Focusing primarily on the dopamine levels in obese (cancer/non cancer) patients, in vitro tumor culture studies and data from prostrate/ breast cancer patients - this report aims to hint at a possible mechanism which underlies cancer progression on the basis of the data from above studies and explain how obese TTY as a condition, fits In the mechanism of tumor progression. Introduction to obesity - The first aspect regarding obesity is the quantification of the physical condition called 'obese'.
For the purpose of this report (and for most of the studies referred to) - computer tomography generated measurements in the order of ?comma area in the central abdominal regions (I. E. - of visceral fat), Is defined as the condition for obesity. Alternatively, other quantifications, such as waste- Hip ratios, Body Mass Index, etc are also used to define or relate specific aspects of body structure to the condition of being obese or its relate deed metabolic syndromes. 9] Central (visceral) obesity is characterized by metabolic syndromes such as - insulin resistance, hyperglycemia, hyperventilates, displacement, hypertension, and problematic and protoplasm Tory states [81. All of which are fairly conditions that cause many complications in contemporaries occurring dies asses - however the focus of this report details the direct implications of obesity, and the molecules involved - followed by a generalization from this case-study on hormonal cancers. The molecular symptoms and effects of obesity on a patient's physiological system ar Fig. - Diagrammatic representation of some of the possible mechanisms for obesity- related prostate cancer progression. GIF-I = insulin-like growth factor 1; IL- 6 = interleukin 6; VEGA = vascular endothelial growth factor; GHB = sex- hormone binding globulin.  Molecular characteristics of obesity - The following are characteristics/by- products of obesity and their respective roles identified in various hormonal (prostrate/breast) cancer studies - Hypersensitiveness - Geiger serum levels of insulin results in decreased production of Sex-Hormone Binding Globulin (GHB).
GHB mediated inhibition of breast tumors has recently bee n identified in literature . Hence, this characteristic is analogous to loss-of- inhibition for breast-cancer cells. Also, it results in higher levels of free androgen's and estrogen - which have been implicated in proliferation of breast cancers, and progression of hormonal cancers in general. Decreased Testosterone levels - have significance in prostrate cancer, as lower testosterone levels have been associated with high- read prostrate cancers. The characteristic being of higher proliferation and less differentiation in the tumor. 2] Perpetuation of TNT-alpha - by virtue of higher levels of TNT- alpha in serum, there is higher susceptibility to inflammation and inflammation by itself has a potential role as a cancer promoting event at any given site. [Smith's Term Paper] Dopamine secretions by adipose tissue are covered with a few examples - o Lepton - is an dopamine secreted primarily by White Adipose Tissue (WATT), and has been shoo win to be active in the formation of reproductive tissue (including the prostrate). And has be en positively correlated with visceral obesity and large prostrate tumors .
Studies have shown that lepton promotes the proliferation of androgen- independent prostate cancer cell lines. It has also been shown to promote vascular endothelial cell profiler and misdiagnoses in vivo, processes that are crucial to allow cancer progression. Also, it has been positively correlated with increased prostrate cancer cell migration (implying invasion and metastasis) . Mechanism of action - The proliferation response of prostate cancer cells to lepton has been shown o involve intracellular signaling molecules such as physicality-instill 3- kinas (POP-K) and c-June NH-terminal kinas NON). 10] o Interleukin-6 - one third of the circulating level secretion of IL- 6 is from adipose tissue. It is directly proportional to visceral obesity and insulin resistance. Its normal role being in modulo action of immune response and cell-functions - it is basically a growth inhibitor. However, recently it has been shown to undergo a transition in its role from growth inhibitor associated with neuroscience differentiation to stimulator accompanied by androgen receptor cacti action in prostrate cancer progression .
Prostrate cancer cultures have been shown to secrete high levels of IL- 6, and it is believed that chronic exposure to this dopamine leads to loss-of-growth- inhibition in tumor cells. Serum IL-6 levels >7 pig/ ml are associated with a poor prognosis in men with prostate cancer. O Vascular Endothelial Growth Factor (VEGA) - VEGA levels are positively correlated with visceral obesity, and it is a potent nitrogen that allows for cell- migration, misdiagnoses and micro-vascular permeability. It hence, has a direct growth factor effect on tumor progression of all ski ads of cancer.
Aggressive high grade cancers all show high levels of VEGA secretions. It is why apotheosized that obesity driven elevation in VEGA levels is a potent priming event for all forms of c anger, specially hormonal cancers. O Depiction - this is an dopamine that is negatively correlated with obesity and visceral fat. It has been identified as a possible therapeutic agent in many obesity related metabolic co indications, such as diabetes, hypertension, etc. Hence, by virtue of its opposite nature to other adipose nest, it is hypothesized to be the 'anticancer' dopamine. It is also negatively correlated with high h grade prostrate and breast cancers.
The function of depiction is via its two primary receptors, which have a spatial didst fiction that is governed by other growth factors and adipose. Studies have also identified JUNK and signal transducer and activator of transcription 3 (STATS) as common downstream effectors of depiction. Both JUNK an d STATS play of cell proliferation, differentiation, and apotheosis during various physiologic and pathologic events such as tumor development.  Discussion/Analysis - Getting fat - Starting in chronological order of occurrence, in a patient's life - first, one must become obese for any risks to be present.
Is this necessarily, true? Yes. Not that non-obese people are necessarily risk- free or unlikely to get cancer - but obesity is positively correlated with multiple forms of cancer, so that risk is assure deed. Foods containing high levels of saturated fatty acids and cholesterol are specifically t he ones that are implicated in development of central abdominal obesity. Linoleum acid (or Omega 6 polyunsaturated fatty acid) is a constituent of animal- at that has been positively implicated in prostrate cancer migration/ metastasis .
Also, low-fat culture medium for in vitro tumor cultures resulted in decreased proliferation rates and low- fat diets for tumor bearing nude-mice also showed slower progression of tumors. White Adipose Tissue (WATT - a sub- classification of adipose tissue, which is largely present in visceral fat), is significantly co-relatable to consumption of animal- fat and saturated fatty acids. It is recognized as a metabolically active endocrine organ - some of the secretions of which have been listed above. Hence, there is definitely a relation between one's diet and cancer prognosis.
The role of obesity - Obesity has been generically classified as a condition that suppresses non- aggressive diseases and accelerates the aggressive ones. How true this stereotype may be, is not the subject of this report - but nonetheless the statement does hold true for cancer progression. To say that cancer (of any form) may be 'induced' by obesity, is not a Justifiable states .NET on the basis of currently available data. However, 'cancer progression' is definitely a task that obesity is able to remote to sufficiency (of the tumor).