Oestrogen changes neuroblastoma cells into neurons

The female sex hormone oestrogen can perform an important role in neuroblastoma, a form of cancer mainly affecting young children. In laboratory experiments, researchers at Karolinska Institutet in Sweden demonstrate that oestrogen treatment and overexpression of the oestrogen receptor cause malignant neuroblastoma cells to mature into neuron-like cells.

Neuroblastoma forms in the peripheral nervous system and is one of the most common forms of solid cancer in young children. The disease mainly affects babies and young children, and while in some cases the tumours can disappear of their own accord, the majority are aggressive, metastasising cancer tumours that are resistant to modern combinations of surgery, radiotherapy and intensive chemotherapy.

The most aggressive forms of neuroblastoma are often associated with a more active MYCN gene, which drives tumour cell growth and spread and inhibits the maturation of the cells. Researchers focus on the activity of this gene and how it relates to neuroblastoma. MYCN is often seen only as a marker for a poor prognosis, but it's critical to the disease and is a possible target for new drugs.

In a previous study, the group discovered that activation of MYCN results in the formation of specific microRNAs, which are relatively small RNA molecules that regulate proteins. Some of these microRNAs disable the oestrogen receptor ERalpha. The present study shows that the inhibition of these microRNA molecules or oestrogen therapy in combination with an overexpression of the oestrogen receptor can cause aggressive neuroblastoma cells with MYCN activation to mature into neuron-like cells which behave more like normal cells.

The researchers studied tumour tissue from patients, cultivated human tumour cells and tumours in mouse models for neuroblastoma. In the mice, the neuron-like cells did not grow as quickly as the original cancer cells, and analyses of the tumour tissue from patients show that those with a high level of the oestrogen receptor have a better survival rate than those with a low. Oestrogen could be a therapeutic method for patients who express high levels of the oestrogen receptor. Another therapy could involve deregulating MYCN or upregulating the oestrogen receptor and then treating with oestrogen.
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Fasting diets boost brain power

Intermittent fasting may provide brain with more energy, improves memory and learning capabilities. When mice were fed every other day, they grew more neurons and synaptic connections, improving their cognitive functions. During intermittent fasting, the body switches energy sources from glucose, made in the liver, to fat cells, which stimulate activity and cell growth in the brain.

The body runs off of the liver's energy stores for about 10 to 14 hours in humans, when those stores are out, human, as well as animal bodies switch to fat stores, which are converted into compounds called ketones in the blood. Ketones act directly on the nerve cells to stimulate production of BDNF'- a key protein to neuron growth-and may help optimize cognition, learning and memory building.

Simply eating less will not have the same effects, eating three meals a day and having an overall relatively low calorie intake - between 1,800 and 2,000 every time-replenish their liver energy stores. The mice in the study were more alert and showed more activity in the areas of their brains responsible for learning and memory during the fasting period. Every-other-day fasting his team used for the mice wouldn't work in human, two days of fasting each week can help in human.
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Lipid synthesis promotes tumor formation in liver

Lipids comprise an optimal energy source and an important cell component. Researchers from the have discovered that the protein mTOR stimulates the production of lipids in liver tumors to satisfy the increased nutrient turnover and energy needs of cancer cells, among other functions. This process has also been observed in patients with liver cancer as the scientists report in cancer cell.

In mouse models and patient samples, researchers demonstrated that the growth regulator mTOR-mammalian target of rapamycin-promotes de novo lipid synthesis and thus tumorigenesis. The accumulation of fatty acids and lipids in the liver is one of the major causes of hepatocellular carcinoma.

Liver stores and recycles nutrients, produces hormone precursors and detoxifies the body by eliminating harmful substances, such as drugs and alcohol. Obesity and diabetes combined with lack of exercise can damage the liver. A first asymptomatic syndrome is so-called "fatty liver," which may cause inflammation that can progress to hepatocellular carcinoma (HCC). The aggressive and rapidly proliferating HCC cells ultimately destroy the surrounding healthy liver tissue, leading to liver failure.

The researchers initially investigated the progression of the disease in a mouse model. For this purpose, they constitutively activated mTOR specifically in liver cells. mTOR is involved in tumor development as it centrally controls cell growth. The researchers have now discovered that mTORC2-mTOR forms two protein complexes termed mTORC1 and mTORC2-promotes the new synthesis of fatty acids and certain lipids. Human body contains more lipid species than genes. It is assumed that there are thousands of different types.

In hepatocytes, mTORC2 stimulates in particular the production of two lipid species important for cell growth: sphingolipids and cardiolipins. The first are structural components of cell membranes, which have to be continuously supplied in rapidly proliferating cells. Cardiolipins are located in the cellular powerhouse, the mitochondria, and are involved in energy production. By enhancing cardiolipin synthesis, the energy-hungry tumor cells ensure their energy supply.

Cancer cells depend on the new synthesis of fatty acids and lipids. Analysis of tissue samples from patients with HCC confirmed the observations made in the mouse model. mTORC2 and its signaling pathways, which promote de novo synthesis of fatty acids and lipids, are also activated in tumor samples from patients. Thus, the protein complex plays a critical role in the progression of benign "fatty liver " to aggressive HCC. The study provides important insights for the development of potential therapeutic interventions, as it shows that targeted lipogenesis inhibitors may have the potential to prevent tumor development.
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Zinc can stop the growth of cancer cell

Zinc is essential for maintaining human health and protecting the esophagus from cancer. According to the latest research, zinc supplements can prevent the proliferation of esophageal cancer cells. Clinical data and animal studies have shown that this mineral is very important for overall body health and for cancer prevention.

Esophageal cancer is the sixth leading cause of deaths across the globe, zinc deficiency has been found in many cancer patients, zinc is an important element in many proteins and many enzymes and the absence of zinc makes it impossible for cells to function properly.

Zinc impedes overactive calcium signals in cancer cells, which is absent in normal cells, and thus zinc selectively inhibits cancer cell growth. Insufficient amount of zinc can lead to the development of cancers and other diseases, foods rich in zinc are spinach, flax seeds, beef, pumpkin seeds, shrimp and oysters.

It is needed in small amounts every day for sound health, apart from cancer prevention, some other benefits of zinc are production of hormones, maintaining proper growth, it improves immunity, it facilitates digestion and reverses heart disease.
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Aliqopa for treating follicular lymphoma

Aliqopa drug (copanlisib) is for the treatment of adults with relapsed follicular lymphoma who have received systemic therapies. For patients with relapsed follicular lymphoma, the cancer often comes after multiple treatments.

Follicular lymphoma is a slow-growing type of non-Hodgkin lymphoma, a cancer of the lymph system. The lymph system is part of the body’s immune system and is made up of lymph tissue, lymph nodes, the spleen, thymus, tonsils and bone marrow.

Aliqopa is a kinase inhibitor that works by blocking several enzymes that promote cell growth. Common side effects of Aliqopa include high blood sugar levels, diarrhea, fatigue, high blood pressure, low levels of certain white blood cells, nausea, lower respiratory tract infections, and low levels of blood platelets.

Serious side effects include infections, high blood sugar levels, hypertension, inflammation of the lung tissues, low neutropenia and severe skin reactions. Women who are pregnant or breastfeeding should not take Aliqopa because it may cause harm to a developing fetus or newborn baby.
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Foods that kill bowel cancer

Eating more of plants based diet can increase rate of surviving bowel cancer after chemotherapy or prevent the cancer. Saturated fat and heterocyclic amines in red meat can cause bowel cancer, replace red meat with fish and white meat like chicken.

Add plant-based antioxidants to your food, eat red or green apples, yellow or orange bell peppers, broccoli, brussels sprouts, green leafy vegetables, avocados, blueberries, carrots, tomatoes, raspberries and strawberries.
They are rich in fiber.

Eat foods rich in selenium like brown rice, oats, whole grains, sunflower seeds, onions, salmon, halibut and tuna. Selenium has anti carcinogenic properties.

Cook with extra-virgin olive oil. It is a good source of omega-3 fatty acids, vitamin E, and antioxidant phenolic compounds. The phenolic compounds, has anti tumor properties.

 Add garlic to your food, the sulfur compound in garlic reduces colon cancer cell growth from induced apoptotic cell death.

Eat lower-glycemic-index foods.
Foods like green peas, cherries, plums, carrots, celery, asparagus, cabbage and broccoli. Low glycerin index foods decrease risk of bowel cancer.
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How to hinder cancer cells growth

Cancer is the abnormal and uncontrollable growth of cells. Researchers from the University of Rochester's Center for RNA Biology have identified a new way to potentially slow the fast-growing cells that cause  different cancer.

Cancer grows when cell cycle gone wrong, all cells undergo  "cell cycle," a series of events that culminate in orderly cell growth and division. When cancer grow, cells divide without stopping and destroy tissues.

Researchers identified a protein called Tudor-SN that is important in the "preparatory" phase of the cell cycle -- the period when the cell gets ready to divide. When scientists eliminated this protein from cells, using the gene editing technology CRISPR-Cas9, cells took longer to gear up for division.

 The loss of Tudor-SN slowed the cell cycle. Tudor-SN is plenty in cancer cells than healthy cells, and our study suggests that targeting this protein could hinder fast-growing cancer cells.
The cell now moves more slowly from the preparatory phase to the cell division phase.

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