This hypothesis has now been confirmed by experimental evidence showing that doxycycline reduces tumor burden in a mouse model of breast cancer-derived osteolytic bone metastasis
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Targeting matrix metalloproteinases in cancer: Bringing new life to old ideas - Science... - 0 views
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Doxycycline and other tetracyclines in the treatment of bone... : Anti-Cancer Drugs - 0 views
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Matrix metalloproteinases in the pathogenesis of estradiol-induced nonbacterial prostat... - 0 views
www.mendeley.com/...teral-prostate-lobe-wistar-rat
prostate estradiol E2 testosterone T DHT inflammation
shared by Nathan Goodyear on 01 May 12
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Complex role of matrix metalloproteinases in angiogenesis | Cell Research - 0 views
Frontiers | Role of Matrix Metalloproteinases in Angiogenesis and Cancer | Oncology - 0 views
www.frontiersin.org/...full
inflammation VEGFR HIF-1alpha MMP2 MMP9 angiogenesis matrix metalloproteinase hypoxia cancer VEGF
shared by Nathan Goodyear on 17 Sep 20
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Thrita | Matrix Metalloproteinases and Breast Cancer - 0 views
sites.kowsarpub.com/...18213.html
MMP angiogenesis EMT metastasis matrix metalloproteinase breast cancer carcinogenesis epithelial to mesenchymal transition
shared by Nathan Goodyear on 17 Sep 20
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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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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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Even externally palpitating tumors for diagnosis could increase the numbers of CTCs in skin cancer and breast cancer
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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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second phase of tumor recurrence and metastasis, which are newly acquired events, rather than just outcomes of incomplete treatment.
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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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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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neutrophil elastase, myeloperoxidase, cathepsin G, proteinase 3, lactoferrin, gelatinase, lysozyme C, calprotectin, neutrophil defensins, and cathelicidins
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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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the proliferative cytokines TGFβ and IL-10 and the angiogenic factor VEGF are representative of neutrophil-derived tissue repair proteins.
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when neutrophils are excessively stimulated, they produce excess NETs, thereby leading to pathological consequences
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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 and platelets wrap CTCs, which protects them from attack by immune cells and shearing force by blood flow
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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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NET-associated proteases NE and MMP-9 were found to be responsible for the reactivation of dormant cancer cells
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Matrix metalloproteinases in the pathogenesis of estradiol-induced nonbacterial prostat... - 0 views
www.ncbi.nlm.nih.gov/...15215045
estrogen estradiol prostate inflammation cytokines male men hormones
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Inhibitors of Prostaglandin Synthesis Inhibit Human Prostate Tumor Cell Invasiveness an... - 0 views
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Role of Oxidative Stress and the Microenvironment in Breast Cancer Development and Prog... - 0 views
www.ncbi.nlm.nih.gov/...PMC3950899
cancer oxidative stress warburg effect reverse warburg effect ROS
shared by Nathan Goodyear on 11 Nov 14
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Oxidative stress generated by breast cancer cells activates HIF-1α and NFκB in fibroblasts, leading to autophagy and lysosomal degradation of Cav-1
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increased levels of hydrogen peroxide in exhaled breath condensate from patients with localized breast malignancy, associated with increased clinical severity
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Comparing mitochondrial metabolic activity revealed a difference between stroma and epithelial cells
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Overexpression of NOX4 in normal breast epithelial cells results in cellular senescence, resistance to apoptosis, and tumorigenic transformation, as well as increased aggressiveness of breast cancer cells
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metalloproteinases (MMP) such as MMP-2, MMP-3, and MMP-9 increase extracellular matrix turnover and are themselves activated by oxidative stress
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Lowered expression of Cav-1 not only leads to myofibroblast conversion and inflammation but also seems to impact aerobic glycolysis, leading to secretion of high energy metabolites such as pyruvate and lactate that drive mitochondrial oxidative phosphorylation in cancer cells
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secreted transforming growth factor β (TGFβ), insulin-like growth factor (IGF), platelet-derived growth factor (PDGF), fibroblast growth factor 2, and stromal-derived factor 1 (SDF1) are able to activate fibroblasts and increase cancer cell proliferation
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oxidative stress has an important role in the initiation and preservation of breast cancer progression
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the cancer cells produce hydrogen peroxide and by driving the “Reverse Warburg Effect” initiate oxidative stress in fibroblasts. As a result of this process, fibroblasts exhibited reduced mitochondrial activity, increased glucose uptake, ROS, and metabolite production.
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Oxidative stress results from an imbalance between unstable reactive species lacking one or more unpaired electrons (superoxide anion, hydrogen peroxide, hydroxyl radical, reactive nitrogen species) and antioxidants
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cancer cells are able to induce drivers of oxidative stress, autophagy and mitophagy: HIF-1α and NFκB in surrounding stroma fibro-blasts
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Studies show that loss of Cav-1 in adjacent breast cancer stroma fibroblasts can be prevented by treatment with N-acetyl cysteine, quercetin, or metformin
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hydrogen peroxide is one of the main factors that can push fibroblasts and cancer cells into senescence
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It is widely held that HIF-1α function is dependent upon its location within the tumor microenvironment. It acts as a tumor promoter in CAFs and as a tumor suppressor in cancer cells
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It was reported that overexpression of recombinant (SOD2) (Trimmer et al., 2011) or injection of SOD, catalase, or their pegylated counterparts can block recurrence and metastasis in mice
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obstructing oxidative stress in the tumor microenvironment can lead to mitophagy and promote breast cancer shutdown is a promising discovery for the development of future therapeutic interventions.
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Recent studies show that in the breast cancer microenvironment, oxidative stress causes mitochondrial dysfunction
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Really fascinating article on tumor signaling. The article points to a complex signaling between cancer cells and stromal fibroblasts that results in myofibroblast transformation that increases the microenvironment favorability of cancer. This article points to oxidative stress as the primary driving force.
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Antitumor effect of pretreatment for colon cancer cells with hyperthermia plus geranylg... - 0 views
pubmed.ncbi.nlm.nih.gov/19337914
nitric oxide colon cancer NO metastasis COX2 matrix metalloproteinase hyperthermia NF-KappaB heat shock proteins MMP HSP HSP70
shared by Nathan Goodyear on 25 Feb 21
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Repurposing Drugs in Oncology (ReDO)-chloroquine and hydroxychloroquine as anti-cancer ... - 0 views
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daily doses up to 400 mg of HCQ or 250 mg CQ for several years are considered to carry an acceptable risk for CQ-induced retinopathies, with the exception of individuals of short stature
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chronic CQ or HCQ therapy be monitored through regular ophthalmic examinations (3–6 month intervals), full blood counts and blood glucose level checks
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long-term HCQ exposure, skeletal muscle function and tendon reflexes should be monitored for weakness
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both CQ and HCQ, specific caution is advised in patients suffering from impaired hepatic function (especially when associated with cirrhosis), porphyria, renal disease, epilepsy, psoriasis, glucose-6-phosphate dehydrogenase deficiency and known hypersensitivity to 4-aminoquinoline compounds
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CQ can prevent the entrapment of protonated chemotherapeutic drugs by buffering the extracellular tumour environment and intracellular acidic spaces
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the expression levels of TLR9 are higher in hepatocellular carcinoma, oesophageal, lung, breast, gastric and prostate cancer cells as compared with adjacent noncancerous cells, and high expression is often linked with poor prognosis
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TLR9-mediated activation of the NF-κB signalling pathway and the associated enhanced expression of matrix metalloproteinase-2 (MMP-2), MMP-7 and cyclo-oxygenase 2 mRNA
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HCQ can activate caspase-3 and modulate the Bcl-2/Bax ratio inducing apoptosis in CLL, B-cell CLL and glioblastoma cells
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In triple-negative breast cancer, CQ was shown to eliminate cancer stem cells through reduction of the expression of Janus-activated kinase 2 and DNA methyl transferase 1 [106] or through induction of mitochondrial dysfunction, subsequently causing oxidative DNA damage and impaired repair of double-stranded DNA breaks
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Therapies used in combination with CQ or HCQ include chemotherapeutic drugs, tyrosine kinase inhibitors, various monoclonal antibodies, hormone therapies and radiotherapy
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Most studies hypothesise that CQ and HCQ could increase the efficacy of other anti-cancer drugs by blocking pro-survival autophagy.
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daily doses between 400 and 1200 mg for HCQ are safe and well tolerated, but two studies identified 600-mg HCQ daily as the MTD