Table 2.
Analysis of CTC count in patients treated with agents targeting programmed cell death protein ligand 1 (PD-L1) and epidermal growth factor receptor (EGFR). TKI, tyrosine kinase inhibitor.
| Patient Characteristics | Clinical Finding | Ref. |
|---|---|---|
| 104 patients with stage IIIB or IV disease; agents targeting PD-L1 or PD-1, 6 weeks (The Netherlands) | ≥1 (32%) 1 | [89] |
| CTC count for prediction 2 (baseline): ≥1; (OS (12.1 vs. 4.5) and PFS (4.8 vs. 1.4) | ||
| 7.5 mL, CellSearch (Veridex LLC, Raritan, NJ, USA) | ||
| 68 patients with stage IIIB or IV disease; first-line TKI treatment failure, EGFR-T790M (China) | CTC distribution: ≥5 (75%) | [104] |
| CTC count for prediction (baseline): ≥5; PFS (9.3 vs. 6.5) | ||
| 7.5 mL, CellSearch (Veridex LLC, Raritan, NJ, USA) | ||
| 107 patients with stage IIIB (ineligible for sequential radiotherapy or concurrent chemo/radiotherapy) or stage IV disease; erlotinib/gefitinib therapy, 28 days 3 (China) | CTC distribution: ≥2 (44%) and ≥5 (15%) | [118] |
| CTC count for prediction (baseline): ≥5; PFS (11.1 vs. 6.8) | ||
| 7.5 mL, CellSearch (Veridex LLC, Raritan, NJ, USA) | ||
| 41 relapsed or refractory NSCLC patients; erlotinib/pertuzumab, 3 weeks (USA) | CTC distribution: ≥1 (78%) and ≥5 (42%) | [105] |
| Agreement (cDNA, tumour biopsy) of EGFR and KRAS mutations was not observed between CTCs and tumour tissues | ||
| CellSearch; EGFR status was determined by immunofluorescence; mutations in EGFR, KRAS, PIK3CA, BRAF, NRAS, and AKT1 were assessed by DxS kits and TaqMan genotyping assays (Qiagen, Venlo, Netherlands) | ||
| 37 patients with stage IIIB or IV disease; no previous chemotherapy, EGFR mutations (Italy) | CTC distribution: ≥1 (13%) | [100] |
| 84% 4 had EGFR mutations, 81% had in-frame deletions (exon 19), 19% had point mutations (exon 21), 13% had multiple mutations, 94% had mutations in tumour tissue | ||
| 7.5 mL of peripheral blood was used for CellSearch analysis, PCR amplification (MIDs), and next-generation sequencing (massively parallel pyrosequencing) | ||
| 40 patients with stage III recurrent disease following locoregional treatment who developed resistance to a primary EGFR TKI, 30 days (USA) | 76% were suitable for genotyping, 57% of CTC samples had T790M mutation, 74% had biopsy agreement (CTC and tumour biopsy agreement) | [103] |
| 10 mL of blood was used for HbCTC-Chip (EpCAM) assessment of specific T790M amplification | ||
| 10 patients with the EGFR DelEx19 mutation (Germany) | Low mutation burden (40% of patients) delayed treatment failure (116 vs. 355 days) | [111] |
| 20 mL of peripheral blood was used for assessment with anti-EpCAM (CD326, positive) and anti-CD45 (negative) microbeads (Miltenyi Biotech, Bergisch Gladbach, Germany), real time-PCR, and melting curve analysis | ||
1 Proportion of patients with a given number of CTCs. 2 OS and PFS shown in months. 3 Length of the therapy. 4 Proportion of CTC samples/patients.