Showing papers in "Seminars in Cancer Biology in 2010"

TL;DR: Data is described that support the important role of MMPs and TIMPs in cancer cell adhesion and tumor progression and tissue remodeling and decisively regulate tumor cell progression including tumor angiogenesis.

TL;DR: There is accumulating evidence for the potential of selectins to contribute to a number of pathophysiological processes, including cancer metastasis, and current evidence for selectins as potential facilitators of metastasis is discussed.

TL;DR: The role of TEs in genome instability, with particular focus on non-LTR retrotransposons, is reviewed, and examples that impact cancer predisposition and/or development are provided.

TL;DR: This review is focused on the cellular mechanisms that control human TE-associated mutagenesis in cancer and summarizes the current understanding of TE contribution to genetic instability in human malignancies.

TL;DR: It appears reasonable to conclude that there is sufficient evidence now for the existence of cancer stem cells in several epithelial tumors and that these cancers stem cells pose a significant threat via their resistance to standard therapies.

TL;DR: The characterization of a considerable number of rearrangement breakpoints has now been accomplished at the nucleotide sequence level, thereby providing an invaluable resource for the detailed study of the mutational mechanisms which underlie genomic recombination events.

TL;DR: The pathways governing DNA replication fidelity are reviewed and evidence implicating replication errors (point mutation instability or PIN) in carcinogenesis is discussed.

TL;DR: SVA biology is reviewed, including SVA insertions associated with known diseases, and a model describing the initial formation of SVA is discussed and the mechanisms by which SVA may impact the host are discussed.

TL;DR: A 'back to Darwin' model for cancer propagation is suggested, in which cells with self-renewal potency or 'stem-ness' provide genetically diverse units of evolutionary selection in cancer progression.

TL;DR: Although tumorigenic cells and normal stem cells are similar in some ways, they are also fundamentally different in other ways, and understanding both shared and distinguishing mechanisms that regulate normal stem cell proliferation and tumor propagation is likely to reveal opportunities for improving the treatment of patients with cancer.

TL;DR: Some of the physico-mechanical characteristics of tumor-associated ECMs believed to play important roles in regulating epithelial tumorigenic behaviors are described.

TL;DR: Clinical and cellular features of these cancer predisposition syndromes are outlined, and the emerging role for RECQ helicases as predictors of disease risk and the response to therapy is discussed.

TL;DR: It is concluded that CSC-based endpoints and biomarkers are eventually expected to considerably improve tumour cure rates in the clinics through individualised tailoring of treatment.

TL;DR: CXCR4, the most prominent chemokine receptor in CLL, is now targeted in a first clinical trial, emphasizing that chemokines and their receptors have become a highly dynamic translational research field.

TL;DR: Evidence suggests that cancer-associated epigenetic changes most likely underlie potential HERV-mediated effects on genome and transcriptome instability and may play a role in malignancy.

TL;DR: Several approaches are being developed to disrupt the activities of adhesion molecules in multiple myeloma cells, including small antagonist molecules, direct targeting by immunoconjugates, stimulation of immune responses against these molecules, and signal transduction inhibitors.

TL;DR: The fidelity of DNA replication performed by eukaryotic DNA polymerases involved in replicating the nuclear genome is considered.

TL;DR: Observations that all CLL, independent of their IgV gene somatic mutation status, express B-cell receptors that show evidence of antigen-experience strongly support the notion that antigen plays a critical role in CLL pathogenesis.

TL;DR: The cellular and molecular mechanisms underlying tumour progression are outlined, focussing on the acquisition of metastatic capacity and resistance to therapy.

TL;DR: The first compounds that have been shown in model systems to be able selectively to kill cancer cells in this way are now entering clinical trials and the promise of MDM2 inhibitors as a new therapeutic anticancer modality should therefore become clear in the not-too-distant future.

TL;DR: The latest developments in the search for small molecules which rescue p53 function by targeting the p53 protein are discussed.

TL;DR: How evidence first illustrated a link between certain B cell receptor (BCR) specificities and disease outcome and the subsequent large-scale IG analyses which revealed the extent of "stereotyped" BCRs in CLL are discussed are discussed.

TL;DR: The presence of a LSC that solely possesses the ability to initiate and sustain leukemia has implications for the treatment of patients with this disease and some of the recent controversies regarding LSC frequency and alternative theories of leukemogenesis are discussed.

TL;DR: Here it is discussed how lethal mutagenesis may represent a novel therapeutic approach for the treatment of solid cancers and how it is proposed that cancers express a mutator phenotype.

TL;DR: Current knowledge of the signalling mechanisms that focus on MDM2, and indeed MDMX, through both phosphorylation mechanisms and peptide-docking events are reviewed to consider the wider implications of these regulatory events in the context of coordinated regulation of the p53 response.

TL;DR: Over 100 germline single nucleotide polymorphisms in genes that function in base excision repair and that result in non-synonymous amino acid substitutions in the proteins they encode are found.

TL;DR: Molecular details of how activation of TCL1, a critical oncogene in aggressive CLL, results in the initiation of this malignancy were clarified and importance of these pathways was supported by investigations of several mouse models of CLL.

TL;DR: Recent progress in heparanase research is summarized emphasizing the molecular mechanisms that govern its pro-tumorigenic and pro-adhesive properties, suggesting that enzyme function exceeds beyond the enzymatic aspect, thus significantly expanding the scope of the functional proteome.

TL;DR: Better understanding of p53 tumour suppressor activity and the interaction between p53 family members and their isoforms is likely to bring us closer to cancer therapy.

TL;DR: Targeting cancer stem cells and their microenvironments may provide new therapies to eradicate tumors.