Recently, new genomics technologies have uncovered several additional oncogenic mechanisms that cooperate with MYC to create this highly aggressive cancer.
We suggest that ATAD2 links the E2F and MYC pathways and contributes to the development of aggressive cancer through the enhancement of MYC-dependent transcription.
4K, PHI and PCA3 have been validated in prospective clinical trials for initial detection of prostate cancer and recent evidence points to potential differentiation between indolent and aggressive cancer.
Patients ≥75 showed a tendency toward more aggressive cancer and more frequent nodal involvement; we found a higher percentage of R1-resections (19.5% vs. 30.4%, p < 0.05) and PSA relapse after 1 year (12.3% vs. 22.8%, p < 0.05).
On multivariate regression analysis, which included Likert score in the apex, age, prostate-specific antigen (PSA) level, prostate size and presence of any cancer on apical biopsy, only Likert score (P = 0.005) and PSA level (P = 0.025) were significant and independent predictors of aggressive cancer in the distal apex.
PCA3 and TMPRSS2:ERG had additional independent predictive value for the prediction of PCa detection and progression, although PCA3 was limited in predicting aggressive cancer.
Malignant melanoma is a highly aggressive cancer that retains functional p53 and p73, and drug unresponsiveness largely depends on defects in death pathways after epigenetic gene silencing in conjunction with an imbalanced p73/DNp73 ratio.
Previous genomic profiling experiments have identified EWS-FLI1-regulated genes and genes that discriminate ESFT from other sarcomas, but so far a comprehensive analysis of EWS-FLI1-dependent molecular functions characterizing this aggressive cancer is lacking.
We evaluated the clinicopathologic significance of p53 gene mutations, including a comparison of DNA analysis and immunohistochemical examination, in Japanese patients with esophageal squamous cell carcinoma, a highly aggressive cancer.
CCDC6 (coiled-coil domain containing 6) is a player of the HR response to DNA damage and has been predicted to interact with BAP1, another HR-DNA repair gene highly mutated in Malignant Pleural Mesothelioma (MPM), an aggressive cancer with poor prognosis.
These findings highlight NUDT5 as an upstream regulator of tumour drivers and may provide a biomarker for cancer stratification, as well as a novel target for drug discovery for combinatorial drug regimens for the treatment of aggressive cancer types and metastasis.
CCDC6 (coiled-coil domain containing 6) is a player of the HR response to DNA damage and has been predicted to interact with BAP1, another HR-DNA repair gene highly mutated in Malignant Pleural Mesothelioma (MPM), an aggressive cancer with poor prognosis.
Krüppel-like factor 5 (KLF5), a member of the SP/KLF family of zinc finger transcription factors, is overexpressed in human colorectal cancer specimens, and this overabundance is associated with aggressive cancer development and progression.
The transcription factor transcription factor 7-like 1 (TCF7L1) is an embryonic stem cell signature gene that is upregulated in multiple aggressive cancer types, but its role in gastric cancer has seldom been discussed.
In summary, these data reveal a compartment depending prognostic effect of CD138 expression in BCa with cytoplasmic positivity being linked to aggressive cancer and stromal CD138 being linked to a more favorable prognosis.
Patients ≥75 showed a tendency toward more aggressive cancer and more frequent nodal involvement; we found a higher percentage of R1-resections (19.5% vs. 30.4%, p < 0.05) and PSA relapse after 1 year (12.3% vs. 22.8%, p < 0.05).
These results demonstrated that miR‑448 may serve as a tumour suppressor in RB by directly targeting ROCK1 and regulating the PI3K/AKT signalling pathway, thereby suggesting that miR‑448 may be an effective therapeutic target for treating this aggressive cancer.
We found protein methyltransferase 6 (PRMT6) to be frequently downregulated in hepatocellular carcinoma (HCC) and its expression to negatively correlate with aggressive cancer features in HCC patients.