Our objective was to identify TP53 mutations in 138 stage I-IV colorectal adenocarcinomas and liver metastases without first enriching for tumor cells by microdissection.
The in vivo VDEPT experiment with RCM-1 and the adenovirus vector driven by the CEA promoter revealed attenuation of liver metastases in the treatment group.
The <sup>18</sup>F-FDG PET/CT detected more pulmonary nodules in four patients (one PMCRC in each of these patients) and more extrapulmonary disease in six patients (four mediastinal lymph nodes, one retroperitoneal lymph node and one liver metastases) that the CT-scan had not detected.
This signature was lost when primary tumors were compared with all metastatic sites combined.<b>Conclusions:</b> Breast cancer patients with liver metastasis may represent a molecularly homogenized cohort with increased incidence of <i>PIK3CA</i> mutations and activation of the PI3K-AKT-mTOR signaling network.<i></i>.
The present results suggest that protein-truncating mutations of the p53 gene are more relevant than missense mutations as one of the prognostic factors in liver metastasis of colorectal carcinomas.
Overall, the prevalence of KRAS exon 2 was 36.8%, and it was lower in liver metastases (N = 138/490; 28.2%) in comparison with primary tumors (N = 442/1086; 40.7%), lung metastases (16/32; 50%), or other metastatic sites (15/51; 29.4%; P < 0.0001).
KRAS mutational status impacts pathologic response to pre-hepatectomy chemotherapy: a study from the International Genetic Consortium for Liver Metastases.
The in vivo VDEPT experiment with RCM-1 and the adenovirus vector driven by the CEA promoter revealed attenuation of liver metastases in the treatment group.
Tumor material was analyzed for p53 mutations in primary colorectal tumors and subsequent liver metastases from 41 consecutive patients who were scheduled to undergo surgical liver resection.
Patients with resected CRLM treated at MSKCC with and without adjuvant HAI who had available KRAS status (wild-type, WT; mutated, MUT) were reviewed from a prospectively maintained institutional database.
Significantly shorter OS was noted in patients with multiple brain metastases (hazard ratio [HR]: 2.43, p = 0.007), uncommon EGFR mutations (HR: 3.75, p = 0.009), and liver metastases.
We examined 12 human acinar cell carcinomas and 42 transgenic mouse carcinomas (including 36 acinar cell tumors, four islet cell tumors, and two liver metastases of primary acinar cell tumors) for evidence of p53 mutation.
BRAF mutation and NRAS mutation were associated with increased odds of developing liver metastasis (aOR 3.09, 95% CI 1.49-6.42, P=0.003; aOR 3.17, 95% CI 1.32-7.58, P=0.01) and central nervous system (CNS) metastasis (aOR 4.65, 95% CI 2.23-9.69, P<0.001; aOR 4.03, 95% CI 1.72-9.44, P=0.001).
The in vivo VDEPT experiment with RCM-1 and the adenovirus vector driven by the CEA promoter revealed attenuation of liver metastases in the treatment group.