An introduction to the progeria a disease which occurs in children and the product is rapid aging

Ageing versus immortality[ edit ] Immortal Hydra, a relative of the jellyfish Human beings and members of other species, especially animals, necessarily experience ageing and mortality. Fungi, too, can age.

An introduction to the progeria a disease which occurs in children and the product is rapid aging

A decade ago it was possible to hope that targetable oncogenes, such as activated tyrosine kinases, might be identified in a high percentage of childhood cancers.

However, it is now clear that the genomic landscape of childhood cancer is highly varied, and in many cases is quite distinctive from that of the common adult cancers. There are examples of genomic lesions that have provided immediate therapeutic direction, including the following: ALK point mutations associated with a subset of neuroblastoma cases.

BRAF and other kinase genomic alterations associated with subsets of pediatric glioma cases.

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And, for the health professionals who serve them. Many topics and insights I would now include are missing.

Hedgehog pathway mutations associated with a subset of medulloblastoma cases. For some cancers, the genomic findings have been highly illuminating in the identification of genomically defined subsets of patients within histologies that have distinctive biological features and distinctive clinical characteristics particularly in terms of prognosis.

In some instances, identification of these subtypes has resulted in early clinical translation as exemplified by the WNT subgroup of medulloblastoma. Because of its excellent outcome, the WNT subgroup will be studied separately in future medulloblastoma clinical trials so that reductions in therapy can be evaluated with the goal of maintaining favorable outcome while reducing long-term morbidity.

However, the prognostic significance of the recurring genomic lesions for some other cancers remains to be defined. A key finding from genomic studies is the extent to which the molecular characteristics of childhood cancers correlate with their tissue cell of origin.

As with most adult cancers, mutations in childhood cancers do not arise at random, but rather are linked in specific constellations to disease categories. A few examples include the following: The presence of H3.

An introduction to the progeria a disease which occurs in children and the product is rapid aging

The presence of RELA translocations in supratentorial ependymomas. The presence of specific fusion proteins in different pediatric sarcomas. Another theme across multiple childhood cancers is the contribution of mutations of genes involved in normal development of the tissue of origin of the cancer and the contribution of genes involved in epigenomic regulation.

Childhood Cancer Genomics (PDQ®)—Health Professional Version - National Cancer Institute

Structural variations play an important role for many childhood cancers. Translocations resulting in oncogenic fusion genes or overexpression of oncogenes play a central role, particularly for the leukemias and sarcomas. However, for other childhood cancers that are primarily characterized by structural variations, functional fusion genes are not produced.

Mechanisms by which these recurring structural variations have oncogenic effects have been identified for osteosarcoma translocations confined to the first intron of TP53 and medulloblastoma structural variants juxtapose GFI1 or GFI1B coding sequences proximal to active enhancer elements leading to transcriptional activation [enhancer hijacking].

Understanding of the contribution of germline mutations to childhood cancer etiology is being advanced by the application of whole-genome and exome sequencing to cohorts of children with cancer. The germline contribution to the development of specific cancers is discussed in the disease-specific sections that follow.

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Each section of this document is meant to provide readers with a brief summary of current knowledge about the genomic landscape of specific childhood cancers, an understanding that is critical in considering how to apply precision medicine concepts to childhood cancers.

Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma. Recurrent somatic structural variations contribute to tumorigenesis in pediatric osteosarcoma. Cell Rep 7 1: N Engl J Med Subclassification of childhood ALL. The genomic landscape of B-precursor ALL is typified by a range of genomic alterations that disrupt normal B-cell development and in some cases by mutations in genes that provide a proliferation signal e.

Genomic alterations leading to blockage of B-cell development include translocations e. Cases with recurring chromosomal translocations e. Activating point mutations in kinase genes are uncommon in high-risk B-precursor ALL, and JAK genes are the primary kinases that are found to be mutated. Childhood ALL is often polyclonal at diagnosis and under the selective influence of therapy, some clones may be extinguished and new clones with distinctive genomic profiles may arise.

The PRSP1 mutations observed in relapsed cases induce resistance to thiopurines in leukemia cell lines. CREBBP mutations are also enriched at relapse and appear to be associated with increased resistance to glucocorticoids. Specific genomic and chromosomal alterations are provided below, with a focus on their prognostic significance.

Some chromosomal alterations are associated with more favorable outcomes, such as high hyperdiploidy 51—65 chromosomes and the ETV6-RUNX1 fusion. Others historically have been associated with a poorer prognosis, including the Philadelphia chromosome t 9;22 q34;q These and other chromosomal and genomic abnormalities for childhood ALL are described below.

Chromosome number High hyperdiploidy 51—65 chromosomes High hyperdiploidy, defined as 51 to 65 chromosomes per cell or a DNA index greater than 1. In cases with a normal karyotype or in which standard cytogenetic analysis was unsuccessful, interphase fluorescence in situ hybridization FISH may detect hidden hyperdiploidy.

While the overall outcome of patients with high hyperdiploidy is considered to be favorable, factors such as age, WBC count, specific trisomies, and early response to treatment have been shown to modify its prognostic significance.

Certain patients with hyperdiploid ALL may have a hypodiploid clone that has doubled masked hypodiploidy. These patients have an unfavorable outcome, similar to those with hypodiploidy.Oxidative phosphorylation. Oxidative phosphorylation is the principal purpose of oxygen respiration and the principal use of breathed in oxygen to generate energy in the body.

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This Childhood Cancer Genomics summary provides a brief synopsis of current knowledge about the genomic landscape of specific childhood cancers. Get detailed information about various genetic alterations and precision medicine concepts in childhood cancers in this summary for clinicians.

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