Abstract 2224P
Background
Approximately 50% of metastatic DTC will become RR, with a substantial impact on its prognosis, when we can either initiate treatment with TKI or establish a watch-and-wait strategy. We aim to evaluate the influence of basal clinical factors in OS and OS since starting TKI (OS-TKI).
Methods
We retrospectively analysed data from 109 patients diagnosed with RR-DTC between 2006 and 2022 treated with TKI included in the REGETNE registry. A descriptive (Table) and statistical analysis of the clinical and histological variables and their association with OS and OS-TKI was performed. Follow-up data were gathered until April 2023.
Results
Median OS and OS-TKI were 138 months (m) and 45m, respectively. Most of our patients had papillary carcinoma (56%). Molecular analysis was available in 67 patients (61.5%), being BRAF V600E the most common molecular alteration identified (25.7%). Patients with poorly differentiated (PD) histology had a significantly poorer OS compared to patients with other histologies (61m vs 153m [papillary, p=0.001] vs 127m [follicular, p=0.01) vs 215m [oncocytic, p=0.03]. The presence of bone metastases (n=34) significantly reduced OS (147m vs 81m, HR 2.08, p=0.007) whilst brain metastases (n=3) influenced OS-TKI (48m vs 21m, HR 4,14, p=0.019). By establishing the RR cut-off point before 24m a significant impact on OS was observed (154m vs 99m, HR 2,03, p=0.016).
Conclusions
Our results suggest that PD histology, the presence of bone metastases and RR≤24m significantly reduce OS and, therefore, these patients could benefit from a closer follow-up and early start of TKI. The development of brain lesions influences OS-TKI and a molecular study of this subgroup of patients could offer a more efficient therapeutic alternative. Table: 2224P
N (%) | ||
Age at diagnosis, median [range] | 59 [5-83] | |
Sex (male/female) | 32/77 | |
Histology | ||
Papillary | 61 (56) | |
Follicular | 22 (20.2) | |
Oncocytic | 11 (10.1) | |
Poorly differentiated | 13 (11.9) | |
Unknown | 2 (1.8) | |
Molecular analysis | 67 (61,5) | |
BRAF (V600E) | 28 (25,7) | |
RET (2 CCDC6-RET, 1 NCOA4-RET, 1 mutation RETC380R) | 4 (3,7) | |
RAS (1 KRAS Q61R, 2 HRAS Q61R and 11 NRAS [3 NRAS Q61R, 1 NRAS Q61K, 7 unknown]) | 14 (12,8) | |
TERT | 4 (3.7) | |
PI3K/AKT | 2 (1.8) | |
PAX8-PPARγ-1 | 3 (2.8) | |
PTEN | 3 (2.8) | |
Radioiodine treatment | 98 (89.9) | |
Time to RR, median | 15,5m | |
Doses received, median [range] | 2 [1-8] | |
Accumulated mCi, median [range] | 300 [100-1294] | |
First-line TKI | ||
Lenvatinib | 34 (31.2) | |
Sorafenib | 54 (49.5) | |
Vandetanib | 6 (5.5) | |
Sunitinib | 12 (11) | |
Axitinib | 3 (2.8) |
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
GETNE.
Funding
Has not received any funding.
Disclosure
J. Hernando: Financial Interests, Personal, Advisory Board: Eisai, Ipsen, Novartis, AAA, Angelini, Pfizer, Roche. A. Garcia Alvarez: Financial Interests, Personal, Advisory Board: ADACAP (Novartis); Other, Expenses (Travel, Congress inscription): Advanz, Eisai, Ipsen, ADACAP (Novartis). T. Alonso Gordoa: Financial Interests, Personal, Advisory Board: Ipsen, Pfizer, Roche, Sanofi, Bayer, Eisai, Novartis Advanced Accelerator Applications, Lilly, Bristol Myers Squibb, Astellas; Financial Interests, Personal, Invited Speaker: Janssen-Cilag; Non-Financial Interests, Project Lead: Pfizer, Ipsen. J. Capdevila Castillon: Financial Interests, Personal, Invited Speaker: Novartis, Novartis, Pfizer, Ipsen, Exelis, Bayer, Eisai, Advanced Accelerator Applications, Amgen, Sanofi, Lilly, Merck Serono; Financial Interests, Personal, Advisory Board: Pfizer, Ipsen, Exelis, Bayer, Eisai, Advanced Accelerator Applications, Amgen, Sanofi, Lilly, Merck Serono, Esteve, ITM; Financial Interests, Personal, Research Grant: Novartis, Pfizer, AstraZeneca, Advanced Accelerator Applications, Eisai, Bayer. All other authors have declared no conflicts of interest.
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