Thymidine kinase 1 (TK1) is a proliferation biomarker
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Estrogen Metabolism and Breast Cancer : Epidemiology - 0 views
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estrogen metabolism estrogen metabolism estrogen metabolite metabolite metabolites breast cancer 2-OH-estrone 16alpha-OH-estrone 2:16alpha-OHE1
shared by Nathan Goodyear on 21 Aug 14
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Maybe the risks of estrogen metabolism is age dependent? This Long Island Breast Cancer Study Project found that an increased 2:16alphOH-estrone ratio was associated with a reduced premenopausal, invasive breast cancer risk. This association declined when looked at in postmenopausal women.
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Nuclear TK1 expression is an independent prognostic factor for survival in pre-malignan... - 0 views
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Nuclear TK1 expression in early grade CIN predicts risk for progression to malignancy
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Nuclear TK1 expression is also a prognostic factor for treatment outcome
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TK1 LI was found to be a more reliable prognostic marker for 5-year survival than pathological stages, FIGO stages and Ki-67,
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nuclear TK1 expression is a reliable prognostic factor in CIN patients, a group of cervical lesion patients that respond positively to treatment
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nuclear TK1 expression is correlated with advanced stage of invasive cervical carcinomas
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a low TK1 LI can help to identify with a better survival
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low TK1 expression in the tumors in these patients might indicate that these tumors have a lower proliferation rate
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TK1 is a key kinase in the one-step salvage pathway by which thymidine is introduced into DNA via the salvage pathway
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TK1 participates in DNA synthesis and is therefore closely related to the S-phase of the cell cycle, and is correlated with proliferation
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TK1 intensity (TK1 synthesis rate) increases from CIN grade I to CIN grade III, but does not further increase in invasive cervical carcinomas.
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TK1 intensity seems to be a prognostic factor particularly when pre-malignant cervical lesions progress to malignancy
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TK-1 is a proliferation biomarker of DNA repair. TK-1 is a nuclear biomarker of cancer prognosis, survival, recurrence and predicts risk of progression of pre-malignant disease.
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shared by Nathan Goodyear on 21 Oct 14
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Influence of Sex Hormones on Melanoma - 0 views
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cancer melanoma ER alpha ER-alpha ER beta ER-beta ER estrogen receptor hormones hormone
shared by Nathan Goodyear on 21 Oct 14
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Men show lower skin levels of ERβ than women, in whom ERβ expression decreases with age and more rapidly after menopause as a result of loss of estradiol-positive feedback
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Recent immunohistochemical analyses of ERβ protein level in melanoma tissues15,16 have shown that ERβ protein expression decreases with increasing Breslow thickness—the most important independent prognostic factor in melanoma.
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melanoma ERβ levels correlated with both the tumor microenvironment and the depth of invasion
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lower ERβ (mRNA and protein) levels in thicker, more invasive melanomas
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As in breast cancer, we maintain that ERα and ERβ status also has to be determined in melanoma with the aim of identifying those displaying a high ERα/ERβ ratio
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An ideal hormone therapy in melanoma should selectively block the proliferative ERα protein and promote the antiproliferative action of ERβ
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Melanoma is a known estrogen sensitive cancer. This study finds ER Beta loss correlates with thickness of lesion. The authors propose ERalpha/ERbeta ratio be assessed. ERbeta has been shown to decrease proliferation, promotes differentiation, and decrease inflammation in breast studies. In contrast, ERalpha promotes proliferation, decreases differentiation, and promotes inflammation. Here, the same effects seem to apply to melanoma. Of interesting note, men have lower skin ERbeta than women and ERbeta declines with age and menopause in women. Essentially, the loss of the ability to differentiate, decrease proliferation and inflammation occurs with increase estrogen stimulus--set up for estrogen promoting cancers.
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Antiangiogenic activity of the endocannabinoid anandamide: Correlation to its... - 0 views
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endocannabinoids inhibit angiogenesis as well as cancer cell growth, invasion, and metastasis.
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shared by Nathan Goodyear on 09 Jul 17
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Press-pulse: a novel therapeutic strategy for the metabolic management of cancer | Nutr... - 0 views
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ketogenic diet ketogenic press-pulse hyperbaric oxygen therapy HBOTnutrition diet cancer HBOT IVC IV vitamin C DCA dichloracetic acid cancer therapy cancer treatment alternative cancer treatment
shared by Nathan Goodyear on 09 Jul 17
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mamdouh_hfz liked it
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A “press” disturbance was considered a chronic environmental stress on all organisms in an ecological community
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“pulse” disturbances were considered acute events that disrupted biological communities to produce high mortality
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Neoplasia involving dysregulated cell growth is the biological endpoint of the disease
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Data from the American Cancer Society show that the rate of increase in cancer deaths/year (3.4%) was two-fold greater than the rate of increase in new cases/year (1.7%) from 2013 to 2017
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cancer is predicted to overtake heart disease as the leading cause of death in Western societies
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cancer can also be recognized as a metabolic disease.
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glucose is first split into two molecules of pyruvate through the Embden–Meyerhof–Parnas glycolytic pathway in the cytosol
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Aerobic fermentation, on the other hand, involves the production of lactic acid under normoxic conditions
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persistent lactic acid production in the presence of adequate oxygen is indicative of abnormal respiration
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Otto Warburg first proposed that all cancers arise from damage to cellular respiration
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The Crabtree effect is an artifact of the in vitro environment and involves the glucose-induced suppression of respiration with a corresponding elevation of lactic acid production even under hyperoxic (pO2 = 120–160 mmHg) conditions associated with cell culture
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the Warburg theory of insufficient aerobic respiration remains as the most credible explanation for the origin of tumor cells [2, 37, 51, 52, 53, 54, 55, 56, 57].
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The main points of Warburg’s theory are; 1) insufficient respiration is the predisposing initiator of tumorigenesis and ultimately cancer, 2) energy through glycolysis gradually compensates for insufficient energy through respiration, 3) cancer cells continue to produce lactic acid in the presence of oxygen, and 4) respiratory insufficiency eventually becomes irreversible
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Efraim Racker coined the term “Warburg effect”, which refers to the aerobic glycolysis that occurs in cancer cells
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Warburg clearly demonstrated that aerobic fermentation (aerobic glycolysis) is an effect, and not the cause, of insufficient respiration
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all tumor cells that have been examined to date contain abnormalities in the content or composition of cardiolipin
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The evidence supporting Warburg’s original theory comes from a broad range of cancers and is now overwhelming
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respiratory insufficiency, arising from any number mitochondrial defects, can contribute to the fermentation metabolism seen in tumor cells.
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data from the nuclear and mitochondrial transfer experiments suggest that oncogene changes are effects, rather than causes, of tumorigenesis
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Normal mitochondria can suppress tumorigenesis, whereas abnormal mitochondria can enhance tumorigenesis
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In addition to glucose, cancer cells also rely heavily on glutamine for growth and survival
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Glutamine is anapleurotic and can be rapidly metabolized to glutamate and then to α-ketoglutarate for entry into the TCA cycle
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Glucose and glutamine act synergistically for driving rapid tumor cell growth
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Glutamine metabolism can produce ATP from the TCA cycle under aerobic conditions
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Amino acid fermentation can generate energy through TCA cycle substrate level phosphorylation under hypoxic conditions
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Hif-1α stabilization enhances aerobic fermentation
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targeting glucose and glutamine will deprive the microenvironment of fermentable fuels
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Although Warburg’s hypothesis on the origin of cancer has created confusion and controversy [37, 38, 39, 40], his hypothesis has never been disproved
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Warburg referred to the phenomenon of enhanced glycolysis in cancer cells as “aerobic fermentation” to highlight the abnormal production of lactic acid in the presence of oxygen
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Emerging evidence indicates that macrophages, or their fusion hybridization with neoplastic stem cells, are the origin of metastatic cancer cells
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Radiation therapy can enhance fusion hybridization that could increase risk for invasive and metastatic tumor cells
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Kamphorst et al. in showing that pancreatic ductal adenocarcinoma cells could obtain glutamine under nutrient poor conditions through lysosomal digestion of extracellular proteins
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It will therefore become necessary to also target lysosomal digestion, under reduced glucose and glutamine conditions, to effectively manage those invasive and metastatic cancers that express cannibalism and phagocytosis.
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Previous studies in yeast and mammalian cells show that disruption of aerobic respiration can cause mutations (loss of heterozygosity, chromosome instability, and epigenetic modifications etc.) in the nuclear genome
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The somatic mutations and genomic instability seen in tumor cells thus arise from a protracted reliance on fermentation energy metabolism and a disruption of redox balance through excess oxidative stress.
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According to the mitochondrial metabolic theory of cancer, the large genomic heterogeneity seen in tumor cells arises as a consequence, rather than as a cause, of mitochondrial dysfunction
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A therapeutic strategy targeting the metabolic abnormality common to most tumor cells should therefore be more effective in managing cancer than would a strategy targeting genetic mutations that vary widely between tumors of the same histological grade and even within the same tumor
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Tumor cells are more fit than normal cells to survive in the hypoxic niche of the tumor microenvironment
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Hypoxic adaptation of tumor cells allows for them to avoid apoptosis due to their metabolic reprograming following a gradual loss of respiratory function
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The high rates of tumor cell glycolysis and glutaminolysis will also make them resistant to apoptosis, ROS, and chemotherapy drugs
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Despite having high levels of ROS, glutamate-derived from glutamine contributes to glutathione production that can protect tumor cells from ROS
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reason to eliminate glutamine in cancer patients and even GSH with cancer patients
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It is clear that adaptability to environmental stress is greater in normal cells than in tumor cells, as normal cells can transition from the metabolism of glucose to the metabolism of ketone bodies when glucose becomes limiting
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Mitochondrial respiratory chain defects will prevent tumor cells from using ketone bodies for energy
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glycolysis-dependent tumor cells are less adaptable to metabolic stress than are the normal cells. This vulnerability can be exploited for targeting tumor cell energy metabolism
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In contrast to dietary energy reduction, radiation and toxic drugs can damage the microenvironment and transform normal cells into tumor cells while also creating tumor cells that become highly resistant to drugs and radiation
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Drug-resistant tumor cells arise in large part from the damage to respiration in bystander pre-cancerous cells
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Because energy generated through substrate level phosphorylation is greater in tumor cells than in normal cells, tumor cells are more dependent than normal cells on the availability of fermentable fuels (glucose and glutamine)
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Ketone bodies and fats are non-fermentable fuels
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Although some tumor cells might appear to oxidize ketone bodies by the presence of ketolytic enzymes [181], it is not clear if ketone bodies and fats can provide sufficient energy for cell viability in the absence of glucose and glutamine
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Apoptosis under energy stress is greater in tumor cells than in normal cells
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A calorie restricted ketogenic diet or dietary energy reduction creates chronic metabolic stress in the body
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. This energy stress acts as a press disturbance
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Drugs that target availability of glucose and glutamine would act as pulse disturbances
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Hyperbaric oxygen therapy can also be considered another pulse disturbance
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The KD can more effectively reduce glucose and elevate blood ketone bodies than can CR alone making the KD potentially more therapeutic against tumors than CR
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Campbell showed that tumor growth in rats is greater under high protein (>20%) than under low protein content (<10%) in the diet
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Protein amino acids can be metabolized to glucose through the Cori cycle
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The fats in KDs used clinically also contain more medium chain triglycerides
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Calorie restriction, fasting, and restricted KDs are anti-angiogenic, anti-inflammatory, and pro-apoptotic and thus can target and eliminate tumor cells through multiple mechanisms
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Ketogenic diets can also spare muscle protein, enhance immunity, and delay cancer cachexia, which is a major problem in managing metastatic cancer
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GKI values of 1.0 or below are considered therapeutic
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The GKI can therefore serve as a biomarker to assess the therapeutic efficacy of various diets in a broad range of cancers.
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It is important to remember that insulin drives glycolysis through stimulation of the pyruvate dehydrogenase complex
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The water-soluble ketone bodies (D-β-hydroxybutyrate and acetoacetate) are produced largely in the liver from adipocyte-derived fatty acids and ketogenic dietary fat. Ketone bodies bypass glycolysis and directly enter the mitochondria for metabolism to acetyl-CoA
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Due to mitochondrial defects, tumor cells cannot exploit the therapeutic benefits of burning ketone bodies as normal cells would
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Therapeutic ketosis with racemic ketone esters can also make it feasible to safely sustain hypoglycemia for inducing metabolic stress on cancer cells
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Ketones are much more than energy adaptabilit, but actually are therapeutic.
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ketone bodies can inhibit histone deacetylases (HDAC) [229]. HDAC inhibitors play a role in targeting the cancer epigenome
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Therapeutic ketosis reduces circulating inflammatory markers, and ketones directly inhibit the NLRP3 inflammasome, an important pro-inflammatory pathway linked to carcinogenesis and an important target for cancer treatment response
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Chronic psychological stress is known to promote tumorigenesis through elevations of blood glucose, glucocorticoids, catecholamines, and insulin-like growth factor (IGF-1)
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In addition to calorie-restricted ketogenic diets, psychological stress management involving exercise, yoga, music etc. also act as press disturbances that can help reduce fatigue, depression, and anxiety in cancer patients and in animal models
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Ketone supplementation has also been shown to reduce anxiety behavior in animal models
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This physiological state also enhances the efficacy of chemotherapy and radiation therapy, while reducing the side effects
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lower dosages of chemotherapeutic drugs can be used when administered together with calorie restriction or restricted ketogenic diets (KD-R)
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Besides 2-DG, a range of other glycolysis inhibitors might also produce similar therapeutic effects when combined with the KD-R including 3-bromopyruvate, oxaloacetate, and lonidamine
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A synergistic interaction of the KD diet plus radiation was seen
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It is important to recognize, however, that the radiotherapy used in glioma patients can damage the respiration of normal cells and increase availability of glutamine in the microenvironment, which can increase risk of tumor recurrence especially when used together with the steroid drug dexamethasone
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Poff and colleagues demonstrated that hyperbaric oxygen therapy (HBOT) enhanced the ability of the KD to reduce tumor growth and metastasis
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HBOT also increases oxidative stress and membrane lipid peroxidation of GBM cells in vitro
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The effects of the KD and HBOT can be enhanced with administration of exogenous ketones, which further suppressed tumor growth and metastasis
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Besides HBOT, intravenous vitamin C and dichloroacetate (DCA) can also be used with the KD to selectively increase oxidative stress in tumor cells
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Recent evidence also shows that ketone supplementation may enhance or preserve overall physical and mental health
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Some tumors use glucose as a prime fuel for growth, whereas other tumors use glutamine as a prime fuel [102, 186, 262, 263, 264]. Glutamine-dependent tumors are generally less detectable than glucose-dependent under FDG-PET imaging, but could be detected under glutamine-based PET imaging
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GBM and use glutamine as a major fuel
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Many of the current treatments used for cancer management are based on the view that cancer is a genetic disease
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Emerging evidence indicates that cancer is a mitochondrial metabolic disease that depends on availability of fermentable fuels for tumor cell growth and survival
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Glucose and glutamine are the most abundant fermentable fuels present in the circulation and in the tumor microenvironment
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Low-carbohydrate, high fat-ketogenic diets coupled with glycolysis inhibitors will reduce metabolic flux through the glycolytic and pentose phosphate pathways needed for synthesis of ATP, lipids, glutathione, and nucleotides
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Cancer is a mitochondrial disease? So says the well published Dr Seyfried. Glucose and glutamine drive cancer growth.
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How is the Immune System Suppressed by Cancer - 1 views
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nitric oxide (NO) released by tumor cells
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Excellent work by Prof de Groot of Essen, indicated by adding exogenous xanthine oxidase ( XO) in hepatoma cells, hydrogen peroxide was produced to destroy the hepatoma cells
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NO from eNOS in cancer cells can travel through membranes and over long distances in the body
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NO also is co linked to VEGF which in turn increases the antiapoptotic gene bcl-2
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The other important influence of NO is in its inhibition of the proapoptoic caspases cascade. This in turn protects the cells from intracellular preprogrammed death.
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nitric oxide in immune suppression in relation to oxygen radicals is its inhibitory effect on the binding of leukocytes (PMN) at the endothelial surface
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Inhibition of inducible Nitric Oxide Synthase (iNOS)
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NO from the tumor cells actually suppresses the iNOS, and in addition it reduces oxygen radicals to stop the formation of peroxynitrite in these cells. But NO is not the only inhibitor of iNOS in cancer.
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Spermine and spermidine, from the rate limiting enzyme for DNA synthases, ODC, also inhibit iNOS
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tolerance in the immune system that decreases the immune response to antigens on the tumors
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Freund’s adjuvant
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increase in kinases in these cells which phosphorylate serine, and tyrosine
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responsible for activation of many growth factors and enzymes
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phosphorylated amino acids suppress iNOS activity
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Hexokinase II
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Prostaglandin E2, released from tumor cells is also an inhibitor of iNOS, as well as suppressing the immune system
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Th-1 subset of T-cells. These cells are responsible for anti-viral and anti-cancer activities, via their cytokine production including Interleukin-2, (IL-2), and Interleukin-12 which stimulates T-killer cell replication and further activation and release of tumor fighting cytokines.
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Th1 cells stimulate NK and other tumor fighting macrophages via IL-2 and IL-12; In contrast, Th2, which is stimulated in allergies and parasitic infections, produce IL-4 and IL-10. IL-4 and IL-10 inhibit TH-1 activation and the histamine released from mast cell degranulation upregulates T suppressor cells to further immune suppression.
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Th-2 subset of lymphocytes, on the other hand are activated in allergies and parasitic infections to release Interleukin-4 and Interleukin-10
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These have respectively inhibitory effects on iNOS and lymphocyte Th-1 activation
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Mast cells contain histamine which when released increases the T suppressor cells, to lower the immune system and also acts directly on many tumor Histamine receptors to stimulate tumor growth
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Tumor cells release IL-10, and this is thought to be one of the important areas of Th-1 suppression in cancer patients
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IL-10 is also increased in cancer causing viral diseases such as HIV, HBV, HCV, and EBV
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IL-10 is also a central regulator of cyclooxygenase-2 expression and prostaglandin production in tumor cells stimulating their angiogenesis and NO production
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nitric oxide in tumor cells even prevents the activation of caspases responsible for apoptosis
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NO produced by cancer cells inhibits proapoptotic pathways such as the caspases.
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early stages of carcinogenesis, which we call tumor promotion, one needs a strong immune system, and fewer oxygen radicals to prevent mutations but still enough to destroy the tumor cells should they develop
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later stages of cancer development, the oxygen radicals are decreased around the tumors and in the tumor cells themselves, and the entire cancer fighting Th-1 cell replication and movement are suppressed. The results are a decrease in direct toxicity and apoptosis, which is prevented by NO, a suppression of the macrophage and leukocyte toxicity and finally, a suppression of the T-cell induced tumor toxicity
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cGMP is increased by NO
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NO in cancer is its ability to increase platelet-tumor cell aggregates, which enhances metastases
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the greater the malignancies and the greater the metastatic potential of these tumors
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The greater the NO production in many types of tumors,
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gynecological
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elevated lactic acid which neutralizes the toxicity and activity of Lymphocyte immune response and mobility
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The lactic acid is also feeding fungi around tumors and that leads to elevated histamine which increases T-suppressor cells. Histamine alone stimulates many tumor cells.
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The warburg effect in cancer cells results in the increase in local lactic acid production which suppresses lymphocyte activity and toxicity as well as stimulates histamine production with further stimulates tumor cell growth.
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T-regulatory cells (formerly,T suppressor cells) down regulate the activity of Natural killer cells
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last but not least, the Lactic acid from tumor cells and acidic diets shifts the lymphocyte activity to reduce its efficacy against cancer cells and pathogens in addition to altering the bacteria of the intestinal tract.
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intestinal tract bacteria in cancer cells release sterols that suppress the immune system and down regulate anticancer activity from lymphocytes.
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In addition to the lactic acid, adenosine is also released from tumors. Through IL-10, adenosine and other molecules secreted by regulatory T cells, the CD8+ cells can be inactivated to an anergic state
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Adenosine up regulates the PD1 receptor in T-1 Lymphocytes and inhibits their activity
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Adenosine is a purine nucleoside found within the interstitial fluid of solid tumors at concentrations that are able to inhibit cell-mediated immune responses to tumor cells
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Adenosine appears to up-regulate the PD1 receptor in T-1 Lymphocytes and inhibits the immune system further
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Mast cells with their release of histamine lower the immune system and also stimulate tumor growth and activate the metalloproteinases involved in angiogenesis and metastases
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COX 2 inhibitors or all trans-retinoic acid
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Cimetidine, an antihistamine has been actually shown to increase in apoptosis in MDSC via a separate mechanism than the antihistamine effect
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interleukin-8 (IL-8), a chemokine related to invasion and angiogenesis
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In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha)
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these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target
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Great review of the immunosuppression in cancer driven by the likes of NO.
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Phosphodiesterase 4D Inhibitors Limit Prostate Cancer Growth Potential - 0 views
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PDE inhibitors increase cAMP and useful to inhibit invasion and mobility of prostate cancer.
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[Full text] High-dose vitamin C suppresses the invasion and metastasis of breast c | OTT - 0 views
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epithelial to mesenchymal transition EMT vitamin C cancer
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Cancer's Invasion Equation | The New Yorker - 0 views
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Affordable Top Hospitals for Spinal Fusion India Leads to Better Outcomes - 0 views
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Affordable top hospitals for spinal fusion India cost of spine surgery affordable spinal fusion doctors in India Spinal Fusion Surgery in india Top Spinal Fusion Doctors india Low Cost Spinal Fusion Surgery in india
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Affordable top hospitals for spinal fusion India are recommended while non-invasive methods have failed to provide relief from pain. The cost of spine surgery offered by affordable spinal fusion doctors in India is almost 40-70% lower in comparison to the US and UK. Helpline Number: +91-9325887033 Email id: enquiry@spineandneurosurgeryhospitalindia.com
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Le Dr Rajiv Parakh propose des méthodes endovasculaires mini-invasives qui obtiennent les meilleurs effets même en diminuant les séjours. Pour un rendez-vous accéléré et une consultation avec le Dr Rajiv Parakh Veuillez appeler le +91-9370586696 ou vous pouvez nous envoyer un courrier Identifiant de l'e-mail : - enquiry@indiacardiacsurgerysite.com
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Les meilleurs hôpitaux cardiaques de Delhi prolongent la vie des patients sou... - 0 views
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Heart Valve Program At Best Cardiology Hospitals in Chennai - 0 views
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Cardiac surgery India Cardiac surgery Best Cardiologists List of top 10 cardiologists Chennai Best cardiology hospitals in Chennai India Best Cardiology Hospitals Top 12 Cardiology Hospitals in Chennai list of 12 cardiology hospitals in chennai
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List of top 10 cardiologists Chennai provides the finest in patient care presenting modern, minimally invasive strategies and strategies whenever possible.
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Robotic Spine Surgery Program By Dr. Vidyadhara S Spine Surgeon in Bangalore - 0 views
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Dr. Vidyadhara S spine surgeon in Bangalore Manipal Hospital Bangalore
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Dr. Vidyadhara S spine surgeon in Bangalore specializes in complex reconstructions and revision surgery, along with treatment of spinal deformity, tumors, and minimally invasive techniques to the spinal column.
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Latest Gamma Knife Radiosurgery® Perfexion™ Installed for Non-invasive Treatm... - 0 views
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The best gamma knife neurosurgeon in Delhi India now offers the latest Gamma knife radiosurgery ® technology for even greater precision to reduce or eliminate tumors or lesions in the brain without traditional surgery.
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Tumor regionalization after surgery: Roles of the tumor microenvironment and neutrophil... - 0 views
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tumor surgery must be carefully considered because the risk of metastasis could be increased by the surgical procedure.
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NETosis, which is the process of forming neutrophil extracellular traps (NETs)
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surgery-induced metastasis
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surgery per se can promote cancer metastasis through a series of local and systemic events
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surgery results in a serious wound that disrupts the structural barrier preventing the outspreading of cancer cells, change the properties of the cancer cells and stromal cells remaining in the tumor microenvironment, or impairs the host defense systems against cancers
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After the primary tumor is surgically removed, the metastases can start to grow vigorously via neoangiogenesis because the circulating inhibitors disappear
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infection and inflammation during the postoperative period have been reported to increase the risk of cancer recurrence in patients
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Surgeons have long suspected that surgery, even if it is a necessary step in cancer treatment, facilitates cancer metastasis
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Surgery-induced cancer metastasis has been well established in animal models
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tumor cell dissemination, tumor-favoring immune responses, and neoangiogenesis
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the surgical resection of primary tumors is beneficial is controversial
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CTCs abruptly increase just after surgery
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Even externally palpitating tumors for diagnosis could increase the numbers of CTCs in skin cancer and breast cancer
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excessive glucocorticoids negatively modulate immune functions
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immune surveillance against tumors is considered to be impaired by surgical stress
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In addition to glucocorticoids, during stimulation of the HPA axis, the catecholamine hormones epinephrine and norepinephrine are released from the adrenal medulla
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NK cell suppression may be attributed to increased levels of catecholamines as well as glucocorticoids
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In mice bearing a primary tumor, it was observed that the removal of the primary tumor facilitated the growth of highly vascularized metastases
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primary tumors may secrete angiogenic inhibitors as well as angiogenic activators
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second phase of tumor recurrence and metastasis, which are newly acquired events, rather than just outcomes of incomplete treatment.
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double-edged sword
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HIF-1 in neutrophils plays a critical role in NETosis and bacteria-killing activity
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neutrophils play various roles in the initiation and progression of cancer
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NETosis
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many inflammatory and neoplastic diseases
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formation of neutrophil extracellular traps (NETs), which are large extracellular complexes composed of chromatin and cytoplasmic/granular proteins1
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NETosis has been highlighted as an inflammatory event that promotes cancer metastasis
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Once activated, neutrophils produce intracellular precursors by using DNA, histones, and granular and cytoplasmic proteins and then spread the mature form of NETs out around themselves
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A series of these events is called NETosis.
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neutrophil elastase, myeloperoxidase, cathepsin G, proteinase 3, lactoferrin, gelatinase, lysozyme C, calprotectin, neutrophil defensins, and cathelicidins
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innate immune response against infection
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Neutrophils are the most abundant type of granulocytes, comprising 40–70% of all white blood cells
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two types of NEToses, suicidal (or lytic) NETosis and vital NETosis
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Suicidal NETosis mainly depends on the production of reactive oxygen species (ROS)
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Since neutrophils die during this process, it is called suicidal NETosis.
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vital NETosis
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vital NETosis occurs independently of ROS production
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Vital NETosis can be induced by Gram-negative bacteria. LPS
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NETs are present in a variety of cancers, such as lung cancer, colon cancer, ovarian cancer, and leukemia
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neutrophils actively undergo NETosis in the tumor microenvironment
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Hypoxia
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NETosis plays a pivotal role in noninfectious autoimmune diseases,
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cytokines
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tumor-derived proteases
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tumor exosomes
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NETosis generally actively progresses in the tumor microenvironment.
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the proliferative cytokines TGFβ and IL-10 and the angiogenic factor VEGF are representative of neutrophil-derived tissue repair proteins.
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NETosis is a defense system to protect the body from invading pathogens
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when neutrophils are excessively stimulated, they produce excess NETs, thereby leading to pathological consequences
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plasma levels of NETosis markers are elevated after major surgeries
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local invasion, intravasation into the blood or lymphatic vessels, escape from the immune system, anchoring to capillaries in target organs, extravasation into the organs, transformation from dormant cells to proliferating cells, colonization to micrometastases, and growth to macrometastases
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NETs promote metastasis at multiple steps
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NETs loosen the ECM and capillary wall to promote the intravasation of cancer cells
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NETs and platelets wrap CTCs, which protects them from attack by immune cells and shearing force by blood flow
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NETs promote the local invasion of cancer cells by degrading the extracellular matrix (ECM)
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neutrophil elastase, matrix metalloproteinase 9, and cathepsin G
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NETs also promote the intravasation of cancer cells
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millions of tumor cells are released into the circulation every day,
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NETs can wrap up CTCs with platelets
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β1-integrin plays an important role in the interaction between CTCs and NETs
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NET-platelet-CTC aggregates.
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After metastasizing to distant tissues, tumor cells are often found to remain dormant for a period of time and unexpectedly regrow late
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NETs are believed to participate in the reactivation of dormant cancer cells in metastatic regions
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NET-associated proteases NE and MMP-9 were found to be responsible for the reactivation of dormant cancer cells
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shared by Nathan Goodyear on 24 Sep 23
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Suppressive impact of metronomic chemotherapy using UFT and/or cyclophosphamide on medi... - 0 views
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cancer low-dose chemotherapy invasion metastasis LDMC low-dose metronomic chemotherapy
shared by Nathan Goodyear on 24 Sep 23
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Evidence starting to mount that LDMC is equal and maybe even superior to MTD without all the side effects.
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shared by spineneuro on 24 Jun 23
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Mastermind of Neurological Care: Unleashing the Expertise of Dr. Sandeep Vaishya in Delhi - 0 views
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Dr. Sandeep Vaishya Dr. Sandeep Vaishya in Delhi best neurologist in Delhi Dr. Sandeep Vaishya best neurologist in Delhi
shared by spineneuro on 24 Jun 23
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From pioneering new minimally invasive surgery techniques to developing surgical alternatives to traditional treatments for better management of chronic conditions like epilepsy, Dr. Sandeep Vaishya strives to provide the best care possible in India.
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shared by harshitatyagi on 13 May 23
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Hysteroscopy and Its Role in IVF - 0 views
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Hysteroscopy Hysteroscopy in ivf hysteroscopy procedure hysteroscopy steps hysteroscopy risks hysteroscopy benefits
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Hysteroscopy is a less-invasive diagnostic procedure in fertility treatments like in vitro fertilization (IVF). The process involves inserting a small, lighted telescope known as a hysteroscope through the vagina and cervix and into the uterus. Lets explore the role of hysteroscopy in IVF, benefits, Risks, procedure etc.