Nieodwracalne inhibitory kinaz tyrozynowych receptorów rodziny naskórkowego czynnika wzrostu – nowa, obiecująca strategia terapeutyczna Artykuł przeglądowy
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Opublikowane:
mar 30, 2012
Słowa kluczowe:
nieodwracalne inhibitory kinaz tyrozynowych, rak pierski, rak płuca, HER2, EGFR
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Abstrakt
Inhibitory kinaz tyrozynowych receptorów rodziny naskórkowego czynnika wzrostu (ErbB) znalazły miejsce w rutynowej praktyce klinicznej. Niestety, u części chorych nie stwierdza się odpowiedzi na leczenie pomimo istnienia czynników predykcyjnych, a u tych, którzy odnoszą korzyść terapeutyczną, nieuchronnie rozwija się oporność. Dokładne badanie funkcjonowania receptorów błonowych i związanych z nimi szlaków sygnałowych wykazało, że nietrwała blokada receptorów ErbB jest jedną z przyczyn rozwoju oporności na terapie ukierunkowane molekularnie. Ten wniosek stał się podstawą stworzenia nieodwracalnych inhibitorów kinaz tyrozynowych receptorów rodziny ErbB. W wyniku całkowitej i nieodwracalnej blokady tych receptorów błonowych dochodzi do zahamowania aktywności szlaków sygnałowych warunkujących wzrost i progresję procesu nowotworowego. W niniejszym artykule omówiono znaczenie nieodwracalnej blokady receptorów rodziny ErbB oraz dane dotyczące efektywności tych leków w warunkach klinicznych.
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Wysocki PJ. Nieodwracalne inhibitory kinaz tyrozynowych receptorów rodziny naskórkowego czynnika wzrostu – nowa, obiecująca strategia terapeutyczna. OncoReview [Internet]. 30 marzec 2012 [cytowane 4 grudzień 2024];2(1(5):21-6. Dostępne na: https://journalsmededu.pl/index.php/OncoReview/article/view/290
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Utwór dostępny jest na licencji Creative Commons Uznanie autorstwa – Użycie niekomercyjne 4.0 Międzynarodowe.
Copyright: © Medical Education sp. z o.o. This is an Open Access article distributed under the terms of the Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). License (https://creativecommons.org/licenses/by-nc/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Address reprint requests to: Medical Education, Marcin Kuźma (marcin.kuzma@mededu.pl)
Bibliografia
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17. Sergina N.V., Rausch M., Wang D. et al.: Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3. Nature 2007; 445: 437-41.
18. Kwak E.L., Sordella R., Bell D.W. et al.: Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib. Proc. Natl. Acad. Sci. USA 2005; 102: 7665-70.
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26. Metro G., Crino L.: The LUX-Lung clinical trial program of afatinib for non-small-cell lung cancer. Expert. Rev. Anticancer. Ther. 2011; 11: 673-82.
27. Yang C., Shih J.Y., Su W.C. et al.: BIBW 2992, an irreversible EGFR/HER2 tyrosine kinase inhibitor, in chemonaive patients with adenocarcinoma of the lung and activating EGFR mutations. 13th World Conference on Lung Cancer 2009: 2009.
28. Engelman J.A., Zejnullahu K., Gale C.M. et al.: PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib. Cancer Res. 2007; 67: 11924-32.
29. Janne P.A., Schellens J.A., Engelman J.A., Eckhard S.G., Millham R., Denis L.J.: Preliminary activity and safety results from a phase I clinical trial of PF-00299804, an irreversible pan-HER inhibitor, in patients (pts) with NSCLC. (abstract no 8027). ASCO Annual Meeting 2008: 2008.
30. Janne P.A., Reckamp K.L., Koczywas M.: Efficacy and safety of PF-00299804 (PF299) in patietns (pt) with advanced NSCLC after failure of at least one prior chemotherapy regimen and prior treatment with erlotinib (E): a two-arm phase II trial (abstract n. 8063). ASCO Annual Meeting 2009: 2009.
2. Kumar A., Petri E.T., Halmos B., Boggon T.J.: Structure and clinical relevance of the epidermal growth factor receptor in human cancer. J. Clin. Oncol. 2008; 26: 1742-51.
3. Lemmon M.A., Schlessinger J.: Cell signaling by receptor tyrosine kinases. Cell 2010; 141: 1117-34.
4. Slamon D.J., Godolphin W., Jones L.A. et al.: Studies of the HER-2/neu proto-oncogene in human breast and ovarian cancer. Science 1989; 244: 707-12.
5. Sliwkowski M.X., Lofgren J.A., Lewis G.D., Hotaling T.E., Fendly B.M., Fox J.A.: Nonclinical studies addressing the mechanism of action of trastuzumab (Herceptin). Semin. Oncol. 1999; 26: 60-70.
6. Junttila T.T., Akita R.W., Parsons K. et al.: Ligand-independent HER2/HER3/PI3K complex is disrupted by trastuzumab and is effectively inhibited by the PI3K inhibitor GDC-0941. Cancer Cell. 2009; 15: 429-40.
7. Xia W., Mullin R.J., Keith B.R. et al.: Anti-tumor activity of GW572016: a dual tyrosine kinase inhibitor blocks EGF activation of EGFR/erbB2 and downstream Erk1/2 and AKT pathways. Oncogene 2002; 21: 6255-63.
8. Geyer C.E., Forster J., Lindquist D. et al.: Lapatinib plus capecitabine for HER2-positive advanced breast cancer. N. Engl. J. Med. 2006; 355: 2733-43.
9. Schwartzberg L.S., Franco S.X., Florance A., O’Rourke L., Maltzman J., Johnston S.: Lapatinib plus letrozole as first-line therapy for HER-2+ hormone receptor-positive metastatic breast cancer. Oncologist 2010; 15: 122-9.
10. Sharma S.V., Bell D.W., Settleman J., Haber D.A.: Epidermal growth factor receptor mutations in lung cancer. Nat. Rev. Cancer 2007; 7: 169-81.
11. Politi K., Zakowski M.F., Fan P.D., Schonfeld E.A., Pao W., Varmus H.E.: Lung adenocarcinomas induced in mice by mutant EGF receptors found in human lung cancers respond to a tyrosine kinase inhibitor or to down-regulation of the receptors. Genes Dev. 2006; 20: 1496-510.
12. Gazdar A.F.: Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors. Oncogene 2009; 28 (Suppl. 1): S24-31.
13. Greulich H., Chen T.H., Feng W. et al.: Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants. PLoS Med. 2005; 2: e313.
14. Pao W., Wang T.Y., Riely G.J. et al.: KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib. PLoS Med. 2005; 2: e17.
15. Tang J.M., He Q.Y., Guo R.X., Chang X.J.: Phosphorylated Akt overexpression and loss of PTEN expression in non-small cell lung cancer confers poor prognosis. Lung Cancer 2006; 51: 181-91.
16. Cappuzzo F., Janne P.A., Skokan M. et al.: MET increased gene copy number and primary resistance to gefitinib therapy in non-small-cell lung cancer patients. Ann. Oncol. 2009; 20: 298-304.
17. Sergina N.V., Rausch M., Wang D. et al.: Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3. Nature 2007; 445: 437-41.
18. Kwak E.L., Sordella R., Bell D.W. et al.: Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib. Proc. Natl. Acad. Sci. USA 2005; 102: 7665-70.
19. Ji H., Li D., Chen L. et al.: The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies. Cancer Cell. 2006; 9: 485-95.
20. Rabindran S.K., Discafani C.M., Rosfjord E.C. et al.: Antitumor activity of HKI-272, an orally active, irreversible inhibitor of the HER-2 tyrosine kinase. Cancer Res. 2004; 64: 3958-65.
21. Wong K.K., Fracasso P.M., Bukowski R.M. et al.: A phase I study with neratinib (HKI-272), an irreversible pan ErbB receptor tyrosine kinase inhibitor, in patients with solid tumors. Clin. Cancer Res. 2009; 15: 2552-8.
22. Burstein H.J., Sun Y., Dirix L.Y. et al.: Neratinib, an irreversible ErbB receptor tyrosine kinase inhibitor, in patients with advanced ErbB2-positive breast cancer. J. Clin. Oncol. 2010; 28: 1301-7.
23. Li D., Ambrogio L., Shimamura T. et al.: BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models. Oncogene 2008; 27: 4702-11.
24. Yap T.A., Vidal L., Adam J. et al.: Phase I trial of the irreversible EGFR and HER2 kinase inhibitor BIBW 2992 in patients with advanced solid tumors. J. Clin. Oncol. 2010; 28: 3965-72.
25. Shih J., Yang C., Su W.C. et al.: A phase II study of BIBW 2992, a novel irreversible dual EGFR and HER2 tyrosine kinase inhibitor (TKI) in patients with adenocarcinoma of the lung and activating EGFR mutations after failure of one line of chemotherapy (LUX Lung 2). ASCO Annual Meeting 2009: 2009.
26. Metro G., Crino L.: The LUX-Lung clinical trial program of afatinib for non-small-cell lung cancer. Expert. Rev. Anticancer. Ther. 2011; 11: 673-82.
27. Yang C., Shih J.Y., Su W.C. et al.: BIBW 2992, an irreversible EGFR/HER2 tyrosine kinase inhibitor, in chemonaive patients with adenocarcinoma of the lung and activating EGFR mutations. 13th World Conference on Lung Cancer 2009: 2009.
28. Engelman J.A., Zejnullahu K., Gale C.M. et al.: PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib. Cancer Res. 2007; 67: 11924-32.
29. Janne P.A., Schellens J.A., Engelman J.A., Eckhard S.G., Millham R., Denis L.J.: Preliminary activity and safety results from a phase I clinical trial of PF-00299804, an irreversible pan-HER inhibitor, in patients (pts) with NSCLC. (abstract no 8027). ASCO Annual Meeting 2008: 2008.
30. Janne P.A., Reckamp K.L., Koczywas M.: Efficacy and safety of PF-00299804 (PF299) in patietns (pt) with advanced NSCLC after failure of at least one prior chemotherapy regimen and prior treatment with erlotinib (E): a two-arm phase II trial (abstract n. 8063). ASCO Annual Meeting 2009: 2009.