2020
DOI: 10.1016/j.ebiom.2020.103103
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Longitudinal therapy monitoring of ALK-positive lung cancer by combined copy number and targeted mutation profiling of cell-free DNA

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Cited by 35 publications
(60 citation statements)
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“…In addition a tissue biopsy should be pursued in cases of suspected small cell lung cancer transformation and also when a LB does not reveal a likely resistance mechanism. Moreover, the knowledge obtained from different analyses that integrate over time tissue and LB will certainly lead to the development of novel therapeutic molecules [ 123 , 124 ]. It is certainly too premature to assert that liquid biopsies will replace tissue biopsies for the evaluation of the status of ALK at the time of diagnosis and/or on progression of all the mechanisms of resistance of a tumor of a patient treated with TKI that target an ALK rearrangement.…”
Section: Discussionmentioning
confidence: 99%
“…In addition a tissue biopsy should be pursued in cases of suspected small cell lung cancer transformation and also when a LB does not reveal a likely resistance mechanism. Moreover, the knowledge obtained from different analyses that integrate over time tissue and LB will certainly lead to the development of novel therapeutic molecules [ 123 , 124 ]. It is certainly too premature to assert that liquid biopsies will replace tissue biopsies for the evaluation of the status of ALK at the time of diagnosis and/or on progression of all the mechanisms of resistance of a tumor of a patient treated with TKI that target an ALK rearrangement.…”
Section: Discussionmentioning
confidence: 99%
“…Older TKI are generally not helpful for these patients, because lorlatinib has the greatest potency against the ALK kinase, and the broadest activity against ALK resistance mutations among all currently available ALK inhibitors ( Figure 1 c) [ 10 , 35 ]. One potential exception is brigatinib, which has a slightly better activity than lorlatinib for the p.G1269A mutation [ 66 ] and produced clinically relevant benefit with a median time-to-next-treatment of 7.5 months in the lorlatinib-pretreated subcohort of the international expanded access program (including mostly European patients, Table 1 and Figure 2 ) [ 70 ], as well as in several case reports (e.g., [ 71 ] and patient 28 in [ 72 ]). Of note, due to the good activity of lorlatinib against all individual ALK mutations analyzed so far, on-target lorlatinib resistance usually results from compound (i.e., multiple coexistent) ALK mutations, which also confer resistance to all other currently available ALK TKI [ 73 , 74 ].…”
Section: State-of-the-art After the First Linementioning
confidence: 99%
“…However, improved prognostication can affect patient management in several other ways, for example it can assist selection of unfavorable cases for more aggressive surveillance and local treatment strategies, or for preferential participation in early phase clinical trials. Luckily, inasmuch as high-risk V3-positive and/or TP53 -mutated cases need closer monitoring, they also have a higher number and higher abundance (variant allele frequencies) of molecular alterations in the blood circulating tumor DNA (ctDNA), which can be used for remission tracking and earlier identification of treatment failure [ 72 , 91 ]. Besides single-nucleotide variants (SNV), copy number alterations, as captured globally by low-pass (0.5–1x) whole-genome sequencing and quantified with the trimmed median absolute deviation from copy number neutrality (tMAD) score across the genome, are also increased in high-risk cases, accumulate further during the course of the disease, and correlate independently with the risk of death [ 72 ].…”
Section: State-of-the-art After the First Linementioning
confidence: 99%
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