Search results for "Blastoma"
showing 10 items of 603 documents
The apoptotic effects of cisplatin and carboplatin in retinoblastoma Y79 cells.
1998
This study demonstrated that cisplatin and carboplatin stimulate apoptosis in human retinoblastoma Y79 cells, cisplatin being the most effective compound. The apoptotic effect appeared after 8 h and then increased in a time-dependent manner. Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2. The prolonged exposure of Y79 cells to cisplatin induced resistance to cisplatin, carboplatin and etoposide. The basal level of p53 was in resistant cells higher than in untreated cells, while Bcl-2 was not modified. p53 and Bcl-2 levels did not change after treating of resistant cells with cisplatin, carboplatin or etoposide. However…
Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression
2015
As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.
OS1.5 Harnessing soluble LRIG1 for pan-RTK targeting in glioblastoma
2018
INTRODUCTION: The role of receptor tyrosine kinases (RTKs) in glioblastoma is widely acknowledged. However, therapies based on RTK targeting have been continuously unsuccessful in GBM patients, highlighting the complexity of RTK signaling and biology. LRIG1 (Leucine-rich Repeats and ImmunoGlobulin domains protein 1) was identified as an endogenous inhibitor of epidermal growth factor receptor (EGFR) and other RTKs, and was confirmed as a tumor suppressor in various cancer types. We previously identified the soluble form of LRIG1 as a potent inhibitor of GBM growth in vivo, irrespective of EGFR status. Here, we aim to shed light on the molecular mechanisms underlying its anti-cancer activity…
Bmi1 and Cell of Origin Determinants of Brain Tumor Phenotype
2007
Glioblastomas frequently express oncogenic EGFR and loss of the Ink4a/Arf locus. Bmi1, a positive regulator of stem cell self renewal, may be critical to drive brain tumor growth. In this issue of Cancer Cell, Bruggeman and colleagues suggest that brain tumors with these molecular alterations can be initiated in both neural precursor and differentiated cell compartments in the absence of Bmi1; however, tumorigenicity is reduced, and tumors contain fewer precursor cells. Surprisingly, tumors appear less malignant when initiated in precursor cells. Bmi1-deficient tumors also had fewer neuronal lineage cells, suggesting a role for Bmi1 in determination of cell lineage and tumor phenotype.
RB acute loss induces centrosome amplification and aneuploidy in murine primary fibroblasts
2006
AbstractBackgroundIncorrect segregation of whole chromosomes or parts of chromosome leads to aneuploidy commonly observed in cancer. The correct centrosome duplication, assuring assembly of a bipolar mitotic spindle, is essential for chromosome segregation fidelity and preventing aneuploidy. Alteration of p53 and pRb functions by expression of HPV16-E6 and E7 oncoproteins has been associated with centrosome amplification. However, these last findings could be the result of targeting cellular proteins in addition to pRb by HPV16-E7 oncoprotein. To get a more detailed picture on the role of pRb in chromosomal instability and centrosome amplification, we analyzed the effects of the acute loss …
pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…
2003
The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…
RNA-sequencing and bioinformatic analysis to pre-assess sensitivity to targeted therapeutics in recurrent glioblastoma.
2019
e13533 Background: This study developed molecular guided tools for individualized selection of chemotherapeutics for recurrent glioblastoma (rGB). A consortium involving clinical neurooncologists, molecular biologists and bioinformaticians identified gene expression patterns in rGB and quantitatively analyzed pathways involved in response to FDA approved oncodrugs. Methods: From2016 to 2018 biopsies from GB were collected using a multisampling approach. Biopsy material was used to isolate glioma stem-like cells and examined by RNA-sequencing. RNA-seq results were subjected to differential expression (DE) analysis and Oncobox analysis – a bioinformatic tool for quantitative pathway activati…
Neuroblastoma with MYCN amplification plus 11q deletion: immunohistochemical expression of angiogenic factors
2010
Neuroblastoma (NB) is an extra-cranial solid neoplasm in childhood. Genetic markers as MYCN amplification (MNA) and deletion of 11q (11q ) are considered factors with an adverse prognosis. Usually, an inverse relationship between MNA and 11q is found. Approximately 13% of the MNA cases present with 11q . These cases show a dramatic decline in survival rates. Hypoxia-inducible factor-2a (HIF-2a) protein expression has been described as an indicator of poor outcome, has been correlated with an aggressive phenotype in NB, and serves as a marker for stem cell-like phenotypes. Additionally, HIF-2a positive cells strongly express vascular endothelial growth factor (VEGF) and, as such, could be in…
SuperHistopath: A Deep Learning Pipeline for Mapping Tumor Heterogeneity on Low-Resolution Whole-Slide Digital Histopathology Images.
2021
High computational cost associated with digital pathology image analysis approaches is a challenge towards their translation in routine pathology clinic. Here, we propose a computationally efficient framework (SuperHistopath), designed to map global context features reflecting the rich tumor morphological heterogeneity. SuperHistopath efficiently combines i) a segmentation approach using the linear iterative clustering (SLIC) superpixels algorithm applied directly on the whole-slide images at low resolution (5x magnification) to adhere to region boundaries and form homogeneous spatial units at tissue-level, followed by ii) classification of superpixels using a convolution neural network (CN…
Experimental models of kidney tumors.
1993
We here present in outline some outstanding results on the animal models of renal tumors submitted to the highest attention, which include two kinds of epithelial neoplams: those developed from the epithelium lining each the renal tubules (renal cell tumors) and pelvis; the mesenchymal tumor of rat; and tumors with embryonal appearance: the nephroplastoma as well as the variant of it known as the estrogen-induced tumor in the hamster. The review deals with methods for tumor induction and the pathobiology of tumors, the latter mainly focussed on the indendification of the precise types of renal cells committed in tumor origin. The existence of closely related counterparts of these animal tum…