Clonal expansion

Recent sequencing studies on healthy skin and esophagus have found that, as we age, these tissues become colonized by mutant clones of cells carrying driver mutations in traditional cancer genes. This comment summarizes these findings and discusses their possible implications for our understanding of cancer, ageing, and other diseases.

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The classical genetic model of colorectal cancer presents APC mutations as the earliest genomic alterations, followed by KRAS and TP53 mutations. However, the timing and relative order of clonal expansion and other types of genomic alterations, such as genomic rearrangements, are still unclear.

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The integration of a viral genome into the host genome has a major impact on the trajectory of the infected cell. Integration location and variation within the associated viral genome can influence both clonal expansion and persistence of infected cells.

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Increased reports of Neisseria meningitidis urethritis in multiple U.S. cities during 2015 have been attributed to the emergence of a novel clade of nongroupable N. meningitidis within the ST-11 clonal complex, the “U.S. NmNG urethritis clade”. Genetic recombination with N. gonorrhoeae has been proposed to enable efficient sexual transmission by this clade. To understand the evolutionary origin and diversification of the U.S. NmNG urethritis clade, whole-genome phylogenetic analysis was performed to identify its members among the N.

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Bacterial cells during many replication cycles accumulate spontaneous mutations, which result in the birth of novel clones. As a result of this clonal expansion, an evolving bacterial population has different clonal composition over time, as revealed in the long-term evolution experiments (LTEEs).

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Genetic aberrations are required for the progression of HPV-induced cervical precancers. A prerequisite for clonal expansion of cancer cells is unlimited proliferative capacity. In a cell culture model for cervical carcinogenesis loss of genes located on chromosome 4q35→qter and chromosome 10p14-p15 were found to be associated with escape from senescence.

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Adipogenesis is accomplished via a complex series of steps, and the events at the earliest stage remain to be elucidated. To clarify the molecular mech-anisms of adipocyte differentiation, we previously isolated 102 genes expressed early in mouse 3T3-L1 preadipocyte cells using a PCR subtrac-tion system.

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Abstract To overcome loss of stem-like properties and spontaneous differentiation those hinder the expansion and application of human mesenchymal stem cells (hMSCs), we have clonally isolated permanent and stable human MSC lines by ectopic overexpression of primary cell cultures of hMSCs with HPV 16 E6E7 and human telomerase reverse transcriptase (hTERT) genes. These cells were found to have a differentiation potential far beyond the ordinary hMSCs. They expressed trophoectoderm and germline specific markers upon differentiation with BMP4 and retinoic acid, respectively.

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Table 125-3 Controlling Antibiotic Resistance: Approaches to Consider Conduct surveillance for antibiotic resistance. Perform molecular typing (e.g., pulsed-field gel electrophoresis) when rates increase. For clonal expansion (e.g., single-strain outbreaks): Stress hand hygiene (alcohol hand rub and universal gloving); monitor adherence and give feedback. For polyclonal expansion (e.g., multistrain outbreaks): Stress antibiotic prudence (consider antibiotic rotation for ICUs); monitor adherence and give feedback.

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Chronic Myelogenous Leukemia Incidence The incidence of chronic myelogenous leukemia (CML) is 1.5 per 100,000 people per year, and the age-adjusted incidence is higher in men than in women (2.0 versus 1.2). The incidence of CML increases slowly with age until the middle forties, when it starts to rise rapidly. CML incidence for males decreased slightly (4.4%) between 1997 and 2003 as compared to 1977–1997. Definition The diagnosis of CML is established by identifying a clonal expansion of a hematopoietic stem cell possessing a reciprocal translocation between chromosomes 9 and 22.

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