Effects of obesity on bone marrow cells

According to new research, obesity causes durable and harmful changes to the hematopoietic stem cell compartment-the blood-making factory in human body. Blood stem cell compartment is made up of numerous cell subsets, age and environmental stresses can lessen the healthy diversity of cells in human blood-making machinery. This can include skewing blood cell formation toward myeloid cells and possibly promoting pre-leukemic fates.

Obesity related stresses alter the cellular architecture of the hematopoietic stem cell compartment and reduce its long-term functional fitness. Tests in obese mice show these effects are progressive and that some of the harmful manifestations persist even after researchers normalize the animals' weight through dietary controls. Alterations of the body's blood-making system appear to be linked to over- expression of a transcription factor called Gfi1- a regulatory gene that controls other genes. The researchers show that oxidative stresses in the body caused by obesity drive overexpression of Gfi1.

 This produces a lasting alteration of hematopoietic stem cell compartment and molecular mayhem. The study also provides groundwork to investigate how lifestyle choices, such as diet, can durably impact blood formation and may contribute to the development of blood cancer. Hematopoietic stem cells are an important tool for treating leukemia and other blood diseases.
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How protein breakdown causes leukemias and brain cancer

An enzyme that is responsible for the breakdown of specific amino acids in food plays a key role in the development of leukemias and brain cancer. The researchers have discovered a surprising link between energy metabolism and the epigenetic code. These labels in the DNA of cancer stem cells determine the activity of genes and many cellular functions.

Acute myeloid leukemia AML is an aggressive type of blood cancer that often relapses in the wake of successful initial treatment. Stem cells that are resistant to therapy are believed to be responsible. Reseachers examined patient samples by comparing the composition of proteins of AML stem cells and leukemia cells without stem cells properties.

The investigators found suspiciously high levels of an enzyme called BCAT1 in the stem cells. These levels rose even higher during a cancer recurrence. The researchers considered this to be a clue that BCAT1 might be linked to therapy resistance. Cancer researchers have suspected for some time that the BCAT1 enzyme, which is responsible for the breakdown of specific proteins in food, plays a role in the development of malignant tumors.

 They discovered that an overproduction of BCAT1 increases the aggressiveness of malignant brain tumors and breast cancer. BCAT1 reduces the levels of this key molecule and this leads to increased levels of chemical labels in the DNA. The tiny methyl groups that are attached to DNA determine whether particular genes are active or silent and, thus, have an immense impact on all cellular functions.

They increase cancer-promoting methylation of DNA. AML is known for an extremely heterogeneous pattern of genetic alterations. However, misregulated methylation with its drastic consequences for the whole cell appears to be a common characteristic of this malignant disease.

The finding that BCAT1 drives cancer-promoting methylation in AML stem cells and other cancer stem cells opens up new options for therapy. A blockade of the enzyme using a targeted agent might normalize DNA methylation and thereby reduce cancer spread and therapy resistance.
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Blood cancer gene could prevents heart failure

Coronary heart disease is the leading cause of death across the globe. Most of these deaths are caused by a heart attack-myocardial infarction where the blood flow to the heart is acutely blocked causing irreversible damage to the heart muscle.

People may survive a heart attack, but the damage that has occurred to the heart muscle can develop to heart failure – a debilitating condition in which the heart cannot pump blood around the body.

The gene Runx1 increases in damaged heart muscle after a heart attack. Mice with a limited capacity to increase Runx1 gene activation were protected against the adverse changes that lead to heart failure.

The Runx1 gene has been extensively studied in the context of its role in leukaemia and normal blood cell development, however until now its role in the heart was unknown.
Now researchers believe that the increased expression of the Runx1 gene, which happens after a heart attack, contributes to adverse changes in the shape and pumping action of the heart.
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Vitamin C can stop the spread of blood cancer

Faulty stem cells in bone marrow often multiply, increasing the growth of fatal tumours. The diseases can lead to anaemia and bleeding as abnormal stem cells multiply in the bone marrow and interfere with blood cell production.

Vitamin C can kill and prevents the spread of the tumours. Vitamin C found in high levels in kale, oranges and peppers could prevents blood cancer but it is impossible to get the required amount through fruits and vegetables in high quantities.

High quantities of vitamin C required for killing the tumours can be given by injecting cancer patients intravenously, the patients can get up to 500 times the amount they would get through eating fruit and vegetables.

Vitamin C prevents the breakdown of glucose, the mitochondria - the strength of the cancer cells are unable to gain vital energy it needs to grow with vitamin C injection.

Researchers discovered that vitamin C suppressed the growth of leukaemia cancer stem cells from human patients implanted into the mice. Combining vitamin C with a cancer drug is more effective in cancer treatment.
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Arthritis drug for blood cancer treatment

Polycythemia Vera PV, is a blood cancer that causes an excess production of red blood cells. Common symptoms of PV are: itching, headache, weight loss, fatigue and night sweats.

Researchers have discovered that methotrexate MTX- a drug for treatment of arthritis can be useful for treating blood cancer.

 The drug works by directly inhibiting the molecular pathway causing the disease. Blood cancer could be treated with methotrexate MTX an arthritis drug.

Methotrexate acts as a potent suppressor in cells carrying the mutated gene responsible for myeloproliferative neoplasms MPNs in patients.

Low-dose of MTX suppresses JAnus kinase JAK/STAT Signal Transducer and Activation of Transcription pathway activity and is able to normalise the raised blood counts and the increase in spleen size associated with blood cancer.

Methotrexate MTX has the potential to provide a new molecularly targeted treatment for myeloproliferative neoplasms patients MNP
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Impacts of proteins on immune system

Different genetic make-up can impact on the activity of the immune system and our ability to fight cancer.

Proteins are made up of thousands of smaller units called amino acids, which are attached to one another in long chains.

Proteins do most of the work in cells and are required for the structure, function, and regulation of the body's tissues and organs.

 A protein called ULBP6 leads to the removal of damaged cells. There are two types of this protein found in different people.

The ULBP6 protein is found on the surface of damaged cells, including several types of cancer cells, and acts as a signal to white cells in our immune system that the damaged cell should be killed.

There are two major types of protein in the population and people who inherit a certain subtype have been shown to have a poor outcome after stem cell transplantation, a procedure used to treat leukemia, which is commonly referred to as bone marrow treatment.

The two types of ULBP6 differ only by two amino acids out of a total of around 180 and it has important influence on patient outcomes. One form of ULBP6
 forms a very strong bond indeed with its receptor NKG2D on the immune system.

This shows why transplants work less well in some people, which is an important step on the path to developing better transplant therapy for more people living with blood cancer.

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