Detection of TP53 mutations in tissue or liquid rebiopsies at progression identifies ALK+ lung cancer patients with poor survival
Anaplastic lymphoma kinase (ALK) sequencing can identify resistance mechanisms and guide next-line therapy in ALK+ non-small-cell lung cancer (NSCLC), but the clinical significance of other rebiopsy findings remains unclear. We analysed all stage-IV ALK+ NSCLC patients with longitudinally assessable...
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| Hauptverfasser: | , , , , , , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
21 January 2019
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| In: |
Cancers
Year: 2019, Jahrgang: 11, Heft: 1 |
| ISSN: | 2072-6694 |
| DOI: | 10.3390/cancers11010124 |
| Online-Zugang: | Verlag, Volltext: https://doi.org/10.3390/cancers11010124 Verlag, Volltext: https://www.mdpi.com/2072-6694/11/1/124 
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| Verfasserangaben: | Petros Christopoulos, Steffen Dietz, Martina Kirchner, Anna-Lena Volckmar, Volker Endris, Olaf Neumann, Simon Ogrodnik, Claus-Peter Heussel, Felix J. Herth, Martin Eichhorn, Michael Meister, Jan Budczies, Michael Allgäuer, Jonas Leichsenring, Tomasz Zemojtel, Helge Bischoff, Peter Schirmacher, Michael Thomas, Holger Sültmann, Albrecht Stenzinger |
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| 245 | 1 | 0 | |a Detection of TP53 mutations in tissue or liquid rebiopsies at progression identifies ALK+ lung cancer patients with poor survival |c Petros Christopoulos, Steffen Dietz, Martina Kirchner, Anna-Lena Volckmar, Volker Endris, Olaf Neumann, Simon Ogrodnik, Claus-Peter Heussel, Felix J. Herth, Martin Eichhorn, Michael Meister, Jan Budczies, Michael Allgäuer, Jonas Leichsenring, Tomasz Zemojtel, Helge Bischoff, Peter Schirmacher, Michael Thomas, Holger Sültmann, Albrecht Stenzinger |
| 246 | 3 | 3 | |a Detection of TP 53 mutations in tissue or liquid rebiopsies at progression identifies ALK plus lung cancer patients with poor survival |
| 264 | 1 | |c 21 January 2019 | |
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| 520 | |a Anaplastic lymphoma kinase (ALK) sequencing can identify resistance mechanisms and guide next-line therapy in ALK+ non-small-cell lung cancer (NSCLC), but the clinical significance of other rebiopsy findings remains unclear. We analysed all stage-IV ALK+ NSCLC patients with longitudinally assessable TP53 status treated in our institutions (n = 62). Patients with TP53 mutations at baseline (TP53mutbas, n = 23) had worse overall survival (OS) than patients with initially wild-type tumours (TP53wtbas, n = 39, 44 vs. 62 months in median, p = 0.018). Within the generally favourable TP53wtbas group, detection of TP53 mutations at progression defined a “converted” subgroup (TP53mutconv, n = 9) with inferior OS, similar to that of TP53mutbas and shorter than that of patients remaining TP53 wild-type (TP53wtprogr, 45 vs. 94 months, p = 0.043). Progression-free survival (PFS) under treatment with tyrosine kinase inhibitors (TKI) for TP53mutconv was comparable to that of TP53mutbas and also shorter than that of TP53wtprogr cases (5 and 8 vs. 13 months, p = 0.0039). Fewer TP53wtprogr than TP53mutbas or TP53mutconv cases presented with metastatic disease at diagnosis (67% vs. 91% or 100%, p < 0.05). Thus, acquisition of TP53 mutations at progression is associated with more aggressive disease, shorter TKI responses and inferior OS in ALK+ NSCLC, comparable to primary TP53 mutated cases. | ||
| 650 | 4 | |a anaplastic lymphoma kinase positive (ALK+) non-small cell lung cancer (NSCLC) | |
| 650 | 4 | |a overall survival | |
| 650 | 4 | |a progression-free survival | |
| 650 | 4 | |a tumor protein p53 gene (TP53) mutation | |
| 650 | 4 | |a tyrosine kinase inhibitor | |
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