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There is evidence of an anticancer effect of metformin through Duloxetine Hcl (Cymbalta)- Multum inhibition of mTOR activity. On the one hand, some studies have shown that metformin lowers the level of insulin and mTOR activity. According Duloxetine Hcl (Cymbalta)- Multum in vivo and in vitro results, metformin, by reducing the expression of G1 cyclins, causes a barrier Duloxetine Hcl (Cymbalta)- Multum the activity of the G1 cell cycle and thus halts the cycle of the cell.

In the indirect mechanism, metformin activates AMPK, which results in AMPK preventing the transcription of the gene responsible for glycogenesis in liver cells (Figure 2). In this process, glycogenosis decreases and, as a result, glucose uptake in muscle cells increases. Glucose uptake in Duloxetine Hcl (Cymbalta)- Multum muscle cells leads to a decrease in blood glucose levels and subsequently insulin levels. Since high levels of insulin in the blood, due to the high number of insulin receptors in the cancer cells, have mitogenic effects and can cause tumor growth and proliferation, reducing insulin levels in the blood reduces the likelihood of malignity and prevents cancer cell proliferation.

For example, several studies have shown metformin use to lower insulin levels in the blood for the treatment of breast cancer in women.

Preventing mTOR activity reduces the levels of 4E-BPs (4E-binding proteins) and S6Ks (ribosomal protein S6 kinase) factors and decreases protein synthesis and proliferation. Thus, the metformin affects AMPK and mTOR and Duloxetine Hcl (Cymbalta)- Multum cancer cell growth and proliferation. One of the advantages of metformin, which demonstrates its high potential for increasing the therapeutic response in cancer cells observed in several animal models, is the prevention of the proliferation and growth of tumors.

For example, there is evidence for metformin preventing the growth of cancer cells in lung, prostate, colon, and genograph. Moreover, the Duloxetine Hcl (Cymbalta)- Multum of the ZODIAC trial showed a lower incidence of death among metformin-taking patients.

In their study, the incidence of death per 1,000 patients taking sulfonylurea, metformin, and insulin, who were under observation for one year, was 4. Furthermore, according to a study by Campagnoli et al on women with breast cancer, the use of metformin reduced the level of testosterone and insulin and its destructive effects, such as insulin resistance. The outcomes for this study recommended that metformin is a better treatment model in women, compared with sulfonylurea or insulin.

For Duloxetine Hcl (Cymbalta)- Multum, Rieken et al reported better Duloxetine Hcl (Cymbalta)- Multum survival (RFS) in 6,863 patients treated with radical prostatectomy. For example, according to some evidence, metformin has been shown to inhibit the proliferation of breast, prostate, colon, uterine, ovarian, and glioma cancer cells. For example, several studies have reported an increase in OS index and a reduction in prostate cancer risk due to metformin use.

In general, according to reports, clinical and experimental pharmacology and physiology nigella sativa articles, as well as animal and human models, the risk of cancer is reduced by the use of metformin, especially in diabetic patients.

One of the greatest clinical trials conducted to date is called NCT01101438. NCT01101438 is a 3-phase experiment that go to see the efficacy of metformin in the treatment of cancers such as breast cancer, non-metastatic cancers, and cancers with a low degree of malignity. Patients received metformin twice a day for 5 years after diagnosis. Patients with prior use of metformin, insulin or other oral hypoglycemia were excluded.

So far, gemcitabine combined with other agents has shown a modest, but statistically significant, benefit in OS in patients Duloxetine Hcl (Cymbalta)- Multum advanced disease. Patients were excluded from the study if they had previously used metformin. NCT01210911 also registered 120 patients who were examined whether a dose of 1,000 mg twice daily in the 6-month period of metformin in combination with erlotinib and gemcitabine is more effective than the combination of these two agents in prolonging PFS.

Consumers before metformin and patients with reading pa diabetes were also excluded from the study.

Metformin was given twice a day for 12 months. In this study, diabetic patients or former metformin users were excluded from the study and glycemic control was a secondary outcome. This randomized phase II trial study reported that metformin may seeds flax some enzymes active.

These enzymes may block other enzymes Duloxetine Hcl (Cymbalta)- Multum for cell growth and stop the growth of tumor cells. NCT01433913 studied varietal effects of metformin in a different condition, such as adenocarcinomas of the prostate and stage I, IIA and IIB prostate cancer. Also, NCT00659568 (a phase I trial) studied the side effects and best dose of metformin when given together with temsirolimus in treating patients with metastatic or unresectable solid tumor or lymphoma.

One of the ongoing clinical trials is NCT01666730 (phase II trial) that studies the effects of metformin and some drugs in chemotherapy such as leucovorin calcium, fluorouracil, and oxaliplatin. According to this trial, drugs used in chemotherapy work in availability heuristic ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Giving metformin together with combination chemotherapy may kill more tumor cells.

Other clinical trials are summarized and shown medical Table 2. Several studies have shown increased intrinsic sensitivity of cells due to the use of metformin (in combination amok radiotherapy), measured by markers such as phosphorylation of histone H2AX protein or olive tail moment.

As a result of increased ROS in the cell, damage to the DNA increases and the production of protein and fat decreases. There is also evidence of a metformin-induced reduction in glutathione in the cell. Therefore, Duloxetine Hcl (Cymbalta)- Multum can increase the likelihood of damage to DNA. Hence, in general, metformin when used in combination with radiotherapy can cause damage to the DNA and the death of cancer cells by increasing the level of ROS.

Several cases have been reported that patients with head and neck squamous cell carcinoma (HNSCC) who underwent radiotherapy (after surgery) showed no sign of illness recurrence.

The result of the study showed that patients using metformin who were treated with chemoradiotherapy had a better response to treatment than the other two groups. One of the factors affecting the response of patients who did not use metformin is the high levels of insulin and insulin resistance. Several papers suggest that metformin increases cell sensitivity by lowering insulin levels, increasing apoptosis, increasing oxygen in the tumor, and increasing the damage to DNA, thereby causing the death of cancer cells.

The expression of the p53 gene is regulated by AMPK, and the presence of AMPK leads to the expression of this gene. P53 gene is a tumor suppressor, and the sleep disorder article of this gene leads to autophagy and apoptosis.

Metformin, like radiotherapy, activates the p53 gene, resulting in a rapid transcription of the p21 gene, which itself is a tumor suppressor. The activity of this gene results in the activity of the inhibitors of CDK (cyclin-dependent kinase), such as CDKN1A, which are barriers of cell division. This Duloxetine Hcl (Cymbalta)- Multum also forces the cell to apoptosis. Therefore, the p21 gene can reduce the proliferation of cancer cells and also Duloxetine Hcl (Cymbalta)- Multum the cellular cycle by regulating and applying therapy-induced cellular senescence (TCS).

All the material and evidence available reflect the anti-tumor properties of metformin. This drug can be used as a complementary therapeutic agent for cancer treatment.

Given the potential of metformin in the treatment of cancer, it can be safely used in radiotherapy and chemotherapy to improve therapeutic response in ADT (androgen deprivation therapy).



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