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We utilized RNA-ISH in primary tumor specimens to identify the potential colocalization of these three highly enriched CTC genes.

Indeed, there was no correlation between the tumor fraction present in cfDNA or enriched CTCs in the 28 samples that were performed on the same liquid biopsy, Fig. 1b, (Pearson correlation 0.081, p = 0.680).

We first examined tumor fractions in matched samples of cfDNA and enriched CTCs obtained from the same blood draw from 28 patients with MM (Fig. 1a, b).

Interestingly, beside one patient (MM_2205), we found a wide discrepancy in the tumor fraction obtained from cfDNA and enriched CTCs, including several patients with higher tumor fractions in cfDNA than enriched CTCs or vice versa.

Highly enriched CTCs are collected in the product outlet in PBS containing 1% (w/v) Pluronic F-68 (Sigma).

We first sought to evaluate the prevalence of circulating tumor DNA (tumor-derived cfDNA) and enriched CTCs in patients with MM.

(3) The most highly enriched CTC-specific transcripts shared by almost all classical CTCs encode extracellular matrix proteins, such as Sparc.

We selected rigorous criteria to identify the most highly enriched CTC-c transcripts (RP score < 300), expressed at very high levels (>100 rpm) in ≥90% of all classical CTCs.

Another technique to enrich CTC which is solely based on the size of the cells is filtration.

This system immunomagnetically enriches CTC from 7.5 ml of blood targeting the epithelial cell adhesion molecules (EpCAM).

Figure 4(a) shows our new strategy using a combination of microbeads coated with anti-CK and anti-EpCAM antibodies to enrich CTCs from patient blood samples.