Wait-and-See Treatment Strategy Could be Considered for Lung Adenocarcinoma with Special Pleural Dissemination Lesions, and Low Genomic Instability Correlates with Better Survival.
Journal
Annals of surgical oncology
ISSN: 1534-4681
Titre abrégé: Ann Surg Oncol
Pays: United States
ID NLM: 9420840
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
received:
02
06
2019
pubmed:
3
4
2020
medline:
5
5
2021
entrez:
3
4
2020
Statut:
ppublish
Résumé
This study aimed to evaluate the feasibility of a wait-and-see strategy for non-small cell lung cancer (NSCLC) patients with special pleural dissemination lesions (r-pM1a and s-pM1a). Furthermore, the study characterized genomic alternations about disease progression. For this study, 131 NSCLC patients with a diagnosis of pM1a were retrospectively selected. Survival differences were evaluated among patients treated with three different initial postoperative treatments: chemotherapy, targeted therapy, and wait-and-see strategy. Whole-exome sequencing (WES) was performed on primary and metastatic tumors of 10 patients with dramatic progression and 13 patients with gradual progression. The wait-and-see group showed better progression-free survival (PFS) than the chemotherapy group (p < 0.001) but PFS similar to that of targeted group (p = 0.984). This pattern persisted in epidermal growth factor receptor (EGFR)-positive patients. For patients with EGFR-negative/unknown status, PFS was longer in the wait-and-see group than in the two treatment groups. Furthermore, better overall survival (OS) was observed for the patients who received chemotherapy or targeted therapy after the wait-and-see strategy than for those who received chemotherapy or targeted therapy immediately. Lymph node status was an independent prognostic factor for PFS and OS. Finally, WES analysis showed that a high genomic instability index (GIS) and chromosome 18q loss were more common in metastatic tumors, and low GIS was significantly associated with better PFS (p = 0.016). The wait-and-see strategy could be considered for special pM1a patients without lymph nodes metastasis, and patients with a low GIS may be suitable for this strategy.
Sections du résumé
BACKGROUND
BACKGROUND
This study aimed to evaluate the feasibility of a wait-and-see strategy for non-small cell lung cancer (NSCLC) patients with special pleural dissemination lesions (r-pM1a and s-pM1a). Furthermore, the study characterized genomic alternations about disease progression.
METHODS
METHODS
For this study, 131 NSCLC patients with a diagnosis of pM1a were retrospectively selected. Survival differences were evaluated among patients treated with three different initial postoperative treatments: chemotherapy, targeted therapy, and wait-and-see strategy. Whole-exome sequencing (WES) was performed on primary and metastatic tumors of 10 patients with dramatic progression and 13 patients with gradual progression.
RESULTS
RESULTS
The wait-and-see group showed better progression-free survival (PFS) than the chemotherapy group (p < 0.001) but PFS similar to that of targeted group (p = 0.984). This pattern persisted in epidermal growth factor receptor (EGFR)-positive patients. For patients with EGFR-negative/unknown status, PFS was longer in the wait-and-see group than in the two treatment groups. Furthermore, better overall survival (OS) was observed for the patients who received chemotherapy or targeted therapy after the wait-and-see strategy than for those who received chemotherapy or targeted therapy immediately. Lymph node status was an independent prognostic factor for PFS and OS. Finally, WES analysis showed that a high genomic instability index (GIS) and chromosome 18q loss were more common in metastatic tumors, and low GIS was significantly associated with better PFS (p = 0.016).
CONCLUSIONS
CONCLUSIONS
The wait-and-see strategy could be considered for special pM1a patients without lymph nodes metastasis, and patients with a low GIS may be suitable for this strategy.
Identifiants
pubmed: 32239339
doi: 10.1245/s10434-020-08400-1
pii: 10.1245/s10434-020-08400-1
doi:
Substances chimiques
Antineoplastic Agents
0
Protein Kinase Inhibitors
0
ErbB Receptors
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
3808-3818Subventions
Organisme : Health Collaborative Innovation Major Project from Guangzhou Science and Technology Bureau
ID : 201400000001-2
Organisme : Project of National Natural Science Foundation
ID : 81673031
Organisme : Project of National Natural Science Foundation
ID : 81872510
Organisme : Key Lab System Project of Guangdong Science and Technology Department-Guangdong Provincial Key Lab of Translational Medicine in Lung Cancer
ID : 2012A061400006/2017B030314120
Organisme : Guangdong Provincial People's Hospital Young Talent Project
ID : GDPPHYTP201902
Organisme : High-level Hospital Construction Project
ID : DFJH201801
Références
Eberhardt WE, Mitchell A, Crowley J, Kondo H, Kim YT, Turrisi III A, Rami-Porta, R. The IASLC lung cancer staging project: proposals for. J Thorac Oncol. 2015;10:1515–22.
doi: 10.1097/JTO.0000000000000673
Sugiura S, Ando Y, Minami H, et al. Prognostic value of pleural effusion in patients with non-small cell lung cancer. Clin Cancer. 1997;3:47–50.
Jett JR, Scott WJ, Rivera MP, et al. Guidelines on treatment of stage IIIB non-small cell lung cancer.* Chest 2003;123:221.
doi: 10.1378/chest.123.1_suppl.221S
Liu T, Liu H, Wang G, et al. Survival of M1a non-small cell lung cancer treated surgically: a retrospective single-center study. Thorac Cardiovasc Surg. 2015;63:577–82.
doi: 10.1055/s-0034-1396666
Li C, Kuo SW, Hsu HH, et al. Lung adenocarcinoma with intraoperatively diagnosed pleural seeding: is main tumor resection beneficial for prognosis? J Thorac Cardiovasc Surg. 2018;155:1238–49.
doi: 10.1016/j.jtcvs.2017.09.162
Xu Y, Chen N, Wang Z, et al. Should primary tumor be resected for non-small cell lung cancer with malignant pleural disease unexpectedly found during operation? A systemic review and meta-analysis. J Thorac Dis. 2016;8:2843–52.
doi: 10.21037/jtd.2016.10.19
Decanter G, Stoeckle E, Honore C, et al. Watch-and-wait approach for reexcision after unplanned yet macroscopically complete excision of extremity and superficial truncal soft tissue sarcoma is safe and does not affect metastatic risk or amputation rate. Ann Surg Oncol. 2019;26:3526–34.
doi: 10.1245/s10434-019-07494-6
Lockmer S, Østenstad B, Hagberg H, et al. Chemotherapy-free initial treatment of advanced indolent lymphoma has durable effect with low toxicity: results from two Nordic Lymphoma Group trials with more than 10 years of follow-up. J Clin Oncol. 2018;JCO1800262.
McClelland SE. Role of chromosomal instability in cancer progression. Endocrine-Relat Cancer 2017;24:T23–31.
doi: 10.1530/ERC-17-0187
Jamal-Hanjani M, Wilson GA, Mcgranahan N, et al. Tracking the evolution of non-small-cell lung cancer. N Engl J Med. 2017;376:2109–21.
doi: 10.1056/NEJMoa1616288
Greaves M. Evolutionary determinants of cancer. Cancer Discov. 2015;5:806–20.
doi: 10.1158/2159-8290.CD-15-0439
Bolger AM, Marc L, Bjoern U. Trimmomatic: a flexible trimmer for Illumina sequence data. Bioinformatics. 2014;30:2114–20.
doi: 10.1093/bioinformatics/btu170
Li H, Durbin R. Fast and accurate short read alignment with Burrows–Wheeler transform. Hinxton; 2009.
Mark AD, Eric B, Ryan P, et al. A framework for variation discovery and genotyping using next-generation DNA sequencing data. Nat Genet. 2011;43:491–8.
doi: 10.1038/ng.806
Kristian C, Lawrence MS, Carter SL, et al. Sensitive detection of somatic point mutations in impure and heterogeneous cancer samples. Nat Biotechnol. 2013;31:213–9.
doi: 10.1038/nbt.2514
Han F, Bergmann EA, Arora K, et al. Indel variant analysis of short-read sequencing data with Scalpel. Nat Protocols. 2016;11:2529.
doi: 10.1038/nprot.2016.150
Kai W, Mingyao L, Hakon H. ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data. Nucleic Acids Res. 2010;38:e164.
doi: 10.1093/nar/gkq603
Talevich E, Shain AH, Botton T, et al. CNVkit: Genome-wide copy number detection and visualization from targeted DNA sequencing. Plos Comput Biol. 2016;12:e1004873.
doi: 10.1371/journal.pcbi.1004873
Notta F, Chan-Seng-Yue M, Lemire M, et al. A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns. Nature. 2016;538:378.
doi: 10.1038/nature19823
Mcgranahan N, Swanton C. Cancer evolution constrained by the immune microenvironment. Cell 2017;170:825.
doi: 10.1016/j.cell.2017.08.012
Turajlic S, Xu H, Litchfield K, et al. Tracking cancer evolution reveals constrained routes to metastases: TRACERx renal. Cell 2018;173:581.
doi: 10.1016/j.cell.2018.03.057
Makoto M, Akira I, Kunihiko K, et al. Gefitinib or chemotherapy for non-small cell lung cancer with mutated EGFR. N Engl J Med. 2010;362:2380.
doi: 10.1056/NEJMoa0909530
Shaw AT, Kim DW, Nakagawa K, et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N Engl J Med. 2013;368:2385–94.
doi: 10.1056/NEJMoa1214886
Irshad S, Bansal M, Castillomartin M, et al. A molecular signature predictive of indolent prostate cancer. Sci Translat Med. 2013;5:202ra122.
doi: 10.1126/scitranslmed.3006408
Fernàndez V, Salamero O, Espinet B, et al. Genomic and gene expression profiling defines indolent forms of mantle cell lymphoma. Cancer Res. 2010;70:1408–18.
doi: 10.1158/0008-5472.CAN-09-3419