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Critical Reviews in Oncogenesis

Lucia Morbidelli
A new challenge to overcoming tumor resistance to conventional treatment is represented by the development of novel nitric oxide (NO) donors. It is now clear that while low doses of NO have proneoplastic properties, high doses exert antitumor/antiangiogenic activities through multiple mechanisms. This review focuses on the role of exogenous NO in cancer therapy and reports the state of the art regarding different NO-donating agents in cancer treatment, particularly in relation to angiogenesis inhibition.
2016: Critical Reviews in Oncogenesis
Salvatore Rizza, Giuseppe Filomeni
Nitric oxide (NO) is a gaseous pleiotropic molecule that can both induce irreversible oxidative damages and modulate physiological signal transductions by transient protein modifications, the most important of which is the S-nitrosylation of cysteine residues. Being noxious and healthy, the role of NO in cancer is seemingly contradictory, as at low concentrations it mediates tumor growth and proliferation whereas at high concentrations it promotes apoptosis and cancer growth inhibition. However, it is becoming evident that when endogenously produced, such as upon inducible nitric oxide synthase (NOS) activation, NO acts to sustain tumorigenesis...
2016: Critical Reviews in Oncogenesis
Francisco J Molina-Ruiz, Raul Gonzalez, Maria A Rodriguez-Hernandez, Elena Navarro-Villaran, Francisco J Padillo, Jordi Muntané
Sorafenib is an oral multikinase inhibitor approved for the treatment of hepatocellular carcinoma (HCC). Its antitumor activity is attributed to inhibition of tyrosine kinase receptors (VEGFR, PDGFR, c-kit) and intracellular serine/threonine kinases (Raf), which alter gene expression to promote apoptosis and downregulate survival and angiogenesis pathways. The beneficial properties of sorafenib have also been related to a reduction in liver fibrosis trough regulation of TGF-βR-related STAT3 signaling. Sorafenib plays a role in the regulation of mitochondrial function, ATP, and autophagy, a process leading to either survival or apoptotic cell death depending on its intensity and duration, by altering several cellular pathways such as mTOR, AMPK, activating endoplasmic reticulum stress responses, and deregulating miRNAs that modulate autophagy...
2016: Critical Reviews in Oncogenesis
Sarra Bouaouiche, Laurence Dubrez, Ali Bettaieb, Stéphanie Plenchette
The inhibitor of apoptosis (IAP) family members are potent regulators of cell homeostasis able to regulate several fundamental cellular processes that include cell death, cell proliferation, cell differentiation, and inflammation. Regarding this broad spectrum of activity, it is now becoming clear that some members of the family possess oncogenic properties. Analysis of genomic database from tumor sequencing studies has revealed a number of genetic alterations affecting some IAP genes and resulting in gain or loss of function...
2016: Critical Reviews in Oncogenesis
Georg Bauer
Nitric oxide (NO) induces apoptosis selectively in NADPH oxidase-1-expressing malignant cells through peroxynitrite formation after the interaction of NO with extracellular superoxide anions. Membrane-associated proton pumps ensure the protonation of peroxynitrite, followed by decomposition into NO2 and hydroxyl radicals that cause lipid peroxidation and thus trigger the mitochondrial pathway of apoptosis. Distant from the cell membrane, NO is oxidized by oxygen, whereas peroxynitrite preferentially reacts with CO2...
2016: Critical Reviews in Oncogenesis
Albert W Girotti
Many malignant tumors exploit nitric oxide (NO) for a survival, growth, and migration/invasion advantage, and also to withstand the cytotoxic effects of chemo- and radiotherapies. Endogenous NO has also been shown to antagonize photodynamic therapy (PDT), a unique minimally invasive modality involving a photosensitizing (PS) agent, PS-exciting light in the visible- to near-infrared range, and molecular oxygen. The anti-PDT effects of NO were discovered about 20 years ago, but the underlying mechanisms are still not fully understood...
2016: Critical Reviews in Oncogenesis
Elaine M Walsh, Maccon M Keane, David A Wink, Grace Callagy, Sharon A Glynn
Triple negative breast cancers (TNBCs), which are defined as estrogen-receptor, progesterone-receptor, and HER2-receptor negative, account for 10-20% of breast cancers, and they are associated with early metastasis, chemotherapeutic resistance, and poor survival rates. One aspect of TNBC that complicates its prognosis and the development of new molecular therapeutic targets is its clinical and molecular heterogeneity. Herein we compare TNBC and basal cytokeratin-positive breast cancers. We examine the different TNBC molecular subtypes, based on gene expression profiling, which include basal-like, mesenchymal, and luminal androgen receptors, in the context of their biology and impact on TNBC prognosis...
2016: Critical Reviews in Oncogenesis
Sandra Donnini, Lorenzo Bazzani, Marina Ziche, Erika Terzuoli
Nitric oxide (NO) exerts physiopathological effects based mainly on its concentration. Thus, it facilitates or inhibits cancer-promoting characteristics. This review discusses the role of NO and its network of partners in tumor progression and angiogenesis: prostaglandin E 2 (PGE-2) and its producing enzymes, cyclooxigenase 2 (COX-2) and microsomal PGE synthase 1 (mPGES-1), and epidermal growth factor receptor (EGFR) signaling. Understanding the molecular mechanisms and cross-talk modulating NO effects by PGE-2 and EGFR and vice versa allows us to develop better therapeutic strategies for cancer treatment...
2016: Critical Reviews in Oncogenesis
Valentina Rapozzi, Claudia Ferroni, Greta Varchi
Nitric oxide (NO) is an endogenous molecule that performs key physiological signaling functions. The overall biological effect exerted by NO strongly depends on its concentration. Indeed, at a low concentration NO acts as a signal transducer affecting many physiological processes, such as blood flow regulation, iron homeostasis, and neurotransmission, while at a high concentration it preferentially exerts cytotoxic effects. Gaining knowledge about the molecular pathways involved in the NO-tumor response represents a great scientific and clinical challenge for developing novel anticancer strategies based on either endogenous or exogenous NO regulation and induction...
2016: Critical Reviews in Oncogenesis
Marzia Pennati, Graziella Cimino-Reale, Laura Gatti, Giuliana Cassinelli
The machinery that maintains cellular and tissue homeostasis in a healthy individual is recruited and hijacked by cancer cells to support tumor growth and progression. Activation of often unpredictable alternative or complementary signaling pathways allows cancer cells to bypass the intrinsic self-destructive machinery and the limited replicative potential present in every cell for correct homeostasis maintenance. Therefore, evasion/resistance to apoptosis/cell death, self-sufficiency in growth/survival signals, and limitless replicative potential remain undoubted hallmarks of cancer, contributing to drug resistance...
2016: Critical Reviews in Oncogenesis
Lisa Nonnenmacher, Sebastian Hasslacher, Julia Zimmermann, Georg Karpel-Massler, Katia La Ferla-Brühl, Sara E Barry, Timo Burster, Markus D Siegelin, Oliver Brühl, Marc-Eric Halatsch, Klaus-Michael Debatin, Mike-Andrew Westhoff
The induction of apoptosis, a physiological type of cell death, is currently the primary therapeutic aim of most cancer therapies. As resistance to apoptosis is an early hallmark of developing cancer, the success of this treatment strategy is already potentially compromised at treatment initiation. In this review, we discuss the tumor in Darwinian terms and describe it as a complex, yet highly unstable, ecosystem. Current therapeutic strategies often focus on directly killing the dominant subclone within the population of mutated cancer cells while ignoring the subclonal complexity within the ecosystem tumor, the complexity of the direct tumor/ microenvironment interaction and the contribution of the ecosystem human - that is, the global environment which provides the tumor with both support and challenges...
2016: Critical Reviews in Oncogenesis
Janis Noonan, Jennifer Zarrer, Brona M Murphy
The role of autophagy in cancer cell survival and cell death has received much attention in recent years; however, scientists are still trying to unravel the complex relationship that exists between autophagy as a tumor suppressor mechanism and as a promoter of tumor progression. In glioblastoma (GBM), the most fatal tumor of the central nervous system, mounting evidence suggests that autophagy processes are tightly intertwined with GBM tumorigenesis and the development of different molecular subtypes. This has led to exciting prospects that autophagy-targeted therapies may improve the efficacy of conventional therapies as well as therapies targeted at specific genetic alterations in individual GBM patients...
2016: Critical Reviews in Oncogenesis
Christine C Dobson, Stephanie Langlois, David Grynspan, Kyle N Cowan, Martin Holcik
Rhabdomyosarcoma (RMS), a malignant neoplasm of presumed mesenchymal origin, is the most common soft tissue cancer of childhood. Despite aggressive treatment, resistance to current therapies remains a challenge. The success of most cytotoxic chemotherapies requires intact programmed cell death (apoptosis) pathways. Defects in the cellular apoptotic program play a key role in the pathogenesis of RMS and contribute to chemotherapeutic resistance to current treatments. Targeting and engaging apoptotic pathways using small-molecule IAP antagonists, death-inducing ligands, reestablishing pannexin channel expression and activity, immunotherapies, or a combination of these approaches is expected to improve outcomes in RMS patients...
2016: Critical Reviews in Oncogenesis
Ahmad R Safa
Accumulating evidence has demonstrated that human cancers arise from various tissues of origin that initiate from cancer stem cells (CSCs) or cancer-initiating cells. The extrinsic and intrinsic apoptotic pathways are dysregulated in CSCs, and these cells play crucial roles in tumor initiation, progression, cell death resistance, chemo- and radiotherapy resistance, and tumor recurrence. Understanding CSC-specific signaling proteins and pathways is necessary to identify specific therapeutic targets that may lead to the development of more efficient therapies selectively targeting CSCs...
2016: Critical Reviews in Oncogenesis
Alex Philchenkov, Koh Miura
Since the acquired resistance of cells to apoptosis is one of the major hallmarks of cancer, the endogenous inhibitors of apoptosis can be regarded as promising targets in the design of anticancer therapeutics. In addition to their antiapoptotic activity, inhibitor of apoptosis proteins (IAPs) are able to regulate numerous other cell functions, including proliferation, differentiation, and migration, as well as proinflammatory and immune responses. Study of the IAP family as target molecules in targeted therapies has recently focused on SMAC mimetics as synthetic IAP antagonists that have been under development as promising therapeutics...
2016: Critical Reviews in Oncogenesis
Elizabeth K Balcer-Kubiczek
Ionizing radiation is an established cause of cancer based on epidemiologic and experimental evidence. According to epidemiological data, virtually all tissues in the human body are sensitive to the carcinogenic action of radiation. Apoptosis represents a major barrier to cancer because apoptotic cell death eliminates dangerous cells that may initiate tumor development. The explosion in research on apoptosis in the 1990s has demonstrated that irradiated cells have differential apoptotic proclivities and has suggested that radiation can affect apoptosis by inducing the type of damage that is eliminated by programmed cell death but may also modulate the efficiency of this damage removal process...
2016: Critical Reviews in Oncogenesis
Zheng Cao, Theodore Livas, Natasha Kyprianou
Anoikis is a unique mode of apoptotic cell death that occurs consequentially to insufficient cell-matrix interactions. Resistance to anoikis is a critical contributor to tumor invasion and metastasis. The phenomenon is regulated by integrins, which upon engagement with components of the extracellular matrix (ECM) form adhesion complexes and the actin cytoskeleton drives the formation of cell protrusions used to adhere to ECM, directing cell migration. The epithelial-mesenchymal transition (EMT) confers stem cell properties and leads to acquisition of a migratory and invasive phenotype by causing adherens junction breakdown and circumventing anoikis in the tumor microenvironment...
2016: Critical Reviews in Oncogenesis
Dave S B Hoon
No abstract text is available yet for this article.
2016: Critical Reviews in Oncogenesis
Kelly Huynh, Dave S B Hoon
The field of genomic biomarkers in melanoma has evolved dramatically in the past few decades. Whereas much of the prior focus was on molecular assessment of tumor tissue, circulating tumor cells (CTCs), and cell-free circulating tumor DNA (ctDNA) as sources of a "liquid biopsy" in cancer patients provide promising potential as a method to assess tumor progression, identify targets for therapy, and evaluate clinical response to treatment. Blood biomarker assays have the advantage of being noninvasive, allow for dynamic evaluation of disease over a serial time frame, and help to address the issue of tissue sampling bias and tumor heterogeneity...
2016: Critical Reviews in Oncogenesis
Carolyn Hall, Lily Valad, Anthony Lucci
Breast cancer is the most commonly diagnosed cancer among women, resulting in an estimated 40,000 deaths in 2014.1 Metastasis, a complex, multi-step process, remains the primary cause of death for these patients. Although the mechanisms involved in metastasis have not been fully elucidated, considerable evidence suggests that metastatic spread is mediated by rare cells within the heterogeneous primary tumor that acquire the ability to invade into the bloodstream. In the bloodstream, they can travel to distant sites, sometimes remaining undetected and in a quiescent state for an extended period of time before they establish distant metastases in the bone, lung, liver, or brain...
2016: Critical Reviews in Oncogenesis
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