250 Chapter 11 Table 3. Continued Reference Level of Testing Name Genes, Molecules or Panel Investigated Type of Analysis Performed Gene or Molecule Name and Mutation or Expression Status (n) No. of Patients with PM (N) and Outcomes (n) No. of Patients without PM (N) and Outcomes (n) MMR Status (MSI/MSS) Findings as Reported by Authors in Studies Jacob et al. 26 RNA PanCancer Progression Panel NanoString analysis N = 6 N = 12 N/A The analysis between patients with PM and M0 did not show a significant down- or upregulation of distinct gene sets. Not described - - Kawazoe et al. 27 DNA KRAS, NRAS, BRAF and PIK3CA PCR N = 52 N = 212 N/A BRAF mutant tumors were more likely to have PM in comparison with BRAF wildtype tumors (50.0% vs. 18.0%, p = 0.009 c). No significant differences for PM according to RAS mutation (p = 0.64 d). BRAF mutant (14) 7 7 RAS pathway mutant (21) 17 4 KRAS exon 2 mutant (90) 75 15 PIK3CA N/A N/A Lan et al. 28 DNA RAS pathway (KRAS, NRAS, HRAS, BRAF) PI3K pathway PCR N = 104 N = 1388 Total: 154/1492 PM was significantly higher in RAS pathway mutated patients compared to wildtype tumors (p = 0.009 d). Tumors with KRAS mutation had a trend toward a higher proportion of PM (p = 0.061 d). There was no association between PM and the presence of a PI3K pathway mutation (p = 0.408 d). PI3K pathway mutant (213) 12 201 36/177 RAS pathway mutant (706) 62 644 91/615 BRAF mutant (70) 8 62 N/A KRAS mutant (602) 51 551 NRAS mutant (49) 5 44 HRAS mutant (21) 4 17
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