Sacrococcygeal teratoma pathophysiology: Difference between revisions

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==Overview==
==Overview==
==Pathogenesis==
==Pathogenesis==
Sacrococcygeal teratomas arise from the primitive knot or Hensen"s node, which is the primary organizers of embryonic development.
==Genetics==
==Genetics==
Development of Sacrococcygeal teratoma is associated with gain of gain of chromosomes 1q32-qter regions and losses of the 6q24-qter and 18q21-qter regions.<ref name = "aa">{{cite journal |vauthors=Harms D, Zahn S, Göbel U, Schneider DT |title=Pathology and molecular biology of teratomas in childhood and adolescence |journal=Klin Padiatr |volume=218 |issue=6 |pages=296–302 |year=2006 |pmid=17080330 |doi=10.1055/s-2006-942271 |url=}}</ref><ref name = "aaa">{{cite journal |vauthors=Veltman I, Veltman J, Janssen I, Hulsbergen-van de Kaa C, Oosterhuis W, Schneider D, Stoop H, Gillis A, Zahn S, Looijenga L, Göbel U, van Kessel AG |title=Identification of recurrent chromosomal aberrations in germ cell tumors of neonates and infants using genomewide array-based comparative genomic hybridization |journal=Genes Chromosomes Cancer |volume=43 |issue=4 |pages=367–76 |year=2005 |pmid=15880464 |doi=10.1002/gcc.20208 |url=}}</ref>
Development of Sacrococcygeal teratoma is associated with gain of gain of chromosomes 1q32-qter regions and losses of the 6q24-qter and 18q21-qter regions.<ref name = "aa">{{cite journal |vauthors=Harms D, Zahn S, Göbel U, Schneider DT |title=Pathology and molecular biology of teratomas in childhood and adolescence |journal=Klin Padiatr |volume=218 |issue=6 |pages=296–302 |year=2006 |pmid=17080330 |doi=10.1055/s-2006-942271 |url=}}</ref><ref name = "aaa">{{cite journal |vauthors=Veltman I, Veltman J, Janssen I, Hulsbergen-van de Kaa C, Oosterhuis W, Schneider D, Stoop H, Gillis A, Zahn S, Looijenga L, Göbel U, van Kessel AG |title=Identification of recurrent chromosomal aberrations in germ cell tumors of neonates and infants using genomewide array-based comparative genomic hybridization |journal=Genes Chromosomes Cancer |volume=43 |issue=4 |pages=367–76 |year=2005 |pmid=15880464 |doi=10.1002/gcc.20208 |url=}}</ref>

Revision as of 17:53, 25 November 2015

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

Overview

Pathogenesis

Sacrococcygeal teratomas arise from the primitive knot or Hensen"s node, which is the primary organizers of embryonic development.

Genetics

Development of Sacrococcygeal teratoma is associated with gain of gain of chromosomes 1q32-qter regions and losses of the 6q24-qter and 18q21-qter regions.[1][2]

Associated Conditions

Gross Pathology

Microscopic Pathology

  • Sacrococcygeal teratoma can be divided into three types depending on the microscopic pathology, as follow:
  • Mature teratoma:may consist of fully differentiated somatic tissue.[3]
  • Immature teratoma: may consist of small fraction of incompletely differentiated tissue.
  • Malignant teratoma:
  • Around 20% of Sacrococcygeal teratomas are malignant.
  • They have elevated tumor markers including yolk sac component secreting alpha fetoprotein or primitive neuroectodermal tumor (PNET).

References

  1. Harms D, Zahn S, Göbel U, Schneider DT (2006). "Pathology and molecular biology of teratomas in childhood and adolescence". Klin Padiatr. 218 (6): 296–302. doi:10.1055/s-2006-942271. PMID 17080330.
  2. Veltman I, Veltman J, Janssen I, Hulsbergen-van de Kaa C, Oosterhuis W, Schneider D, Stoop H, Gillis A, Zahn S, Looijenga L, Göbel U, van Kessel AG (2005). "Identification of recurrent chromosomal aberrations in germ cell tumors of neonates and infants using genomewide array-based comparative genomic hybridization". Genes Chromosomes Cancer. 43 (4): 367–76. doi:10.1002/gcc.20208. PMID 15880464.
  3. Calaminus G, Schneider DT, Bökkerink JP, Gadner H, Harms D, Willers R, Göbel U (2003). "Prognostic value of tumor size, metastases, extension into bone, and increased tumor marker in children with malignant sacrococcygeal germ cell tumors: a prospective evaluation of 71 patients treated in the German cooperative protocols Maligne Keimzelltumoren (MAKEI) 83/86 and MAKEI 89". J. Clin. Oncol. 21 (5): 781–6. PMID 12610174.

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