Evolutionary information dynamics of cancer--论文代写范文精选

率失真参数发现,在疾病过程中，较大的系统能够描述一个自己的形象,加速突变率,和抑郁的突变控制。动力学是类似于简单的进化系统间断平衡,占疾病进展的上位。下面的essay代写范文进行讲述。

Abstract 
‘Racial’ disparities among cancers, particularly of the breast and prostate, are something of a mystery. For the US, in the face of slavery and its sequelae, centuries of interbreeding has greatly leavened genetic differences between ‘Blacks’ and ‘whites’, but marked contrasts in disease prevalence and progression persist. ‘Adjustment’ for socioeconomic status and lifestyle, while statistically accounting for much of the variance in breast cancer, only begs the question of ultimate causality. Here we propose a more basic biological explanation that extends the theory of immune cognition to include an elaborate tumor control mechanism constituting the principal selection pressure acting on pathologically mutating cell clones. 

The interplay between them occurs in the context of an embedding, highly structured, system of culturally-specific psychosocial stress. A Rate Distortion argument finds that larger system able to literally write an image of itself onto the disease process, in terms of enhanced ‘risk behavior’, accelerated mutation rate, and depressed mutation control. The dynamics are analogous to punctuated equilibrium in simple evolutionary systems, accounting for the staged nature of disease progression. We conclude that ‘social exposures’ are, for human populations, far more than incidental cofactors in cancer etiology. Rather, they are part of the ‘basic biology’ of the disorder. The aphorism that ‘culture is as much a part of human biology as the enamel on our teeth’ appears literally true at a fundamental cellular level. 
KEY WORDS: Cancer, cellular cognition, culture, evolution, information theory, interpenetration, mutator, punctuation, renormalization, second order selection, tumorigenesis, universality.

Introduction 
Cardiovascular disease and cancer are major causes of mortality in the United States structured by ‘race’, class, and gender [28]. Cancers of the breast and prostate - ‘hormonal’ cancers - particularly show large disparities by ethnicity and economic class in incidence among young adults, stage at presentation, and mortality rate (e.g. [39]). Although certain genetic alleles predispose individuals to higher susceptibility for these cancers (e.g. [23] for prostate cancer), recent changes of incidence and mortality in time and geography indicate genes alone do not explain the expressed population-level patterns. 

At present, African-American women under age 35 suffer an approximately two-fold higher age-specific rate of breast cancer, compared to white women, and the mortality rate is about three times higher [44]. For prostate cancer, African-American men have a 2-fold higher mortality rate, and 50 percent higher incidence rate, than their white counterparts [43]. During the 1980’s, when ideologies of individualism particularly influenced US scientific thinking, interest in health differentials waned. In its stead, the life style doctrine arose: people get sick because they don’t take responsibility for their own health. 

The connection between diet and breast cancer was an often-cited example of how life style affects health. By the 1990’s, however, a large literature on determinants of risk behaviors explored the bases of ‘life style’ decisions and found them rooted in social and economic processes (e.g. [11, 22, 30, 58, 59]). Many of the risk behaviors associated with AIDS, drug abuse, and violence, were shown to be coping mechanisms for dealing with frustration, pain, deprivation, humiliation, and danger (e.g. [7, 58, 59]). 

The particular modes of coping spread, first between social networks and then within social networks by branching processes [32]. Indeed, one of the classic studies of drug use, The Heroin Epidemics, described all these contagious small-scale processes early on [29]. Risk behaviors may explain part of the pattern in hormonal cancers. Such behaviors, however, may not totally explain population differentials in hormonal cancer incidences and mortality rates. We propose an approach that more fully integrates the biocultural processes that shape the development of humans, their cancers, and differentials in both their susceptibility and pathways of disease progression. We begin with Nunney’s [37] evolutionary history of cancer, as opposed to more conventional local evolutionary dynamic theories of tumorigenesis within an organism (e.g. [8]). Nunney’s analysis suggests that in larger animals, whose lifespans are proportional to about the 4/10 power of their cell count, prevention of cancer in rapidly proliferating tissues becomes more difficult in proportion to their size. Cancer control requires the development of additional mechanisms and systems to address tumorigenesis as body size increases – a synergistic effect of cell number and organism longevity.

Nunney’s work implies, in particular, that different tissues may have evolved markedly different tumor control strategies. All of these, however, are likely to be energetically expensive, permeated with different complex signaling strategies, and subject to a multiplicity of reactions to signals. For modern humans, large animals whose principal selective environment is other 3 humans, this suggests a critical role for the ‘signal’ of psychosocial stress, as mediated by a local ‘sociocultural network’, i.e. an embedding cognitive social structure linked to a cultural practice and history. Contemporary evolutionary anthropology (e.g. [18]) emphasizes that culture, largely defining what social relations are particularly helpful or stressful, has become inextricably intertwined with human biology. 

Recent analysis (e.g. [21]) suggests that psychosocial stress is a very strong signal indeed and severally affects the stages of mutation control: immune surveillance, both DNA damage and repair, apoptosis, and rates of somatic mutation – the ‘mutator phenotype’ we will explore at length below. Atlan and Cohen [3] and Cohen [12] go even further, finding the immune system is itself cognitive. The immune system compares incoming signals of immune challenge with a stored picture of the world in a kind of immune memory and then chooses a fairly precise response from a much larger repertoire. We have extended this characterization [53, 56] to show how an embedding sociocultural network, the local ‘extended family’ in which every human finds him or herself, can interact with both an individual’s central nervous and immune systems. We characterize this synergism as a ‘cognitive condensation’ that links social to psychoneuroimmunologic function. According to our analysis, a systematic pattern of externally-imposed stressors constitutes a ‘language’ that can interact with this condensation. The ‘signal’ of imposed coherent stress then literally writes a distorted image of itself onto the cognitive condensation, and ultimately onto the functioning of the immune system.

Here we will extend that work to look at the effect of structured external stress on tumorigenesis. We will describe the ‘local evolution’ of cancer within a tissue in terms of a ‘punctuated interpenetration’ between a tumorigenic mutator mechanism and an embedding cognitive process of mutation control, including but transcending immune function. Punctuated biological processes are found up and down temporal scales. Evolutionary punctuation is a modern extension of Darwinian evolutionary theory that accounts for the relative stability of a species’ fossil record between the time it first appears and its extinction (e.g. [24]). Species appear ‘suddenly’ on a geologic timescale, persist relatively unchanged for a fairly long time, and then disappear suddenly, again on a geologic timescale. Evolutionary process is vastly speeded up in tumorigenesis, but we believe it to be subject to a version of ‘punctuation’ that accounts for the staged nature of the disease.

In essence, the mutation control process constitutes the Darwinian selection pressure determining the fate of the (path dependent) output of the mutator. Externally-imposed structured psychosocial stress then jointly increases mutation rate while decreasing mutation control effectiveness through an additional level of punctuated interpenetration. We envision this as a single, interlinked process, and, extending Nunney’s work, find the evolutionary anthropologist Robert Boyd’s aphorism that ‘culture is as much a part of human biology as the enamel on our teeth’ likely true at the level of very basic biological mechanisms. For human populations, different forms of ‘social exposures’ can act as carcinogens. Hormonal cancers, since they explicitly involve ‘signaling molecules’, should be especially amenable to the information dynamics formalism we have adapted to our analysis. The central mystery we are addressing does not involve such detailed questions as the relationship between metastatic spread and primary tumor size or the like. We are, instead, focusing on the basic biology of populationlevel differences in disease expression. However, the approach does provide an explanation of the temporally staged nature of cancer, in terms of multiple phase-change-like punctuations.（essay代写)

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