Recent advances in the molecular pathogenesis and targeted therapies of medullary thyroid carcinoma

Imagem de Miniatura
Arquivos
art_ALMEIDA_Recent_advances_in_the_molecular_pathogenesis_and_targeted_2012.PDF (256 KB)
Citações na Scopus
34
Tipo de produção
article
Data de publicação
2012
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
LIPPINCOTT WILLIAMS & WILKINS
Autores
Citação
CURRENT OPINION IN ONCOLOGY, v.24, n.3, p.229-234, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Purpose of review This review will focus on the recent advances in molecular pathogenesis and targeted therapies for medullary thyroid carcinoma (MTC). Unlike hereditary MTC in which rearranged during transfection (RET) mutations are the most important precipitating events, in sporadic MTC the genetic or molecular biomarkers are yet to be established. Recent findings Targeted molecular therapies that inhibit RET and other tyrosine kinase receptors involved in angiogenesis have shown great promise in the treatment of metastatic or locally advanced MTC and are under investigation. In addition, the recent findings of H-RAS mutations in 56% of RET-negative sporadic MTC and the activation of the mammalian target of rapamycin (mTOR) intracellular signaling pathway in hereditary MTC suggests that additional or alternative genetic events are important for MTC pathogenesis. Summary Recently, vandetanib (ZD6474), an inhibitor of vascular endothelial growth factor receptor (VEGFR) 2 and VEGFR 3, RET, and epidermal growth factor receptor (EGFR), was approved for the treatment of adults with symptomatic or progressive MTC. Significant advantages for vandetanib over placebo were seen in terms of response rate, disease control rate, and biochemical response in a phase III study. Furthermore, cabozantinib (XL184), an inhibitor of VEGFR 1 and VEGFR 2, hepatocyte growth factor receptor (MET), and RET, was associated with partial response and stable disease in 29 and 41%, respectively.
Palavras-chave
antiangiogenic agents, medullary thyroid carcinoma, rearranged during transfection, targeted therapy
URI
https://observatorio.fm.usp.br/handle/OPI/1330
Referências
  1. Abraham D, 2011, CLIN CANCER RES, V17, P4772, DOI 10.1158/1078-0432.CCR-11-0242
  2. Ahmed M, 2011, EUR J ENDOCRINOL, V165, P315, DOI 10.1530/EJE-11-0129
  3. Almeida MO, 2011, CANCER GENET CYTOGEN, V203, P30
  4. Roychowdhury S, 2011, SCI TRANSL MED, V3, DOI 10.1126/scitranslmed.3003161
  5. Brandi ML, 2001, J CLIN ENDOCR METAB, V86, P5658, DOI 10.1210/jc.86.12.5658
  6. CARLSON KM, 1994, P NATL ACAD SCI USA, V91, P1579, DOI 10.1073/pnas.91.4.1579
  7. Carr LL, 2011, CLIN CANCER RES, V16, P5260
  8. Cohen EEW, 2008, J CLIN ONCOL, V26, P4708, DOI 10.1200/JCO.2007.15.9566
  9. DONISKELLER H, 1993, HUM MOL GENET, V2, P851, DOI 10.1093/hmg/2.7.851
  10. Druce MR, 2011, CLIN ENDOCRINOL OXF
  11. Ebos JML, 2009, CANCER CELL, V15, P232, DOI 10.1016/j.ccr.2009.01.021
  12. Elisei R, 2008, J CLIN ENDOCR METAB, V93, P682, DOI 10.1210/jc.2007-1714
  13. ENG C, 1995, CLIN ENDOCRINOL, V43, P123, DOI 10.1111/j.1365-2265.1995.tb01903.x
  14. Faggiano A, 2011, J CLIN ENDOCR METAB, V95, pE32
  15. Frank-Raue K, 2011, HUM MUTAT, V32, P51, DOI 10.1002/humu.21385
  16. Fugazzola L, 2008, CLIN ENDOCRINOL, V69, P418, DOI 10.1111/j.1365-2265.2008.03218.x
  17. HAZARD JB, 1959, J CLIN ENDOCR METAB, V19, P152
  18. Hoff AO, 2007, HEMATOL ONCOL CLIN N, V21, P475, DOI 10.1016/j.hoc.2007.04.002
  19. Hogan AR, 2009, J SURG RES, V156, P167, DOI 10.1016/j.jss.2009.03.098
  20. Hong DS, 2011, J CLIN ENDOCR METAB, V96, P997, DOI 10.1210/jc.2010-1899
  21. Iwashita T, 1996, ONCOGENE, V12, P481
  22. Kurzrock R, 2011, J CLIN ONCOL, V29, P2660, DOI 10.1200/JCO.2010.32.4145
  23. Lam ET, 2011, J CLIN ONCOL, V28, P2323
  24. Loges S, 2009, CANCER CELL, V15, P167, DOI 10.1016/j.ccr.2009.02.007
  25. Meijer JA, 2011, CLIN ENDOCRINOL OXF, V72, P534
  26. Mian C, 2011, EUR J ENDOCRINOL, V164, P971, DOI 10.1530/EJE-11-0079
  27. Modigliani E, 1998, CLIN ENDOCRINOL, V48, P265, DOI 10.1046/j.1365-2265.1998.00392.x
  28. Moura MM, 2011, J CLIN ENDOCR METAB, V96, pE863, DOI 10.1210/jc.2010-1921
  29. MULLIGAN LM, 1993, NATURE, V363, P458, DOI 10.1038/363458a0
  30. MYERS SM, 1995, ONCOGENE, V11, P2039
  31. Nicolini V, 2011, BIOCHEM PHARMACOL, V82, P778, DOI 10.1016/j.bcp.2011.06.037
  32. Paez-Ribes M, 2009, CANCER CELL, V15, P220, DOI 10.1016/j.ccr.2009.01.027
  33. Rapa I, 2011, J CLIN ENDOCR METAB, V96, P2146, DOI 10.1210/jc.2010-2655
  34. Robinson BG, 2011, J CLIN ENDOCR METAB, V95, P2664
  35. Rohmer V, 2011, J CLIN ENDOCR METAB, V96, pE509, DOI 10.1210/jc.2010-1234
  36. Santoro M, 2004, CELL MOL LIFE SCI, V61, P2954, DOI 10.1007/s00018-004-4276-8
  37. Schlumberger MJ, 2009, J CLIN ONCOL, V27, P3794, DOI 10.1200/JCO.2008.18.7815
  38. Schwartz DL, 2008, HEAD NECK-J SCI SPEC, V30, P883, DOI 10.1002/hed.20791
  39. Sherman SI, 2011, MODERN PATHOL, V24, pS44, DOI 10.1038/modpathol.2010.165
  40. Takahashi M, 2001, CYTOKINE GROWTH F R, V12, P361, DOI 10.1016/S1359-6101(01)00012-0
  41. Verbeek HHG, 2011, J CLIN ENDOCR METAB, V96, pE991, DOI 10.1210/jc.2010-2381
  42. Waguespack SG, 2011, NAT REV ENDOCRINOL, V7, P596, DOI 10.1038/nrendo.2011.139
  43. Wells Jr SA, 2011, J CLIN ONCOL, V28, P767
  44. Wells SA, 2009, CLIN CANCER RES, V15, P7119, DOI 10.1158/1078-0432.CCR-08-2742
  45. Wells Jr SA, 2011, J CLIN ONCOL, V30, P134, DOI [DOI 10.1200/JCO.2011.35.5040, 10.1200/JCO.2011.35.5040]
  46. WOLFE HJ, 1973, NEW ENGL J MED, V289, P437, DOI 10.1056/NEJM197308302890901

Coleções
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/ICESP
Artigos e Materiais de Revistas Científicas - LIM/42