These results suggest an important role of p53 in regulating tumor cell migration through activating PCDH10 expression and support the notion that non-canonical activities of p53 may contribute to its tumor suppressor function in vivo.
Genetic changes found in human osteogenic sarcoma cells, including loss of the p53 and Rb tumor suppressor elements and overexpression of the cyclin G1 (CYCG1) proto-oncogene, suggest the potential of gene transfer as a treatment for metastatic disease.
Computational analysis of transcription factor-binding sites within ontology-enriched or clustered gene sets suggested that the differentially expressed proliferation- and metastasis-associated genes in FAK-null cells were regulated through a common set of transcription factors, including p53.
Sufficient tumor tissue was present in 184 (97.9%) of 188 primary and 56 (96.6%) of 58 metastatic cases. p53 overexpression was found in 42 (22.8%) of 184 primary RCC specimens and in 29 (51.8%) of 56 metastasis specimens (P = 0.0001). p53 overexpression for papillary, chromophobe, and conventional RCC was 70.0%, 27.3%, and 11.9%, respectively (P <0.0001).
These findings suggest that alteration of p53 protein is an event that occurs in the development of cancer, but not of borderline tumors of the ovary, and that it occurs before metastasis and remains unchanged thereafter.
Our findings indicate that the dsP53-285 can upregulate wild-type p53 expression in human bladder cancer cells through RNA activation, and suppresses cells proliferation and metastasis in vitro and in vivo.
In addition, coinfection either with HPV-6 and -16 or with HPV-6 and -18 was detected in 20 cases (33.3% of HPV DNA-positive cases). p53 over-expression was observed in 60 patients (58.8%). p53 was over-expressed significantly in the poorly-differentiated SCC and in patients with metastasis to lymph nodes (P < 0.05, respectively).
Positive test was found in 38% cases in Stage IIA, 57% in Stage IIB, 45% in Stage III and 50% cases in Stage IV. p53 overexpression was observed in 48% of tumors with lymph nodes metastases, and 41% of tumors without lymph nodes metastases.
Further studies found that the high CRYAB and p53 co-expression was also significantly correlated with pathological grade (<i>P</i>=0.024), lymph node metastasis (<i>P</i>=0.000), Distant metastasis (<i>P</i>=0.015), TNM stage (<i>P</i>=0.013), and survival (<i>P</i>=0.000).
The expressions of protein of mutant-type p53 in presence of lymph nodes metastasis were higher than those in absence of lymph nodes metastasis (p < 0.05).
Among the aneuploid tumors (n = 9, x TW = 298 g, range: 7-1000 g), 6 had good outcome, 2 presented metastasis and 1 was lost to follow-up; Weiss' criteria were 2-8 and p53 reactivity was positive in 3 tumors (2 of them of malignant evolution).
This study aimed at: (1) clarifying whether E-cadherin and β-catenin expression and proliferative activity in metastatic ovarian cancer are inter-related; (2) Identifying possible correlations between cell adhesion molecular expression profiles, the proliferative activity and p53 expression of tumor cells and tumor grade and stage; (3) testing the cytology microarray (CMA) technique in analyzing metastasis formation.
The relationship between miR‑612 and TP53 gene expression and their roles in ESCC invasion and metastasis was further studied by reverse transcription‑quantitative polymerase chain reaction and western blotting in EC109 cells and cancer tissues.
Similarly, p53 overexpression was identified immunohistochemically in the tibial chondrosarcoma and its metastases, while being absent in the femoral enchondroma; LOH at 17p13 however, was not demonstrable.
The FAT10 and mutant p53 levels in gastric cancer tissue were significantly correlated with lymph node metastasis and tumor, nodes, metastasis (TNM) staging.
Overexpression of p53 protein in lymph node metastases was associated with distant metastasis free survival by univariate analysis (P = 0.03), but did not reach statistical significance by multivariate analysis (P = 0.07).
We assessed whether metastases correlate with microvessel counts (i.e. intratumoral vascularity) using the CD-31 monoclonal antibody (MAb) and p53 mutant protein expression, determined in the primary by immunocytochemical methods in 70 patients with locally advanced head and neck cancer.
The combined results of immunohistochemistry and proteomic analysis suggest that H. pylori altered the p53 and 14-3-3 isoforms expression and DENA further enhanced the H. pylori effect, which might be involved in carcinogenesis and metastasis of gastric cancer on Gulo(-/-) mice.
There was a statistically significant correlation between p53 and EGFR overexpression (p < 0.0001), nm23 loss (protein and RNA), lymph node status (p < 0.0001); between the incidence of local recurrence and EGFR RNA overexpression (p= 0.003) as well as between the incidence of metastasis and altered Rb expression (p = 0.026), p53 overexpression (p < 0.0001) and mutation (p = 0.04).