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Head and Neck Carcinogenesis a Product of Complex Evolutionary Forces

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Head & Neck Cancer: Current Perspectives, Advances, and Challenges

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Abstract

This chapter explores carcinogenesis of the head and neck as a product of biologic forces present in micro and macroenviroments. We attempt to present dynamic complex characteristics of head and neck tissues in a framework that explores ecologic selection as a means to understand and explain the risk for cancer. We contend problems with diagnosis and treatment responses results from an inattention to environmental interactions and their impact upon malignant transformation and reversal to a normal physiologic state. Furthermore an emphasis is placed on Darwinism and ecologic selection that determine functional roles and activities of keratinocytes derived from the proliferative stratum of mucosa in response to changes in head and neck environments. In addition, we consider unique features; such as, microbiome, fluids (e.g., saliva, transudate, exudates), epithelial mucosa biology, and immune responses to provide a broader picture for the influence of evolutionary, chemical, and physiologic changes upon head and neck cells and tissues during carcinogenesis.

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Abbreviations

HNSCC:

head and neck squamous carcinoma

OSCC:

oral squamous cell carcinoma

ST:

smokeless tobacco

PAH:

polycyclic aromatic hydrocarbons

TSNA:

tobacco specific nitrosamines

HPV:

human papilloma virus

HHV:

herpes virus

$NQO:

4-Nitroquinoline-1-oxide

MDR:

drug resistant gene

ABC:

ATP-binding protein cassette

XRE:

xenobiotic responsive element

ADH:

alcohol dehydrogenase

ALDH:

aldehyde dehydrogenase

CYP450 :

cytochrome P450

GST:

glutathione-S-transferase

Rb:

retinoblastoma

NF-kB:

nuclear factor kappa-light-chain-enhancer of activated B cells

c-fos:

cell Finkel osteogenic gene

c-jun:

cell JNK related gene

AP-1:

activator protein-1

ATF:

activator transcription factor

JDP:

AP-1 repressor protein

IP3:

Inositol-1,4,5 trisphosphate

MAPK:

mitogen activator protein kinase

E2F:

elongation factor 2

PCNA:

proliferation cell nuclear antigen

E6/E7:

early HPV proteins 6 and 7

NOTCH1:

Notch homolog 1, translocation-associated (Drosophila)

TP63:

tumor protein 63

IF6:

Interferon regulatory factor 6

ARF:

Alternate reading frame of INK4a/ARF locus (CDKN2A)

Nanog:

homeoprotein embryonic stem cell transcription factor

AKT:

Protein Kinase B (PKB), is a serine / threonine protein kinase

PTEN:

Phosphatase and tensin homolog

mTor:

mammalian target of rapamycin

CpG:

cytosine guanine phosphodiesterase islands

TTP:

mpRNA decay factor tristetraprolin

HWE:

Hardy-Weinberg equilibrium

RR:

relative risk

CI:

confidence interval

SNP:

single polymorphic polymorphism

ETOH:

ethyl alcohol

AA:

acetaldehyde

IgA, IgG, IgM:

immunoglobulins A, G, and M

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Authors and Affiliations

  1. Department of Oral Medicine and Diagnostic Sciences, College of Dentistry, 801 S. Paulina Street, Chicago, IL, 60612, USA

    Joel Schwartz

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    James A. Radosevich

Glossary

Fitness

Adaptive optimum phenotype and is the contribution of progeny to next generations. Fitness can also be described by a probability and an array of x phenotypes in a specific environment.

Cryptic Genetic Variation

Genetic variation that does not contribute to range of phenotypes under standard environmental conditions but becomes important ­under changes in environment.

Evolvability

ability of cell or individual to respond to natural or inducible selection. This dependent upon complexity, degeneracy, and robustness. A product of phenotype and genotype in an environment.

Robustness

Invariance of phenotype as a product of genetic and environment.

Pleiotropy

effect of a single genetic locus to produce multiple phenotypic variations for enhanced survival.

Field cancerization

a single mutated stem cell can expand into adjacent expanding clones of cells and produce a tumor mass. This principal asserts that development of a predominant clinical cancer in the head and neck does not completely describe a level of transformation because there are many other sites of malignant transformation identified by chromosomal of gene changes that have not attained clinical relevance.

Senescence

cells in G0, resting phase.

Driver mutations

mutations provide a selective growth advantage to the cell.

Passage mutations

Mutations do not alter fitness but occur coincidentally or subsequently acquired a driver mutation. Passenger mutations occur in every cell that has a driver mutation.

Gatekeeper

gene is an “oncogene”, regulator of cell growth, differentiation and nuclear stability.

Tumor suppressor gene

put the brakes on cancer induction process.

Pluripotential_stem cell populations

high degree of activity which permits differentiation to ectoderm, endoderm mesoderm or neuro-ectoderm.

Phenotypic variation

maintains germ cell line origin (e.g., ectoderm) although offering an opportunity for progression of dedifferentiation.

Epigenetic modifications

These can include methylation regulation of cytosine bases in cytosine guanine islands (e.g., CpG sites) that assist in regulation of expression, but also accompanied by changes in acetylation of histones and phosphorylation of various purine bases that can silence tumor suppressor genes.

Genetic drift

a product of random sampling, which also contributes to phenotypic variability.

Hardy-Weinberg equilibrium (HWE) and disequilibrium

information regarding evolvability of organisms in selected environments to determine selection of the fittest in a particular microenvironment.

Fitness landscape

a stable local maxima for each cell and population until another selective change is introduced.

Allelic frequency

determine a fraction of the copies of one gene shared among offspring to determine genetic drift in a population of know parental genotypes.

Relative risk

a risk assessment for an event relative to exposure compared to a normal environment.

Founder’s effect

cell survivors with an opportunity for selective populations to proliferate from a larger population.

Lotka-Volterra

prey and predator based systems.

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Schwartz, J. (2013). Head and Neck Carcinogenesis a Product of Complex Evolutionary Forces. In: Radosevich, J. (eds) Head & Neck Cancer: Current Perspectives, Advances, and Challenges. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-5827-8_14

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