Using cell lines representative of P53 wild-type ovarian cancer (A2780), and P53 mutant ovarian cancer (SKOV3), cells were implanted in the flank of athymic nude female mice.
We performed genome-wide copy number aberration (CNA) profiles and mutation hotspot screening (KRAS, BRAF, NRAS, ERBB2, PIK3CA, TP53) in 38 LGSOC tumor samples.
Resistance to chemotherapy and high heterogeneity in mutations contribute to ovarian cancer's lethality, including many mutations in tumor suppressor p53.
High expression of the three transketolase genes was associated with unfavorable PFS in patients with TP53-mutated ovarian cancer, but not in patients with TP53 wild-type ovarian cancer.
Because chemokine network is involved in OC progression, we evaluated associations between chemokine expression and survival in tumor suppressor protein p53 (<i>TP53</i>) wild-type (<i>TP53</i>WT) and mutant (<i>TP53</i>m) OC datasets.
The association between p53 protein phosphorylation at serine 15, serine 20 and sensitivity of cells isolated from patients with ovarian cancer and cell lines to chemotherapy in in vitro study.
We evaluated the association between lifestyle and reproductive factors and risk of ovarian cancer defined by p53 and MAPK expression.<b>Methods:</b> Epithelial ovarian cancer cases (<i>n</i> = 274) and controls (<i>n</i> = 1,907) were identified from the Nurses' Health Study and Nurses' Health Study II prospective cohorts, and the population-based New England Case-Control study.
With lead times ≤6 months, ovarian cancer detection sensitivity at 0.98 specificity (SE98) varied from 0.19 [95% CI 0.08-0.40] for CTAG1A, CTAG2 and NUDT1 to 0.23 [0.10-0.44] for P53 (0.33 [0.11-0.68] for high-grade serous tumors).
Positive protein expressions of AIB1, Bcl-2, and p53 were identified in the epithelial ovarian cancer tissues, and with an increase in the tumor staging of ovarian cancer, we found that the positive protein expression rate was gradually augmented.
We analyzed mRNA expression of <i>PD-1</i>, <i>PD-L1</i> and <i>IFNG</i> by quantitative real-time PCR in tissue of 170 patients with low grade-serous (LGSOC), high-grade serous (HGSOC), endometrioid and clear cell OC compared to 28 non-diseased tissues (ovaries and fallopian tubes) in relation to tumor protein 53 (<i>TP53</i>) and breast cancer gene 1/2 (<i>BRCA1/2</i>) mutation status.
Knowing that p53 expression status is used for chemotherapeutic approaches and prognosis in ovarian cancer, the results obtained highlight the importance of locating TP53 mutations.
We demonstrate that deleterious TP53 variants identified in blood-derived DNA of 523 patients with ovarian cancer (AGO-TR1 trial) were not causal for the patients' ovarian cancer in three out of six TP53-positive cases.
In the present study we extended these studies to identify the molecular pathways regulated by QC to promote apoptosis independent of p53 status in OC.