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Search Results: 1 - 10 of 332809 matches for " Michael J. Monument "
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Salient features of mesenchymal stem cells—implications for Ewing sarcoma modeling
Michael J. Monument
Frontiers in Oncology , 2013, DOI: 10.3389/fonc.2013.00024
Abstract: Despite a heightened appreciation of the many defining molecular aberrations in Ewing sarcoma, the cooperative genetic environment and permissive cell of origin essential for EWS/ETS-mediated oncogenesis remain elusive. Consequently, inducible animal and in vitro models of Ewing sarcoma from a native cellular context are unable to fully recapitulate malignant transformation. Despite these shortcomings, human, and murine mesenchymal stem cells (MSCs) are the closest working in vitro systems available. MSCs are tolerant of ectopic EWS/FLI expression, which is accompanied by a molecular signature most similar to Ewing sarcoma. Whether MSCs are the elusive cell of origin or simply a tolerant platform of the EWS/FLI transcriptome, these cells have become an excellent molecular tool to investigate and manipulate oncogenesis in Ewing sarcoma. Our understanding of the biological complexity and heterogeneity of human MSCs (hMSCs) has increased substantially over time and as such, appreciation and utilization of these salient complexities may greatly enhance the efficient use of these cells as surrogate models for Ewing sarcoma tumorigenesis.
Extra-Abdominal Desmoid Tumors Associated with Familial Adenomatous Polyposis
George T. Calvert,Michael J. Monument,Randall W. Burt,Kevin B. Jones,R. Lor Randall
Sarcoma , 2012, DOI: 10.1155/2012/726537
Abstract: Extra-abdominal desmoid tumors are a significant cause of morbidity in patients with familial adenomatous polyposis syndrome. Understanding of the basic biology and natural history of these tumors has increased substantially over the past decade. Accordingly, medical and surgical management of desmoid tumors has also evolved. This paper analyzes recent evidence pertaining to the epidemiology, molecular biology, histopathology, screening, and treatment of extra-abdominal desmoid tumors associated with familial adenomatous polyposis syndrome.
Microsatellite Instability in Sarcoma: Fact or Fiction?
Michael J. Monument,Stephen L. Lessnick,Joshua D. Schiffman,Rl. Tx. Randall
ISRN Oncology , 2012, DOI: 10.5402/2012/473146
Abstract:
Extra-Abdominal Desmoid Tumors Associated with Familial Adenomatous Polyposis
George T. Calvert,Michael J. Monument,Randall W. Burt,Kevin B. Jones,R. Lor Randall
Sarcoma , 2012, DOI: 10.1155/2012/726537
Abstract: Extra-abdominal desmoid tumors are a significant cause of morbidity in patients with familial adenomatous polyposis syndrome. Understanding of the basic biology and natural history of these tumors has increased substantially over the past decade. Accordingly, medical and surgical management of desmoid tumors has also evolved. This paper analyzes recent evidence pertaining to the epidemiology, molecular biology, histopathology, screening, and treatment of extra-abdominal desmoid tumors associated with familial adenomatous polyposis syndrome. 1. Introduction Desmoid tumors (DTs), also known as aggressive fibromatosis, are fibroblastic neoplasms which are often locally aggressive but lack metastatic potential. They may occur sporadically or in association with familial adenomatous polyposis (FAP) syndrome. Among individuals with FAP, desmoids most frequently occur in intra-abdominal and abdominal wall locations with most arising from the peritoneum. These abdominal desmoids range in severity from indolent, asymptomatic lesions to highly invasive, sometimes fatal tumors. Although less common than abdominal desmoids and very rarely fatal, extra-abdominal desmoids are also a significant cause of morbidity in this population. This paper will review recent developments in the diagnosis, screening, treatment, and prognosis of FAP-associated extra-abdominal DTs. 2. Epidemiology of FAP-Associated Desmoid Tumors The overall incidence of DTs has frequently been quoted at 2–4 per million people per year [1, 2]. This estimate is derived from a 1986 Finnish study which used the pathologic records of several regional hospitals and their known catchment area populations to calculate an incidence figure [3]. Recently, the Dutch national pathology database was analyzed, and 519 total desmoid cases in patients over the age of ten were identified from 1999 to 2009. There were 480 sporadic DTs and 39 FAP-DTs. The annual incidence was 3.7 per million overall [4] consistent with the earlier Finnish study. The same nationwide study from The Netherlands identified 1400 patients over the age of ten with FAP during the 1999 to 2009 period. FAP-associated DTs (FAP-DTs) made up 7.5% of all DTs, and the relative risk of an FAP patient developing a DT was over 800-fold higher than the general population [4]. The Dutch study was limited by the use of pathologic specimens as many DTs may be identified based upon history, physical exam, and imaging but not biopsied or surgically excised especially in the FAP cohort. Additionally, some individuals with sporadic DTs may have had as yet
Lost in Translation: Ambiguity in Nerve Sheath Tumor Nomenclature and Its Resultant Treatment Effect
Nicholas M. Bernthal,Kevin B. Jones,Michael J. Monument,Ting Liu,David Viskochil,R. Lor Randall
Cancers , 2013, DOI: 10.3390/cancers5020519
Abstract: There is much ambiguity surrounding the diagnosis of nerve sheath tumors, including atypical neurofibroma and low-grade MPNST, and yet, the distinction between these entities designates either benign or malignant behavior and thus carries presumed profound prognostic importance that often guides treatment. This study reviews the diagnostic criteria used to designate atypical neurofibroma from low-grade MPNSTs and reviews existing literature the natural history of each of these tumors to see if the distinction is, in fact, of importance.
Microsatellite Instability in Sarcoma: Fact or Fiction?
Michael J. Monument,Stephen L. Lessnick,Joshua D. Schiffman,Rl. Tx. Randall
ISRN Oncology , 2012, DOI: 10.5402/2012/473146
Abstract: Microsatellite instability (MSI) is a unique molecular abnormality, indicative of a deficient DNA mismatch repair (MMR) system. Described and characterized in the colorectal cancer literature, the MSI-positive phenotype is predictive of disease susceptibility, pathogenesis, and prognosis. The clinical relevance of MSI in colorectal cancer has inspired similar inquisition within the sarcoma literature, although unfortunately, with very heterogeneous results. Evolving detection techniques, ill-defined sarcoma-specific microsatellite loci and small study numbers have hampered succinct conclusions. The literature does suggest that MSI in sarcoma is observed at a frequency similar to that of sporadic colorectal cancers, although there is little evidence to suggest that MSI-positive tumors share distinct biological attributes. Emerging evidence in Ewing sarcoma has demonstrated an intriguing mechanistic role of microsatellite DNA in the activation of key EWS/FLI-target genes. These findings provide an alternative perspective to the biological implications of microsatellite instability in sarcoma and warrant further investigation using sophisticated detection techniques, sensitive microsatellite loci, and appropriately powered study designs. 1. The Essence of Microsatellite DNA The biological precedence of tandem nucleotide repeats scattered throughout the human genome has intrigued scientific inquiry since these genetic elements were first characterized in the early 1980s. More precisely, the term microsatellite DNA refers to tandem iterations of simple sequence motifs dispersed throughout the genome. The majority of microsatellite DNA is comprised of mono-, di-, tri- and tetra-nucleotide repeats, and these repetitive elements constitute ~3% of the human genome [1]. Current estimates suggest that there are approximately one million microsatellite loci within the human genome, and the vast majority of these sequences are situated within noncoding regions such as intronic and intergenic segments. Consequently, microsatellite DNA has been long regarded as “junk DNA” with a poorly understood biological function. The repetitive nature of microsatellite DNA renders it more susceptible to mutagenesis during DNA replication and furthermore, the lack of evolutionary pressure on these noncoding regions has licensed an impressive rate of microsatellite polymorphisms in the human population overtime. Compared to coding regions of the genome, microsatellite loci are genetically diverse, characterized by high heterozygosity indices and numerous alleles for any given loci
Microsatellites with Macro-Influence in Ewing Sarcoma
Michael J. Monument,Kirsten M. Johnson,Allie H. Grossmann,Joshua D. Schiffman,R. Lor Randall,Stephen L. Lessnick
Genes , 2012, DOI: 10.3390/genes3030444
Abstract: Numerous molecular abnormalities contribute to the genetic derangements involved in tumorigenesis. Chromosomal translocations are a frequent source of these derangements, producing unique fusion proteins with novel oncogenic properties. EWS/ETS fusions in Ewing sarcoma are a prime example of this, resulting in potent chimeric oncoproteins with novel biological properties and a unique transcriptional signature essential for oncogenesis. Recent evidence demonstrates that EWS/FLI, the most common EWS/ETS fusion in Ewing sarcoma, upregulates gene expression using a GGAA microsatellite response element dispersed throughout the human genome. These GGAA microsatellites function as enhancer elements, are sites of epigenetic regulation and are necessary for EWS/FLI DNA binding and upregulation of principal oncogenic targets. An increasing number of GGAA motifs appear to substantially enhance EWS/FLI-mediated gene expression, which has compelling biological implications as these GGAA microsatellites are highly polymorphic within and between ethnically distinct populations. Historically regarded as junk DNA, this emerging evidence clearly demonstrates that microsatellite DNA plays an instrumental role in EWS/FLI-mediated transcriptional regulation and oncogenesis in Ewing sarcoma. This unprecedented role of GGAA microsatellite DNA in Ewing sarcoma provides a unique opportunity to expand our mechanistic understanding of how EWS/ETS fusions influence cancer susceptibility, prognosis and transcriptional regulation.
Population, Development and Deforestation in Songea District, Tanzania  [PDF]
Michael J. Haule
Natural Resources (NR) , 2014, DOI: 10.4236/nr.2014.51004
Abstract:

Deforestation is a phenomenon that forms part of environmental degradation. The fact that deforestation is both a source and contributor to global warming, as it reduces the carbon sinks, cannot be contested [1]. A case study research was carried out in Songea Tanzania aimed at establishing whether there was differential participation of people of different demographic characteristics in those activities that lead into tree cover decline. The study revealed that people of different age group and, sex categories played different roles in activities that lead to deforestation such as felling trees for firewood and felling trees for establishing and/or for expanding farms. It was observed that age group and sex categories influenced one’s involvement or participation in deforestation thus contributing differently by both activity and degree of forest cover reduction. This literally means that people of different demographic characteristics of age and sex contributed differently to the ailing deforestation process. From this end, it is logical and implicit arguing that the identification of actors in deforestation-related activities confirms the disaggregated manner by which population acts on the environment. Development of blanket conservation packages that are not focused on age group and sex categories of members the population in question remains too general and in-effective. To be precise, the planning and implementation of effective conservation initiatives has to take into account demographic characteristics of the population in question. The observed reality is that the population engages with the environment not as a unit but in its disaggregated manner, i.e. based on its demographic sub-categories [2]. The theory behind a successful conservation initiative is based on unveiling the mechanism by which population acts when resulting to deforestation.

The Effect of NeuroGen® Nerve Support Supplement on Pillar Pain after Endoscopic Carpal Tunnel Release  [PDF]
Michael J. Fitzmaurice
Modern Plastic Surgery (MPS) , 2014, DOI: 10.4236/mps.2014.41002
Abstract:

61 patients with clinically diagnosed and electromyographically confirmed carpal tunnel syndrome were enrolled in a prospective study to evaluate the effectiveness of a nerve supplement on pillar pain after carpal tunnel surgery. All of the patients underwent endoscopic carpal tunnel release. 15 of the patients also took the nerve support supplement NeuroGen? as part of their perioperative treatment. The supplement group demonstrated a significantly lower amount of pillar pain (VAS) at initial follow up compared to the control group (1.13 and 4.05 respectively). 46% (7/15) of the supplement group were completely free of pillar pain compared to only 9% (4/46) of the control group at the first follow up. 53% (8/15) of the NeuroGen? group did not require any pain medications compared to 35% (16/46) of the control group. The Nerve supplement NeuroGen? significantly reduces pain after carpal tunnel surgery.

Changes in Human Population Characteristics and Environmental Change in the West Matogoro Catchment Area of Songea, Tanzania  [PDF]
Michael J. Haule
Natural Resources (NR) , 2014, DOI: 10.4236/nr.2014.512064
Abstract: The study was carried out in West Matogoro Catchment Area (WMCA) of Songea, Tanzania, to establish whether for the period between intercensal periods 1978-1988 and 1988-2002, and between 2002 and 2005 characteristics of human population of the area had changed in terms of size, age structure and sex composition. In case it did, then the study had to establish whether such changes may be used to explain the observed forest cover change that occurred in the area. Establishing whether the observed changes were proportionate was important in linking the relationship among factors at hand. The study partly tested the thesis by Liu and others which linked human population changes and their implications to the panda habitat [1]. The findings indicated existence of changes in human population characteristics for the period under review. Variations in terms of population size, age structure and sex composition were realized. While growth was measured by the total population and size of age group of the environmentally active population as identified by the study by Haule, sex composition was determined by sex ratios [2]. The environmentally active age group included males aged 20 to 44 and females aged 10 to 44, i.e. the key actors in felling trees for farm expansion and for firewood respectively. Geographic Information System (GIS) evidence indicated progressive forest cover deterioration. When compared, the changes in human population characteristics and those of the forest cover were noted to be un-proportional. Variations were in terms of increase in human population size and expansion of age group of the “actors” thus attributed to the augmenting deforestation. A positive relationship was demonstrated between population growth, expansion of age segment of the key actors and expanded deforestation. We reiterate that any sustainable measures to address the environmental issues should take into account changes in demographic characteristics of the in Situ population which forms the locus of the interface between population and environment. These factors signify the intensity and duration of the involved forces that characterize forest cover quality.
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