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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
Humberto Lara-Guerra, Jack A Roth
Gene therapy was originally conceived to treat monogenic diseases. The replacement of a defective gene with a functional gene can theoretically cure the disease. In cancer, multiple genetic defects are present and the molecular profile changes during the course of the disease, making the replacement of all defective genes impossible. To overcome these difficulties, various gene therapy strategies have been adopted, including immune stimulation, transfer of suicide genes, inhibition of driver oncogenes, replacement of tumor-suppressor genes that could mediate apoptosis or anti-angiogenesis, and transfer of genes that enhance conventional treatments such as radiotherapy and chemotherapy...
2016: Critical Reviews in Oncogenesis
Farin Amersi, Charles Forscher, Allan W Silberman
INTRODUCTION: Retroperitoneal sarcomas (RS) are rare malignant tumors characterized by high local recurrence rates and poor survival, Aggressive surgical resection may improve local recurrence rates and disease-specific survival (DSS), The aim of our study was to determine predictors of survival and local recurrence in primary RS. METHODS: We performed a retrospective analysis and identified 68 patients who underwent surgical resection of a primary RS between 1985 and 2010, Clinical and pathologic variables were used to create univariate and multivariate models for both survival and recurrence...
2016: Critical Reviews in Oncogenesis
Steve D Colquhoun
As the incidence of hepatocellular carcinoma (HCC) continues to rise, so does our understanding of this disease and the number of available treatment options and strategies. Although surgical intervention often continues to play a central role, it must be placed in the proper context of what has rapidly become a multimodality, multidisciplinary disease. Understanding the nuances of managing HCC and its associations and treatment options are essential for making appropriate surgical decisions.
2016: Critical Reviews in Oncogenesis
Mark C Kelley
Therapies targeting the mitogen-activated protein kinase signaling pathway can induce profound tumor regression in patients with advanced BRAF-mutated melanoma. Most patients develop resistance after several months of treatment, which is typically followed by rapid disease progression and death. BRAF- and mitogen-activated protein kinase kinase (MEK)-targeted therapies were initially thought to exert their therapeutic effects through direct inhibition of signaling within the tumor cell, resulting in cell death...
2016: Critical Reviews in Oncogenesis
Peter C Jones, Reiko F Irie
Tumor-associated gangliosides have been investigated for their potential as antigenic targets for more than 35 years, culminating in the recent Food and Drug Administration approval of dinutuximab (Unituxin), an IgG antibody targeted against GD2, for the treatment of neuroblastoma in children. This review is focused on discoveries and development of therapeutic approaches involving human IgM antibodies directed against gangliosides, which occurred over the past 40 years at University of California-Los Angeles and the John Wayne Cancer Institute, where Dr...
2016: Critical Reviews in Oncogenesis
Mark B Faries
The last few years have yielded exciting developments in immunotherapy for cancer. The promise of cancer immunotherapy has been well known for many years, but had generally produced limited or inconsistent benefit to patients. Intralesional therapies, which are in fact one of the oldest forms of immunotherapy, are also demonstrating benefits in the modern age. This review discusses the origins of intralesional immunotherapy and its underlying rationale. It also discusses the reemergence of this mode of therapy into the modern era, which is where Donald L...
2016: Critical Reviews in Oncogenesis
Elizabeth A Grimm
Melanoma and many other cancers often express cells and molecular features of inflammation. Intrinsic to melanoma is the expression of a continuous cycle of cytokines and oxidative stress markers. The oxidative stress of inflammation is proposed to drive a metastatic process, not only of DNA adducts and crosslinks, but also of posttranslational oxidative modifications to lipids and proteins that we argue support growth and survival. Fortunately, numerous antioxidant agents are available clinically and we further propose that the pharmacological attenuation of these inflammatory processes, particularly the reactive nitrogen species, will restore the cancer cells to an apoptosis-permissive and growth-inhibitory state...
2016: Critical Reviews in Oncogenesis
David W Ollila, Nicole E Lopez, Eddy C Hsueh
There is an increasing body of literature that strongly suggests that complete metastasectomy for stage IV melanoma can improve overall survival. Before 2011, the efficacy of systemic therapy for melanoma was poor, making surgical resection the mainstay for treatment and the only realistic chance for cure. Now, in just a short time span (2011-2014), we have six Food & Drug Administration (FDA)-approved drugs for patients with stage IV metastatic melanoma. In the absence of prospective clinical trials evaluating the most advantageous sequence and timing for systemic therapy and surgical resection in the setting of stage IV melanoma, the treating surgical and medical oncologists must jointly devise individual treatment plans that take into account the advantages and disadvantages of each modality...
2016: Critical Reviews in Oncogenesis
Vernon K Sondak, Damon Reed, Jane L Messina
Pediatric melanoma has been rising in incidence in recent years and its management poses challenges that are frequently exacerbated by diagnostic uncertainty about the benign or malignant nature of many pediatric melanocytic neoplasms. Sentinel lymph node biopsy (SLNB), originally described by Dr. Donald L. Morton, has been incorporated selectively into the management of pediatric atypical melanocytic neoplasms (AMNs), but its value and significance in this scenario have been controversial. Herein, we describe a comprehensive approach to the evaluation and management of pediatric AMNs that involves SLNB as a diagnostic, staging, and potentially therapeutic tool...
2016: Critical Reviews in Oncogenesis
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