3.2 Aging . The Physiology Of Aging Hematopoiesis Represents

Cancer is described as the abnormal growth of cells. Normal cells are replaced with abnormal cells in which their deoxyribonucleic acid (DNA) has been damaged or augmented (McCance & Huether, 2014). Cancer cells with their various DNA changes are characterized by growing uncontrollably, being immortal with an unlimited lifespan

When a tumor suppressor gene is effected by a mutation, it loses its control over the cell and the cell does not stop to get inspected. When this happens, the mutation is copied, the cell divides and damage is passed down to the newly formed daughter cells. The mutation then becomes permanent and the now mutated cell will continue to divide and proliferate when it normally would not.

The changes that occur in the niche are more important than in stem cells themselves when it comes to the failure of stem cell activity with aging. (Fowler, 2012)

Cancer is a disease caused by an uncontrolled division of abnormal cells. The DNA sequence in cells can be changed as a result of copying errors during replication. If these changes whatever their cause are left uncorrected, both growing and non-growing somatic cells might gain many mutations that they could no longer function. The relevance of DNA damage and repair to the generation of cancer was obvious when it was recognized that everything that causes cancer also cause a change in the DNA sequence. Tumor suppressor genes are protective genes and normally they limit cell growth by monitoring the speed of cell division, repair mismatched DNA and control when a cell dies. When a tumor suppressor gene is mutated cells grow

“Myelodysplastic syndromes are a group of disorders caused by poorly formed or dysfunctional blood cells.” (Mayo Clinic 2015) Myelodysplastic syndromes, also known as bone marrow failure syndromes, occur when the bone marrow is not doing its job of providing enough functional, healthy blood cells. These syndromes generally occur with geriatric patients, and are responsible for a host of issues such as abnormal bleeding, infection, bruising, and anemia. People with these syndromes generally present with some form of cytopenia, whether it be anemia, neutropenia, or thrombocytopenia. MDS causes the cells produced to usually have shorter life spans, resulting in less mature blood cells making it out into the circulatory system. These cells tend to have abnormal shapes and appearances in addition to their failure to function correctly. MDS is a progressive disease, and generally is not considered terminal, although some patients will progress into acute myeloid leukemia as a result of the disease. Unlike some other syndromes, MDS is not inherited, and there are many risk factors that will be discussed later that can exacerbate this illness.

Moreover, it’s important to understand that gene mutation occurs in our cell all the time. Accordingly, the prevention of cancer is profoundly dependent on the p53 tumour suppressor protein, which is the process to eliminate excess, damaged or infected cells by apoptosis (Haupt 2003). But if the cell doesn’t die in the process of apoptosis, it may lead a person to developing a cancer. Oncogene are a sequence of deoxyribonucleic acid (DNA) that has been altered or mutated from its original form and induces cancer (Encyclopaedia Britannica 2017). Some people have high risk of developing cancer because they inherited mutations in certain genes (Cancer research UK 2014). Mutation are classified into two, inherited and acquired types of mutation, widely discussed below (ASCO 2017)

Though initial treatment of acute lymphoblastic leukemia (ALL) leads to clinical and hematological remission, 20% of pediatric ALL patients and over 50% of adult ALL patients relapse and cannot achieve remission even after intensified therapy, making disease relapse and resistance to therapy the greatest challenge. This study aims to determine the cellular and genetic mechanisms, specifically with NT5C2, responsible for drug resistance and relapse in ALL. It was hypothesized that relapse-associated NT5C2 mutations may represent gain-of-function alleles with increased enzymatic activity.

Aging is an important factor that impairs humans’ brains structurally and functionally thus leads to cognitive disorders which negatively affect elder people’s normal life. Previous studies have shown that exposing aged animals to young blood can enhance stem cell function in various organs such as liver and brain. Inspired by these studies, Villeda and co-researchers want to find out if exposure to young blood can counteract age-related impairments and enhance aged brains. In Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice, Villeda and co-researchers work with mice to study the effects of exposure to young blood on the aged mice’s brains. Villeda’s research focuses on the hippocampus, a

This article deconstructs the evolution of a tumor during the response to treatment in a retrograde fashion. This information is crucial for this paper because it shows a step by step application of how a particular mutation was assessed. Chromosomal changes are of significant importance since the research being conducted is about genetic markers and what

Genomic profiling has furthered research and understanding of this complex disease process by identifying further tumor subtypes and molecular alterations of the disease. (Stopeck, 2009). Based upon the specific gene

Hematopoiesis is maintained by the renewal of multipotent hematopoietic stem cells that give rise to lineage committed cells. Hematopoietic stem cells are controlled in in the bone marrow, where they reside in a quiescent state (Baker 2014). Hematopoietic transcription factors play a crucial role in the proliferation and commitment of hematopoietic stem cells and during the differentiation into their mature progeny. According to the stochastic model of hematopoiesis, long term hematopoietic stem cells that undergo extensive self-renewal begin to differentiate into short term hematopoietic stem cells with limited self-renewing potential (Baker 2014). Short term hematopoietic stem cells further differentiate into multipotent progenitors that

Cancer occurrs by the production of multiple mutations in a single cell that causes it to proliferate out of control. Cancer cells often different from their normal neighbors by a host of specific phenotypic changes, such as rapid division rate, invasion of new cellular territories, high metabolic rate, and altered shape. Some of those mutations may be transmitted from the parents through the germ line. Others arise de novo in the somatic cell lineage of a particular cell. Cancer-promoting mutations can be identified in a variety of ways. They can be cloned and studied to learn how they can be controlled.

While biologists in the field of aging, known as biogerontologists, work earnestly to understand and investigate the fundamental biology of aging, there are anti-aging entrepreneurs capitalizing on vulnerable populations with false promises of longevity and the fountain of youth. In an attempt to educate the public, and differentiate the pseudoscientists from the legitimate biologists, three scientists published an article stating there was no marketed intervention that could slow, stop, or reverse the aging process, and cautioned that some products may even be dangerous (Binstock, 2003). An international roster of 51 physicians and scientists endorsed these biogerontologists in a position statement expressing the biological research that has been done, and the lack of interventions currently available to slow the progression of aging. The position statement was published in several scientific journals and a summarized version of this statement was published in the AARP bulletin,

In MDS/MPN cases, either normal karyotype or MDS-related chromosome abnormalities have been reported. A high percentage of MDS/MPN patients harbor identifiable mutations in genes recurrently mutated across myeloid neoplasms when undergoing either targeted-panel mutation analysis or whole-exome sequencing with next-generation sequencing technology but no disease defining mutations have been reported [9]. Mutation analysis has emerged as an important ancillary test to accompany a diagnosis of MDS/MPN; especially in the absence of cytogenetic chromosome abnormalities because these may serve as a critical clonality marker confirming its neoplastic nature essential for the diagnosis of a myeloid neoplasm. CMML, among the most well-documented in this group, harbor mutations in genes that include SRSF2, TET2, and ASXL1 in up to 50% of cases, respectively[9, 10]. Mutations in ASXL1 have also been reported as an independent prognostic factor along with other clinicopathologic parameters in a multivariable model [10]. Mutation analysis including these genes can greatly facilitate the diagnosis and prognostic stratification of CMML [11]. However, a more conservative approach toward the mutation analysis results is warranted in older individuals lacking definitive evidence of a myeloid neoplasm, since it is known the presence of mutations in similar set of genes can be identified in such patients [12,

New information about cancer genetics has proliferated, as have cancer cell lines for testing that information.