Galectin 1 In the Regulation of Skeletal Muscle Wasting in Human Cancer Cachexia Introduction

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Galectin-1 in the Regulation of Skeletal Muscle Wasting in Human Cancer Cachexia

The modern oncology can control cancer progression leading to chronic treatments. In the absence of controls, patients reach a state slowly wasting. Orexigenic drugs (corticosteroids, megestrol acetate, medroxyprogesterone acetate, etc.) (Conlisk et al. p1051) Can increase appetite and alleviate anorexia and weight loss. We observe a parallel decrease in nausea and/or vomiting favourable anthropometric and biological parameters, and often an improved quality of life. The appetite stimulants alone are not sufficient to reverse the wasting process and must be associated with treatment of underlying diseases. (DeWys, p491-97)

T it cancer refers to more than one hundred types of diseases characterized by the appearance of malignant tumors. (Bruera, pp1383) This is the second leading cause of death after cardiovascular diseases. Oncogenesis is very similar from one cancer to another, but the clinical and biological characteristics are unique to each cancer. (Barber, p80-86)

The normal cell reproduces itself if it receives a signal from the cells that are close (controlled method of reproduction) and follows a reproductive cycle to apoptosis (programmed cell death). It recognizes its own place and anchored on the extracellular matrix (for an epithelial cell) and neighboring cells. (Feingold, p184-90)

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trolled is due to mutations observed in at least two classes of genes, proto-oncogenes and tumor suppressor genes, play important roles in the regulation and cell reproduction. Oncogenes from proto-oncogenes by mutation, translocation or amplification, act as growth promoters. (Maguid, p843-57)

Introduction on Galectin 1 In the Regulation of Skeletal Muscle Wasting in Human Cancer Cachexia Assignment

The tumor suppressor genes, in turn, have the primary function of acting as a brake on cell proliferation. When the proto-oncogens become carcinogenic, they cause uncontrolled growth of cells. The tumor suppressor genes involved in cancer development when inactivated, a cell cycle is then freed from all bondage inhibitory. (Wright, p120-24) The other feature of cancer cells is the ability to migrate. To avoid being recognized come abnormal cells floating, unable to anchor on other cells, cancer cells use intracellular messengers, suggesting wrongly proper anchoring and no failure. (Whinningham, p23-36)

They detach from the primary tumor and enter the tissues by releasing enzymes, metalloproteinases, which dissolve the basement membrane and other extracellular matrices. Then they cross the basement membrane and the layer of endothelial cells of a small blood vessel to be carried away by the bloodstream (or lymphatic) to another site in the body where they founded a new settlement (metastases). In the successive steps which lead them to their destination, they escape all the controls that subjugate normal cells. (Wigmore et al. p27-30)

Cancer cachexia and skeletal muscle wasting

Cachexia is a state of deep decay generally characterized by weakness, prostration, slow mental capacity, loss of appetite and reduction of fat and muscle mass. (Maguid, p843-57) It happens more often than having to locate internist pathologies underlying this symptom, that is, weight loss and weight loss, with fatigue generalized. Generally, these patients who have diabetes and do not know, eat, drink and urinate all the time and lose weight and lean muscle mass, or cancer patients, especially cancer of the lung or digestive tract. At best, do not eat for stress gastritis or benign ulcer. But let us see what must seek the good internist when encountering these patients. (Warmolts, p374-79)

typical of patients suffering from malignant tumors in pre-terminal (especially if located in the digestive tract, to ' esophagus or the stomach), has complex etiology in which different mechanisms come into play (anorexia, abnormal glucose metabolism and release of substances produced by the tumor from the host is capable of influencing the metabolism back toward catabolism) is often the most debilitating feature of this disease process. (Weindruch, p20-33)

The cancer cachexia is a severely debilitating paraneoplastic syndrome, which is characterized by an early weight loss, lack of appetite, but also and especially a loss of muscle mass, with depletion of fat deposits and deep metabolic changes. (Beller et al. p287) It adversely affects the quality of life of cancer patients. Today is no longer considered a terminal event but is seen as the final consequence of a series of metabolic and molecular alterations that occur very early when it is seen that is substantially non-reversible treatment with common nutritional, metabolic. (Bartlett, p260-67) pathogenesis of loss of muscle mass in the course of cancer has not yet been fully elucidated, as it depends on diverse factors, but it seems mainly by an imbalance between the rate of synthesis and protein degradation in muscles.

Where there is a role played by the proteolytic system the ubiquitin / proteasome-dependent ATP in accelerated muscle protein degradation. (Maguid, p843-57) For these reasons, a substance has been studied, bortezomib proteasome injunction, to block the destruction of lean body mass. (Beal et al. p89-97)

For some 'time is in use megestrol acetate in the treatment of cancer cachexia: a progestin used to treat the source of advanced breast cancer, able to increase appetite and body weight in cancer patients. Such good results are obtained from AIDS-induced anorexia. According to the literature on the megestrol acetate seems well tolerated and does not cause water retention. (Straub, p1591-1611) Ghrelin is a novel growth hormone-releasing peptide (GH) can also induce a positive energy balance by reducing fat and stimulating the use of appetite through GH-independent mechanisms. (Fearon et al. p1345-50)

It appears that ghrelin improves cachexia and functional capacity in patients with COPD. proinflammatory cytokines, particularly TNF-alpha (Tumor Necrosis Factor) play an important role in pathogenesis of cancer cachexia. In addition, they demonstrated that they could lose in the prevention of cancer in mice causes their muscle cells to over produce dystrophin. (Bozzetti et al. p367)

Protein stops muscle brake

The focus of this approach is a messenger protein called activin. It looks like myostatin, hold another chemical messenger that is responsible for muscle growth in check. If omitted, the skeletal muscles begin to proliferate excessively. (Mantovani, p296) The Zhou and her colleagues are now used in cancer cachexia in mice: They blocked the activin in the body of animals with the help of a specially developed protein-antagonist. (Bruera, p113)

Cancer cachexia pathophysiology

In addition, cachexia is described in those patients with involuntary weight loss. Cancerous processes produce an imbalance in the energy balance by decreasing food intake and increased catabolism, resulting in a clearly negative balance. (Kung T. et al. p579-85) They look at different factors determining cachexia, from metabolic unbalances produced by tumoral products and endocrine disorders or inflammatory response produced by cytokines, all leading to increased lipolysis, muscle protein loss and anorexia. (Mantovani, p296)

In addition to the causes of anorexia are multiple, from chemotherapy agents, radiotherapy or immunotherapy, which can produce different degrees of nausea, vomiting, diarrhea, and also to impairments of perceptions in the taste and smell, to obstruction of the digestive system pain, depression, constipation. (Steiner et al. p144-49)

From the knowledge of the different mechanisms producing anorexia-cachexia syndrome have been studied in artificial nutrition-calorie diets with relative success, a variety of drugs that were positive for the appetite gain as progestogens, steroids, and with lesser clinical evidence cannabinoids, cyproheptadine, mirtazapine (antidepressant) and olanzapine (antipsychotic). (Fearon et al. p1345-50) Others have studied for its anti-inflammatory cytokines due to its action, such as melatonin, omega-3 polyunsaturated acids, pentoxifylline and thalidomide, but the latter are still scarce clinical data for everyday use. (Bhattacharyya et al. p56-78)

Same happens with anabolic drugs derived from testosterone or metabolic inhibitors such as hydrazine sulfate. (Warmolts, p374-79) Undoubtedly especially progestogens megestrol and corticosteroids are first-line choice in the anorexia-cachexia syndrome to increase appetite and weight and the first impact in improving the quality of life and comfort in patients with advanced cancer. (Beal et al. p89-97)

The regulation of appetite and eating patterns is mediated by different psychological, gastrointestinal, metabolic and nutritional, as well as various neural and endocrine mechanisms. The anorectic cancer patient experiences a sensation of fullness early and decreased appetite. (Mantovani, p296)

Sometimes the causes of anorexia may result from their own cancer treatment (chemotherapy, radiotherapy or immunotherapy), which may induce nausea and vomiting to varying degrees. (Leppanen et al. p5549-65) They can also contribute to reduced intake alterations in perception of food and psychological reasons (depression). Sometimes, anorexia can be attributed to a direct effect of the tumor, where it is located in the hypothalamus or at the digestive system. (Beal et al. p89-97)

However, in most cases the origin of the anorexia associated with cachexia appears to be the metabolic alterations experienced by the patient as a result of the presence of tumor. (Warmolts, p374-79) Different factors, both humoral and source segregated by the host in response to tumor growth, or secreted by the tumor cells themselves may play an important role in the response anorexic. (Fearon et al. p1345-50)

In short, anorexia appears to be more an effect than the cause of weight loss and, in fact, decreased intake may manifest after it has been weight loss. (Bhattacharyya et al. p56-78) In any case, malnutrition due to reduced food intake only exacerbates the cachectic state, promoting a… [END OF PREVIEW] . . . READ MORE

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