Drooping of the eyelid
    • Dizziness
    • Back pain (if spine involved)
    • Seizures
Also known as:
  • Pseudo-inflammatory tumors
  • Inflammatory pseudotumor
  • Plasma cell granuloma
  • Inflammatory pseudotumor
  • Fibrous histiocytoma
  • Fibroxanthoma
  • Xanthogranuloma
  • Inflammatory pseudosarcoma
  • Atypical fibromyxoid tumor
  • Atypical myfibroblastic tumor
Sclerosing mesenteritis[40][41][42][43][44][45][46][47][48][49][50][51][52]

[53][54][55][56][57][58][59][60]

Unknown exact etiology:
  • Encompasses a spectrum of idiopathic primary inflammatory and fibrotic processes affecting mesentery
Varying components of:
  • Inflammation, fibrosis, and fat necrosis
  • Adipocyte necrosis (mesenteric lipodystrophy)
  • Chronic inflammatory state (mesenteric panniculitis)
  • Fibrosis (sclerosing mesenteritis)
_
  • Non-neoplastic inflammatory and fibrotic disease
  • Abdominal surgery/trauma:
    • Cholecystectomy
    • Appendectomy
    • Hysterectomy
    • Colectomy
    • Pneumatic jackhammer
    • Occult ileal perforation
  • Autoimmunity:
    • Riedel thyroiditis
    • Primary sclerosing cholangitis
    • Retroperitoneal fibrosis
    • Orbital pseudotumor
    • Autoimmune hemolytic anemia
    • Minimal change nephropathy
    • Systemic lupus erythematosus
    • Relapsing polychondritis
    • Multifocal fibrosclerosis
    • Limited systemic sclerosis
    • Celiac-associated T-cell lymphoma
  • Paraneoplastic syndrome:
    • Non-Hodgkin lymphoma(most common)
    • Breast cancer
    • Carcinoid
    • Melanoma
    • Squamous carcinoma and adenocarcinoma of the lung
    • Renal carcinoma
    • Multiple myeloma
    • Hepatocellular carcinoma
    • Prostate adenocarcinoma
    • Ovarian carcinoma
    • Endometrial carcinoma
    • Cervical carcinoma
    • Angiosarcoma
    • Gastrointestinal adenocarcinomas
  • Ischemia and infection history:
    • Typhoid fever
    • Dysentery
    • Tuberculosis
    • Syphilis
    • Malaria
    • Influenza
    • Rheumatic fever
  • Mesentery
  • Asymptomatic
  • Abdominal pain
  • Nausea and vomiting
  • Altered bowel habits (Constipation or diarrhea)
  • Weight loss
  • Fever
  • Malaise
  • Abdominal tenderness
  • Abdominal distension
  • Peritoneal inflammation and ascites (usually chylous)
  • Pleural effusion
  • Protein-losing enteropathy (Fever, edema)
  • Biliary obstruction (hemolytic anemia, jaundice)
  • Bowel obstruction
  • Obstructive uropathy/renal failure
  • Chylous ascites
  • Chronic mesenteric ischemia
  • Anemia
  • Hypoalbuminemia
  • Mesenteric vascular occlusion (both arterial and venous)
Nomenclature used in the medical literature for idiopathic primary inflammatory and fibrotic processes of the mesentery is as follows:
  • Mesenteric lipodystrophy (predominant fat necrosis predominance)
  • Mesenteric fibrosis
  • Mesenteric panniculitis
  • Mesenteric lipodystrophy
  • Retractile mesenteritis
  • Mesenteric Weber-Christian disease
  • Xanthogranulomatous mesenteritis
  • Mesenteric lipogranuloma
  • Liposclerotic mesenteritis
  • Inflammatory pseudotumor
  • Isolated lipodystrophy
  • Retroperitoneal xanthogranuloma
Retroperitoneal fibrosis[61][62][63][64][65][66][67][68][69][70][71][72][73]

Idiopathic (70%) [Ormond's disease] is an immune-mediated disease caused by:

  • Other autoimmune diseases
  • Immunoglobulin G4-related disease (IgG4-RD)
  • Chronic periaortitis
  • Allele HLA‑DRB1*03, D32 polymorphism of the gene encoding CCR5 (chemokine receptor)
  • TTCCAT haplotype of the gene encoding CCL11/eotaxin‑1 (drives the recruitment of eosinophils)

Secondary to:

Fibro-inflammatory disease histologically hallmarked by fibrous tissue and chronic inflammation:
  • Fibrous tissue composed of extracellular matrix containing type I collagen fibers organized in thick irregular bundles, often encircling small retroperitoneal vessels
  • Fibroblasts:
    • Show signs of activation and transition into myofibroblasts (α‑smooth muscle actin expression)
    • Are major source of collagen production
    • Rarely show mitoses, undergo clonal proliferation
  • Inflammatory infiltrate consists of numerous lymphocytes, plasma cells, and macrophages
  • Inflammatory cells maybe:
    • Interspersed within the collagen bundles (“diffuse” pattern) or
    • Organized in nodular aggregates, usually around small vessels, having a B cell core surrounded by CD4+ T cells
  • When IgG4+/total IgG+ plasma cell ratio is >40%, RPF is classified as “IgG4-related” if other features such as storiform fibrosis, eosinophil infiltration, and obliterative phlebitis are also present
  • Tryptase positive (mast cells)
  • Benign immune mediated inflammatory process
  • Idiopathic [Ormond's disease]
  • Secondary to certain drugs (ergot-derivatives, methysergide, bromocriptine, beta blockers, methyldopa, hydralazine, analgesics)
  • Biological agents (etanercept, infliximab)
  • Underlying malignancy (carcinoid, Hodgkin and non-Hodgkin lymphoma, sarcomas, colorectal, breast, prostate and bladder carcinoma)
  • Infections (tuberculosis, histoplasmosis, actinomycosis)
  • Radiation therapy for testicular seminoma, colon and pancreatic cancer
  • Retroperitoneal hemorrhage
  • Surgery (lymphadenectomy, colectomy, aortic aneurysmectomy)
  • Secondary (AA) amyloidosis
  • Trauma
  • Barium enema
  • Mesenteric panniculitis
  • Different forms of histiocytosis particularly Erdheim-Chester disease
  • Exposure to asbestos
  • Tobacco smoke exposure
  • Thoracic aorta
  • Mesenteric arteries
  • Renal arteries and veins
  • Epiaortic arteries
  • Ureters
  • Abdominal organs
  • Pancreas
  • Salivary glands
  • Lymph nodes
  • Pituitary gland
  • Pain in the lower back, abdomen, or flank (most common presentation, bilateral or unilateral flank pain that radiates to the inguinal region, or acute onset pain similar to renal colic)
  • Abdominal aortic aneurysms
  • Malaise
  • Anorexia
  • Weight loss
  • Fever
  • Nausea and vomiting
  • Testicular pain
  • Constipation
  • Venous compression (inferior vena cava) leading to:
    • Lower limb edema (lymphatic compression)
    • Inferior vena cava syndrome
    • Deep vein thrombosis
    • Pulmonary embolism
  • Arterial stenosis (rare) causing:
    • Upper-leg claudication
    • Mesenteric ischemia (mesenteric arteries compression)
    • Thoracic aorta and/or the epi-aortic arteries' compression
  • Recurrent laryngeal nerve paralysis causing hoarsness and dry cough
  • Acute kidney injury (AKI) (due to bilateral encasement of ureteral and renal involvement in peri-iliac retroperitoneal fibrosis)
  • Renal atrophy (due to previous transient unilateral obstruction or renal artery stenosis)
  • Obstructive uropathy
  • Gross hematuria
  • Urinary symptomes (urinary urgency,frequency, and dysuria)
  • Hypertension (due to renal artery impingement)
  • Obstruction of the inferior vena cava and/or iliac veins
  • Thrombophlebitis
  • Deep vein thrombosis
  • Varicocele
  • Hydrocele
Retroperitoneal fibrosis is also known as:
  • Ormond's disease
  • Periureteritis fibrosa
  • Periureteritis plastica
  • Chronic periureteritis
  • Sclerosing retroperitoneal granuloma
  • Fibrous retroperitonitis
Lymphoma
  • Diffuse large B cell lymphoma (DLBCL):
    • Rare MALT1 rearrangements, trisomy 18 in some, possible NFκB activation in minority
  • Extranodal marginal B cell lymphoma arising from mucosal associated lymphoid tissue (MALT lymphoma):
    • Clonal rearrangements of immunoglobulin genes
    • Often trisomy of 3, 12, 18
    • Usually negative for characteristic MALT1 rearrangements t(11;18)(q21;q21) and t(14;18)(q32;q21)
  • Follicular lymphoma:
    • Presence of t(14;18)(q32;q21) translocation has not been systematically assessed in primary breast follicular lymphoma
  • Burkitt lymphoma:
    • t(8;14)(q24;q32) c-Myc and IgH translocation is most frequent
    • t(2;8)(p12;q24) IgΚ and c-Myc
    • t(8;22)(q24;q11) c-Myc and Igλ
Diffuse large B cell lymphoma (DLBCL):
  • Diffuse infiltration by large lymphoid cells, centroblastic > immunoblastic, activated B cell type > germinal center type

Extranodal marginal B cell lymphoma:

  • Vaguely nodular growth pattern, neoplastic cells occupy the marginal zone surrounding the B cell follicle mantle zone but can have diffuse growth pattern if follicles infiltrated / replaced
  • Marginal zone B cells, variable plasma cells, reactive follicles (±)
  • Monocytoid-like cells
  • Plasmacytic differentiation
  • Low mitotic rate

Follicular lymphoma:

  • Follicular and diffuse architectural patterns
  • Monotonous population of small cleaved cells (centrocytes)
  • Variable numbers of centroblasts (large noncleaved cells)
  • Associated sclerosis can cause single file infiltration pattern

Burkitt lymphoma:

  • Sheets of uniform medium sized lymphocytes with round nuclei, multiple basophilic nucleoli, course chromatin, scant to moderate basophilic cytoplasm, minimal intervening stroma
  • High mitotic rate
  • Tingible body macrophages containing apoptotic debris produce a "starry sky" appearance
  • Mantle cell lymphoma:
  • Small to medium sized, slightly irregular cells with scant cytoplasm
  • Classic Hodgkin lymphoma:
  • Reed-Sternberg cells and variants in a reactive background
  • Nodular lymphocyte predominant Hodgkin lymphoma:
  • Vague nodules of small B cells and interspersed large tumor cells (LP cells) with thin nuclear membranes, fine chromatin and variable nucleoli
  • MALT lymphoma:
    • Infiltration of thyroid epithelium creates lymphoepithelial lesions (lymphocytes "stuff" glandular lumina)
    • May have background lymphocytic thyroiditis
Positive for:
  • Diffuse large B cell lymphoma (DLBCL):
    • CD45, CD20, CD79a, PAX5, BCL2, Ki67 (high)
    • Activated B cell type (CD10-, BCL6- or CD10-, BCL6+, MUM1 / IRF+) is more common
    • Germinal center type (CD10+, BCL6+ or CD10-, BCL6+, MUM1 / IRF-)
    • Surface Ig+
    • CD43±
  • Extranodal marginal B cell lymphoma arising from mucosal associated lymphoid tissue (MALT lymphoma):
    • Surface and cytoplasmic Ig+ (IgM > IgG or IgA)
    • CD45, CD20, CD79a, PAX5, variable CD43, variable BCL2, Ki67 (low)
    • Variable monotypic cytoplasmic immunoglobulin seen in cases with plasmacytic differentiation
    • CD21 and CD23 highlight expanded / disrupted follicular dendritic meshworks
    • CD43±
  • Follicular lymphoma:
    • Surface Ig+
    • CD45, CD20, CD79a, CD10, BCL6, BCL2
    • CD21 and CD23 highlight follicular dendritic cell meshworks
  • Burkitt lymphoma:
    • Surface IgM+
    • CD45, CD20, CD79a, PAX5, CD10, BCL6, Ki67 (~100%)
  • Mantle cell lymphoma:
    • Surface IgMD+, CD20+, CD5+, CD10-, CD43+, cyclin D1+
  • Classic Hodgkin lymphoma:
    • R-S cells: CD30+, CD15±, PAX5+
  • Nodular lymphocyte predominant Hodgkin lymphoma:
    • LP cells: CD45+, CD20+
  • Thyroid MALT lymphoma:
    • CD20
    • Keratin
    • Thyroglobulin
    • CD45
  • Anaplastic large T cell lymphoma:
    • CD3, CD10, CD30, CD43, CD99, TdT
  • PreT lymphoblastic lymphoma:
    • CD3, CD10, CD99, TdT

Negative for:

  • Diffuse large B cell lymphoma (DLBCL):
    • EBER
  • Extranodal marginal B cell lymphoma, MALT type:
    • CD5, CD10, CD23, BCL6, cyclin D1
  • Follicular lymphoma:
    • CD5, CD23, cyclin D1
  • Burkitt lymphoma:
    • CD5, CD23, TdT, BCL2
  • Mantle cell lymphoma:
    • CD10-
  • Classic Hodgkin lymphoma:
    • R-S cells: ALK-, CD45-, CD3-
  • Nodular lymphocyte predominant Hodgkin lymphoma:
    • LP cells: CD15-, CD30-
  • Anaplastic large T cell lymphoma:
    • ALK1, bcl6
  • PreT lymphoblastic lymphoma:
    • Bcl6-
  • Malignant
  • MALT lymphoma (Extranodal marginal B cell lymphoma may arise from it)
  • Underlying autoimmune disease
  • EBV (endemic and sporadic Burkitt lymphoma)
  • HIV (immunodeficiency associated Burkitt lymphoma)
  • HHV8
  • Chronic hepatitis C infection
  • Transplants
  • Chemotherapy
Anywhere in body
  • Lymph nodes
  • Esophagus
  • Bladder
  • Bone
  • Oral cavity
  • Thyroid gland
  • Painless palpable mass, with or without ipsilateral lymphadenopathy
  • Fever
  • Night sweats
  • Weight loss
  • Neck mass
  • Dysphagia
  • Odynophagia
  • Chest / abdominal pain
  • Weight loss
  • Hemorrhage
  • Vocal cord paralysis / hoarseness
  • Stricture / obstruction
  • Perforation with esophagomediastinal or esophagotracheobronchial fistula or mediastinitis
  • Vocal cord paralysis
  • Cold nodule
WHO classification of lymphoma:
  • Hodgkin lymphomas arise from precursor B cells (Reed-Sternberg cells)
    • Classic Hodgkin lymphoma (CHL) - 95% is further subclassified as:
      • Nodular sclerosis
      • Lymphocyte rich
      • Mixed cellularity
      • Lymphocyte depleted
    • Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) - 5%
  • Non-Hodgkin lymphomas arise from monoclonal expansion of malignant B or T cells
    • B cell lymphomas
      • B cell acute lymphoblastic lymphoma (ALL)
      • Chronic lymphocytic lymphoma / small lymphocytic leukemia (CLL / SLL)
      • Mantle cell lymphoma
      • Follicular lymphoma
      • Marginal zone B cell lymphoma
      • Extranodal MALT type
      • Hairy cell leukemia
      • Plasmacytoma / plasma cell myeloma
      • Diffuse large B cell lymphoma (DLBCL)
      • Burkitt lymphoma
    • T / NK cell lymphomas
      • T cell acute lymphoblastic lymphoma (ALL)
      • T cell CLL
      • Mycosis fungoides / Sézary syndrome
      • Peripheral T cell lymphoma
      • Angioimmunoblastic T cell lymphoma
      • Enteropathy associated intestinal T cell lymphoma
      • Hepatosplenic T cell lymphoma
      • Anaplastic large cell lymphoma (ALCL)
      • Extranodal NK / T cell lymphoma, nasal type
Rhabdomyosarcoma (RMS)[74][75][76][77][78][79][80][81][82][83]
  • MyoD1 and PIK3CA mutation (sclerosing and spindle cell RMS)
  • Most common translocation is t(2;13)(q35;q14), causingPAX3'FOXO1 gene fusion (alveolar RMS)
  • t(1;13)(p36;q14), causingPAX7'FOXO1 gene fusion
  • Embryonal RMS is associated with:
    • Loss of heterozygosity (LOH) at 11p15 locus (site of IGF-2 gene)
    • Other genes at 11p15.5 locus:
      • H19
      • CDKN1C
      • HOTS
  • Other mutations include pRb, TP53, GLI, CDKN2A, CDKN2B, RAS, FGFR4, PIK3CA, CTNNB1 [beta-catenin] and NF1 genes
  • VGLL2andNCOA2rearrangements
  • Gene fusions include VGLL2-CITED2, VGLL2-NC0A2, TEAD1-NCOA2, PAX3-NCOA2, PAX3-NCOA2, and SRF-NCOA2.
  • Further gene mutations include:
    • RAS
    • RB1
    • PTCH
    • MDM2
    • CDK4
    • MYCN
    • Basic helix-loop-helix [bHLH]
Histologic classification:
  • Embryonal RMS comprises of:
    • Rhabdomyoblasts arranged in sheets and large nests, with infrequent intermixed fusiform cells
    • Myofilaments with cross-striations
  • Botryoid (sarcoma botryoides) and spindle cell (leiomyomatous) RMS:
    • "Grape-like" gross appearance of the tumor
    • Polypoid mass grows beneath an epithelial surface, with dense subepithelial aggregates of rhabdomyoblasts (the so-called "cambrium" layer)
  • Sclerosing and spindle cell RMS
  • Alveolar RMS comprises of:
    • Fibrovascular septae lined with densely packed ovoid to round tumor cells separated by pseudo-alveolar spaces (vaguely resemble pulmonary alveoli)
    • "Loosely adherent" rhabdomyoblasts shed into these pseudo-alveolar spaces
  • Anaplastic RMS comprises of:
    • Large hyperchromatic nuclei with atypical bizarre mitotic figures
    • Nuclear size is threefold larger than that of adjacent "typical" tumor cells
Positive for:
  • Actin
  • Myosin
  • Desmin
  • Myoglobin
  • Z-band protein
  • Myogenic differentiation 1 (MyoD1)

Maybe positive for:

  • Cytokeratin
  • Synaptophysin
  • Neuron-specific enolase
  • S-100 protein
  • Malignant soft tissue tumor
  • Metastatic
  • In utero radiation exposure
  • Accelerated in utero growth
  • Low socioeconomic status
  • Antibiotics receival soon after birth
  • Recreational drugs usage during pregnancy
  • Neurofibromatosis
  • Li-Fraumeni syndrome
  • Beckwith-Wiedemann syndrome
  • Costello syndrome
  • Head and neck (orbit, parameningeal sites including middle ear, nasal cavity, paranasal sinuses, nasopharynx, infratemporal fossa, scalp, parotid gland, oral cavity, pharynx, thyroid and parathyroid glands)
  • Genitourinary tract (bladder, prostate, or the male or female genital tracts)
  • Sarcoma botryoides (urinary bladder wall, vagina, nasopharynx)
  • Extremity
  • Trunk
  • Chest wall
  • Perineal-perianal region
  • Biliary tract
  • Liver
  • Brain
  • Trachea
  • Heart
  • Breast
  • Ovary
  • Proptosis
  • Ophthalmoplegia
  • Nasal, aural, or sinus obstruction with or without a mucopurulent or sanguineous discharge
  • Localized, painless enlarging mass
  • Hematuria
  • Large pelvic mass
  • Urinary obstruction
  • Urinary frequency
  • Constipation
  • Mucosanguineous vaginal discharge
  • Polypoid mass protruding from vagina
  • Scrotal or inguinal enlargement (paratesticular tumors)
Histology of RMS similar to that of other childhood small round blue cell tumors involving bone and soft tissue such as:
  • Lymphoma
  • Small cell osteosarcoma
  • Mesenchymal chondrosarcoma
  • Ewing sarcoma family of tumors (EFT)
Liposarcoma[84][85][86][87][88][89][90][91][92][93] Atypical lipomatous tumor/well differentiated liposarcoma and dedifferentiated liposarcoma are associated with:
  • Presence of a large/giant marker chromosome and/or ring chromosomes at 12q13-15 region
  • Amplification of this chromosome region rich in protooncogenes, including CHOP, CDK4, MDM2, HMGI-C, GLI, SAS, OS1, HMGA2 and OS9

Myxoid liposarcoma is associated with:

  • t(12:16)(q13;p11) - CHOP(DDIT3) / FUS or t(12;22)(q13;q22) - CHOP(DDIT3) / EWS

Pleomorphic liposarcoma is associated with:

  • Complex karyotypic aberrations
Well-differentiated liposarcoma:
  • Sclerosing liposarcoma (distinctive stromal cells distributed across the tissue, associated with lipoblasts filled with multiple vacuoles, and collagenous background of fibrillary appearance)
  • Adipocytic liposarcoma (adipocytes with different cell sizes, hyperchromasia, and nuclear atypia. Fibrous septa containing hyperchromatic stromal cellssurrounding adipocytes)
  • Inflammatory liposarcoma (heavy chronic inflammatory infiltrate composed of different lympho-plasmacytic aggregates)
  • Spindle cell lipocarcinoma (proliferation of neural-like spindle cells organized in a fibrous structure containing lipoblasts)

De-differentiated liposarcoma:

  • Myxoid liposarcoma ( non-homogenous appearance with cystic and solid components)
  • Round Cell liposarcoma ( small, round, or spindle cells with sparse eosinophilic and granular cytoplasm and large nuclei,scattered lipoblasts and areas of necrosis)
  • Pleiomorphic liposarcoma (pleomorphic cells with enlarged round to bizarre nuclei)
Atypical lipomatous tumor/well differentiated liposarcoma is positive for:
  • MDM2
  • CDK4
  • p16
  • S100 (stains adipocytes and lipoblasts)
  • Round cell liposarcoma metstasizes to retroperitoneum, pleural cavity, soft tissue, or pelvis and lungs (poor prognosis)
  • Retroperitoneum
  • Esophagus
  • Bowel
  • Mediastinum
_
Leiomyosarcoma[94][95][96][97][98][99][100][101][102] Positive for:
  • HHF35 (90%)
  • Alpha-smooth muscle actin (90%)
  • Vimentin
  • Desmin (75%)
  • H-caldesmon
  • PTAH (stains myofibrils)
  • Keratin (30%)
  • ER (usually in uterine and female retroperitoneal tumors)
  • S100 (occasionally weak staining)
  • EMA (may be focal)
  • CD34

Negative for:

  • CD117
  • Uterus
  • Abdomen
  • Esophagus
  • Rectum
  • Skin / subcutis
  • Retroperitoneum
  • Extremities
  • Large vessels (inferior vena cava, saphenous vein, femoral vein, pulmonary artery, femoral artery)
  • Superficial or deep soft tissues
  • Bone
  • Breast
  • Colon
  • Epididymis
  • Mediastinum
  • Lungs
_
Neurofibroma[103][104][105][106][107][108][109][106][110][111][112] Can be sporadic or as a part of Neurofibromatosis 1 and 2
  • NF1 gene located at chromosomal region 17q11.2, codes for neurofibromin
  • Functional part of neurofibromin GAP (or GTPase-activating protein) accelerates the conversion of the active GTP-bound RAS to its inactive GDP-bound form
  • Loss of RAS control leads to increased activity of other signaling pathways including RAF, ERK1/2, PI3K, PAK, MAPK, SCF/c-kit and mTOR-S6 kinase
  • Made of nerve fibers, schwann cells (cells that cover the nerve fibers), blood vessels, inflammatory white blood cells (mast cells), and connective tissue (fibroblasts and loose material called extra cellular matrix)
Positive for:
  • S100
  • CD34 (focal)
  • Factor XIIIa (focal)

Negative for:

  • EMA (except in plexiform neurofibromas)
  • Cutaneous neurofibromas are always benign
  • Diffuse neurofibromas can become malignant
  • Neurofibromatosis 1
  • Neurofibromatosis 2 (multiple neurofibromas, meningiomas of the brain or spinal cord, and ependymomas of the spinal cord)
  • Anywhere in body
  • Scalp (diffuse neurofibroma)
  • Soft masses/bumps on or under skin (internal or superficial)
  • Transient itching (mast cells release histamine)
  • Transient pain
  • Numbness and tingling in the affected area
  • Severe bleeding (sign of tumor growth)
  • Physical disfiguration
  • Cognitive disability
  • Stinging
  • Neurological deficits
  • Changes in movement (clumsiness in the hands, trouble walking
  • Changes in bowel or bladder function (a sense of urgency when urinating, bowel or bladder incontinence)
  • Scoliosis (an abnormal curvature of the spine, if the tumor creates muscular imbalance or erodes bones of the spine)
Types of neurofibromas in NF1:
  • Diffuse neurofibromas
  • Cutaneous or Dermal neurofibromas
  • Intramuscular neurofibromas
  • Plexiform neurofibromas
  • Intraneural
Nodular fasciitis[113][114][115][116][117][118][119][120][121][122]
  • Balanced translocation t(17;22)(p13;q13) resulting in MYH9-USP6 gene fusion
  • Histologically vast array of patterns
  • Fibroblasts, spindle-shaped cells found in connective tissue
  • Myofibroblasts, large cells with an appearance between fibroblasts and smooth muscle tissue
  • Sub-membranous "tram track" pattern characteristic of myofibroblasts on immunostaining
  • Short C or S-shaped fascicles or cartwheel formations
  • Feathery appearance cells, with holes or tears in the tissue
  • Visible chromosomes in cells during cell division
  • Fine, pale, and even-looking chromatin
  • Inflammation, accelerated mitotic index with normal mitoses
  • Non-pleomorphic cells with high rate of mitosis
  • Essentially spindle cell proliferation
  • Stroma is rich in collagen and/or myxoid ground substance
Positive for:
  • Smooth muscle actin
  • Muscle specific actin
  • Vimentin
  • Calponin
  • CD68

Negative for:

  • S100
  • Desmin
  • Keratin
  • CD34
  • Caldesmon
  • ALK
  • p53
  • Benign
  • Reparative process secondary to trauma
  • Anywhere in body
  • Arms (34%)
  • Flexor forearm (27%)
  • Head and neck region (24%)
  • Trunk (chest, back) (21%)
  • Thigh (17%)
  • Legs (14%)
  • Upper arm (12%)
  • Hands (rarely)
  • Bladder
  • Breast
  • Cervix
  • Intra-articular
  • Prostate
  • Vagina
  • Vulva
  • Solitary firm non-painful mass
  • Oval or round in shape with irregular margins
  • Tender (maybe)
Also known as:
  • Nodular pseudosarcomatous fasciits
  • Subcutaneous pseudosarcomatous fibromatosis
  • Pseudosarcomatous fasciitis
Hypertrophic scars
  • Overexpression of growth factors such as:
  • TGF-beta
  • VEGF
  • CTGF
  • Decreased production of matrix metalloproteinases
  • Increased numbers of PDGF receptors on fibroblasts
  • Over-activation of signals for insulin-like growth factor-1
  • Decreased fibroblast apoptosis rate
  • Increased expression of thymic stromal lymphopoietin
  • Increased fibrocyte activation via stromal cell-derived factor-1
  • Genes in four susceptibility loci on chromosomes 1q41, 3q22.3-23, and 15q21.3
  • Excess collagen formation with varying numbers of fibroblasts and myofibroblasts
  • Collagen fibers are arranged in a wavy pattern predominantly oriented parallel to the epithelial surface
  • Nodular structures containing myofibroblasts and vertically aligned vessels
_
  • Benign
  • Frequent complication of burn injuries
  • Piercings
  • Cuts
  • Surgical wounds
  • Lacerations

Adverse wound healing factors at the injury site such as:

  • Infection (acne, folliculitis, chicken pox, and vaccinations)
  • Excessive tension
  • Milder than keloids
  • Don’t grow beyond the boundaries of the original skin injury
  • Cosmetic disfigurement
  • Pruritis
  • Pain
  • Functional impairment (from contracture or mechanical irritation)
  • Loss of temperature regulation
  • Dry skin
  • Neuropathic pain
Hypertrophic scars can be classified as:
  • Mature scar
  • Immature scar
  • Linear, hypertrophic scar (surgical/traumatic)
  • Widespread, hypertrophied scar (burn)
Keloids[123][124][125][126]
  • Epigenetic alteration in fibroblast DNA and acetylation of histone proteins
  • Overexpression of growth factors such as:
    • TGF-beta
    • VEGF
    • CTGF
  • Decreased production of matrix metalloproteinases
  • Increased numbers of PDGF receptors on fibroblasts
  • Over-activation of signals for insulin-like growth factor-1
  • Decreased fibroblast apoptosis rate
  • Increased expression of thymic stromal lymphopoietin
  • Increased fibrocyte activation via stromal cell-derived factor-1
  • Genes in following susceptibility loci on chromosomes:
    • 1q41
    • 3q22.3-23
    • 15q21.3
    • 2q23
    • 7p11
    • 10q23.31
  • In Japanese population, 4 SNP loci (rs873549, rs1511412, rs940187, and rs8032158) in 3 chromosomal regions (1q41, 3q22.3–23, and 15q21.3) exhibit significant associations with keloids
  • Hyalinized collagen bundles
  • Excess collagen formation with varying numbers of fibroblasts and myofibroblasts
  • Hypocellular zones of fibrous tissue containing thickened, glassy, eosinophilic collagen bundles
_
  • Benign
  • Minor injuries
  • Insect bites
  • Pimples
  • Earlobe piercings

Adverse wound healing factors at the injury site such as:

  • Infection
  • Inflammation
  • Excessive tension
  • Excessive motion (such as in injuries over a joint),
  • Wound left to heal without stitches

Keloids may be associated with rare inherited syndromes such as:

  • Rubinstein-Taybi syndrome
  • Goeminne syndrome
  • Any part of body having injury
  • Upper chest
  • Shoulders
  • Upper back
  • Head and neck (especially on ears)
  • Cosmetic disfigurement
  • Raised, reddish nodules
  • Skin pigmentation
  • Itchiness
  • Redness
  • Unusual sensations
  • Pain
  • Functional impairment
  • Keloid is Greek for "crab claw"
  • Extend beyond the borders of the original wound
  • Regress spontaneously
  • Recur after excision
  • Darkly pigmented people/African-American, Asians (Han Chinese, Japanese) are more prone to form keloids

Keloids can be prevented by using:

  • Pressure dressing
  • Silicone gel pad
  • Paper tape over the injury site for 23-24hours per day

Keloids can be classified as:

  • Minor keloid
  • Major keloid
Primitive neuroectodermal tumor (PNET)[127][128][129]
  • EWS / FLI1 fusion product by RT-PCR due to t(11;22)(q24/q22;q12) (90%)
  • p53 tumor suppressor gene mutations
  • Small blue cell tumor
  • Round hyperchromatic cells
  • Abundant mitotic figures
  • Homer Wright rosettes
  • Fibrosis
  • Neurosecretory granules on electron microscopy
Positive for:
  • CD99
  • FLI1
  • PAS+ diastase sensitive (glycogen)
  • Vimentin
  • Neuron specific enolase

Negative for:

  • Cytokeratin (usually)
  • Desmin
  • WT1
  • GFAP
  • PAX2
  • Malignant neural crest tumor
  • Highly aggressive (rapid death within 1 year)
  • Metastases to lung, pleura, bone and liver
  • CNS PNET: Intracranial (cerebral hemisphere)
  • Peripheral PNET: kidneys
Also known as:
  • CNS PNET
  • Askin tumor
  • Peripheral neuroepithelioma
  • Ependymoblastoma

WHO classified PNET into 3 subtypes:

  • Central primitive neuroectodermal tumors (PNETs)
  • Neuroblastomas
  • Peripheral primitive neuroectodermal tumors (pPNETs)

Peripheral PNET (pPNET) is now thought to be virtually identical to Ewing sarcoma

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