Errata

doi:10.1590/S0100-69912009000400019

ERRATA

No fascículo Nº 3 (páginas 201/202), na forma impressa, as citações das referências foram colocadas erroneamente em alguns trechos da DISCUSSÂO. Abaixo grafamos os textos como devem ser lidos corretamente. Colocamos também a lista correta das referências. Pedimos desculpas pelos nossos erros. Na apresentação on line os textos estão corretos. (Pinto Rodrigo Pozza, Lima Fernando Krebs Cirne, Kulkzynski Jane M U, Moreira Luis Fernando. Expressão do P16 e do PDGFR-Beta no adenocarcinoma gástrico. Rev. Col. Bras. Cir. [serial on the Internet]. 2009 July [cited 2009 Aug 26] ; 36(3): 199-203. Available from: http://www.scielo.br/ scielo.php?script=sci_arttext&pid=S0100-69912009000300004&lng=en. doi: 10.1590/S0100-69912009000300004.)

"Além isso, resultados promissores no tratamento desses pacientes com inibidores da tirosina-quinase, tais como o imatinib (antes conhecido como STI571, Gleevec, Novartis Pharmaceutical Corp, East Hanover, NJ, USA) foram relatados para tumores gastrointestinais estromais (GISTs), nos quais o PDGFR é superexpressado^13,15,20,21. Em um modelo animal de carcinoma gástrico foi demonstrado aumento dos efeitos antitumorais e citotóxicos da 5-FU e do paclitaxel quando cominados com imatinib²².

A associação entre esse marcador e o adenocarcinoma gástrico não foi encontrada na literatura médica, embora a sua expressão (PDGFR alfa e beta) tenha sido encontrada em outros tumores epiteliais, tais como o colangiocarcinoma²³, e o câncer de ovário²⁴ e de mama²⁵.

Assim como em outro relato⁶, o presente trabalho não encontrou relação da expressão do p16 com sexo ou com idade.

Com relação ao tipo histológico de Lauren, ao contrário das expectativas, predominou o tipo difuso,^1,26-28 não sendo encontrada diferença estatística entre o tipo histológico de Lauren e a expressão de p16 nos dois pontos de corte estudados, conforme reportado anteriormente,¹² embora não se tenha chegado a um acordo a respeito dessa questão^7,27.

Embora se saiba que tumores com perda de p16 tendem a ter um potencial metastático mais alto, não foi realizada no presente estudo a imunoistoquímica para o p16 nos linfonodos, uma vez que a expressão total do p16 é muito mais baixa em linfonodos metastáticos do que na lesão primária⁶.

1. De Vita VT Jr, Hellman S, Rosenberg AS. Cancer - Principles and Practice of Oncology. 6^th Edition. Philadelphia: Lippincott Willians and Wilkins; 2001.
²
AICR - American Institute for Cancer Research. World Cancer Research Fund. Food, nutrition and the prevention of cancer: a global perspective. Washington, DC: Banta Book Group; 1997.
³
INCA - Instituto Nacional do Câncer. Estimativa 2005 - Incidência de Câncer no Brasil. Rio de Janeiro, 2005.
4. Brien TP, Depowski MD, Sheehan CE, Ross JS, McKeenna BJ. Prognostic factors in gastric cancer. Mod Pathol 1998; 11:870-7.
5. Wistuba II, Gazdar AF, Minna JD. Molecular genetics of small cell lung carcinoma. Semin Oncol. 2001 Apr;28(2 Suppl 4):3-13.
6. He XS, Su Q, Chen ZC, et al. Expression, deletion and mutation of p16 gene in human gastric cancer. World J Gastroenterol 2001 Aug; 7(4): 515-21.
7. Zhao GH, Li TC, Shi LH, et al. Relationship between inactivation of p16 gene and gastric carcinoma. World J Gastroenterol 2003 May; 9(5): 905-9.
8. Kanyama Y, Hibi K, Nakayama H, et al. Detection of p16 promoter hypermethylation in serum of gastric cancer patients. Cancer Sci 2003 May; 94(5): 418-20.
9. Ficorella C, Cannita K, Ricevuto E, et al. P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer. Oncol Rep 2003 Jan-Feb; 10(1): 169-73.
10. Tang S, Luo H, Yu J, et al. Relationship between alterations of p16(INK4a) and p14(ARF) genes of CDKN2A locus and gastric cancer. Chin Med J 2003 Jul; 116(7): 1083-7.
11. Lee HS, Lee HK, Kim HS, et al. Tumor suppressor gene expression correlates with gastric cancer prognosis. J Pathol 2003 May; 200(1): 39-46.
12. Rocco A, Schandl L, Nardone G, et al. Loss of expression of tumor suppressor p16(INK4) protein in human primary gastric cancer is related to the grade of differentiation. Dig Dis 2002; 20(1): 102-5.
13. George D. Platelet-derived growth factor receptors: a therapeutic target in solid tumors. Semin Oncol 2001 Oct; 28(5 Suppl 17): 27-33.
14. Heldin CH, Westermark B. Mechanism of action and in vivo role of platelet-derived growth factor. Physiological Reviews 1999 Oct; 79(4): 1283- 316.
15. Koh JS, Trent J, Chen L, et al. Gastrointestinal stromal tumors: overview of pathologic features, molecular biology, and therapy with imatinib mesylate. Histol Histopathol 2004 Apr; 19(2): 565-74.
16. Hirota S, Ohashi A, Nishida T, et al. Gain-of-function mutations of platelet-derived growth factor receptor alpha gene in gastrointestinal stromal tumors. Gastroenterology 2003 Sep; 125(3): 660-7.
17. Liu YC, Chen SC, Chang C, et al. Platelet-derived growth factor is an autocrine stimulator for the growth and survival of human esophageal carcinoma cell lines. Exp Cell Res 1996 Nov 1; 228(2): 206-11.
18. Ashman LK. The biology of stem cell factor and its receptor c-kit. Int J Biochem Cell Biol 1999; 31: 1037-51.
19. Esposito I, KleeffJ, Bischoff SC, et al. The stem cell factor c-kit system and mast cells in human pancreatic cancer. Lab Invest 2002; 82: 1481-92.
20. Shinomura Y, Kinoshita K, Tsutsui S, Hirota S. Pathophysiology, diagnosis and treatment of gastrointestinal stromal tumors. J Gastroenterol 2005; 40: 775-80.
21. von Mehren M. Recent advances in the management of gastrointestinal stromal tumors. Current Oncol Rep 2003; 5(4): 288-94.
22. Kim R, Emi M, Arihiro K, Tanabe K, Uchida Y, Toge T. Chemosensitization by STI571 targeting the platelet derived growth factor/platelet derived growth factor receptor- signaling pathway in the tumor progression and angiogenesis of gastric carcinoma. Cancer 2005; 103(9): 1800-9.
23. Holcombe RF, Gu M, Imagawa D, Milovanovic T. Expression of Kit and platelet derived growth factors alpha and beta in cholangiocarcinoma, and case report of therapy with imatinib mesylate (STI571). Anticancer Drugs 2003; 14(8): 651-7.
24. Wilczynski SP, Chen YY, Chen W, Howell SB, Shively JE, Alberts DS. Expression and mutational analysis of tyrosine kinase receptors c-kit, PDGFR-alpha and PDGFR-beta in ovarian cancers. Human Pathol 2005; 36(3): 242-9.
25. Carvalho I, Milanezi F, Martins A, Reis RM, Schmidt F. Overexpression of platelet-derived growth factor receptor alpha in breast cancer is associated with tumor progression. Brest Cancer Res 2005; 7(5)R788-95.
26. Chow WH, Blot WJ, Vaughan TL, et al. Body mass index and the risk of adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst 1998; 90:150.
27. César AC, Silva AE, Tajara EH. Fatores genéticos e ambientais envolvidos na carcinogênese gástrica. Arq Gastroenterol 2002 Out-Dez; 39(4): 253-59.
28. Marigo C, Okuyama MH, Santos GS. Tipos histológicos e mortalidade por câncer gástrico em São Paulo. 1997 Cad Saúde Pub 13 supl 1.

Datas de Publicação

Publicação nesta coleção
09 Nov 2009
Data do Fascículo
Ago 2009

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. De Vita VT Jr, Hellman S, Rosenberg AS. Cancer - Principles and Practice of Oncology. 6^th Edition. Philadelphia: Lippincott Willians and Wilkins; 2001.

[2] ²
AICR - American Institute for Cancer Research. World Cancer Research Fund. Food, nutrition and the prevention of cancer: a global perspective. Washington, DC: Banta Book Group; 1997.

[3] ³
INCA - Instituto Nacional do Câncer. Estimativa 2005 - Incidência de Câncer no Brasil. Rio de Janeiro, 2005.

[4] 4. Brien TP, Depowski MD, Sheehan CE, Ross JS, McKeenna BJ. Prognostic factors in gastric cancer. Mod Pathol 1998; 11:870-7.

[5] 5. Wistuba II, Gazdar AF, Minna JD. Molecular genetics of small cell lung carcinoma. Semin Oncol. 2001 Apr;28(2 Suppl 4):3-13.

[6] 6. He XS, Su Q, Chen ZC, et al. Expression, deletion and mutation of p16 gene in human gastric cancer. World J Gastroenterol 2001 Aug; 7(4): 515-21.

[7] 7. Zhao GH, Li TC, Shi LH, et al. Relationship between inactivation of p16 gene and gastric carcinoma. World J Gastroenterol 2003 May; 9(5): 905-9.

[8] 8. Kanyama Y, Hibi K, Nakayama H, et al. Detection of p16 promoter hypermethylation in serum of gastric cancer patients. Cancer Sci 2003 May; 94(5): 418-20.

[9] 9. Ficorella C, Cannita K, Ricevuto E, et al. P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer. Oncol Rep 2003 Jan-Feb; 10(1): 169-73.

[10] 10. Tang S, Luo H, Yu J, et al. Relationship between alterations of p16(INK4a) and p14(ARF) genes of CDKN2A locus and gastric cancer. Chin Med J 2003 Jul; 116(7): 1083-7.

[11] 11. Lee HS, Lee HK, Kim HS, et al. Tumor suppressor gene expression correlates with gastric cancer prognosis. J Pathol 2003 May; 200(1): 39-46.

[12] 12. Rocco A, Schandl L, Nardone G, et al. Loss of expression of tumor suppressor p16(INK4) protein in human primary gastric cancer is related to the grade of differentiation. Dig Dis 2002; 20(1): 102-5.

[13] 13. George D. Platelet-derived growth factor receptors: a therapeutic target in solid tumors. Semin Oncol 2001 Oct; 28(5 Suppl 17): 27-33.

[14] 14. Heldin CH, Westermark B. Mechanism of action and in vivo role of platelet-derived growth factor. Physiological Reviews 1999 Oct; 79(4): 1283- 316.

[15] 15. Koh JS, Trent J, Chen L, et al. Gastrointestinal stromal tumors: overview of pathologic features, molecular biology, and therapy with imatinib mesylate. Histol Histopathol 2004 Apr; 19(2): 565-74.

[16] 16. Hirota S, Ohashi A, Nishida T, et al. Gain-of-function mutations of platelet-derived growth factor receptor alpha gene in gastrointestinal stromal tumors. Gastroenterology 2003 Sep; 125(3): 660-7.

[17] 17. Liu YC, Chen SC, Chang C, et al. Platelet-derived growth factor is an autocrine stimulator for the growth and survival of human esophageal carcinoma cell lines. Exp Cell Res 1996 Nov 1; 228(2): 206-11.

[18] 18. Ashman LK. The biology of stem cell factor and its receptor c-kit. Int J Biochem Cell Biol 1999; 31: 1037-51.

[19] 19. Esposito I, KleeffJ, Bischoff SC, et al. The stem cell factor c-kit system and mast cells in human pancreatic cancer. Lab Invest 2002; 82: 1481-92.

[20] 20. Shinomura Y, Kinoshita K, Tsutsui S, Hirota S. Pathophysiology, diagnosis and treatment of gastrointestinal stromal tumors. J Gastroenterol 2005; 40: 775-80.

[21] 21. von Mehren M. Recent advances in the management of gastrointestinal stromal tumors. Current Oncol Rep 2003; 5(4): 288-94.

[22] 22. Kim R, Emi M, Arihiro K, Tanabe K, Uchida Y, Toge T. Chemosensitization by STI571 targeting the platelet derived growth factor/platelet derived growth factor receptor- signaling pathway in the tumor progression and angiogenesis of gastric carcinoma. Cancer 2005; 103(9): 1800-9.

[23] 23. Holcombe RF, Gu M, Imagawa D, Milovanovic T. Expression of Kit and platelet derived growth factors alpha and beta in cholangiocarcinoma, and case report of therapy with imatinib mesylate (STI571). Anticancer Drugs 2003; 14(8): 651-7.

[24] 24. Wilczynski SP, Chen YY, Chen W, Howell SB, Shively JE, Alberts DS. Expression and mutational analysis of tyrosine kinase receptors c-kit, PDGFR-alpha and PDGFR-beta in ovarian cancers. Human Pathol 2005; 36(3): 242-9.

[25] 25. Carvalho I, Milanezi F, Martins A, Reis RM, Schmidt F. Overexpression of platelet-derived growth factor receptor alpha in breast cancer is associated with tumor progression. Brest Cancer Res 2005; 7(5)R788-95.

[26] 26. Chow WH, Blot WJ, Vaughan TL, et al. Body mass index and the risk of adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst 1998; 90:150.

[27] 27. César AC, Silva AE, Tajara EH. Fatores genéticos e ambientais envolvidos na carcinogênese gástrica. Arq Gastroenterol 2002 Out-Dez; 39(4): 253-59.

[28] 28. Marigo C, Okuyama MH, Santos GS. Tipos histológicos e mortalidade por câncer gástrico em São Paulo. 1997 Cad Saúde Pub 13 supl 1.

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