Sentences with phrase «causes of leukemia»

«Making headway in infant leukemia research: Researchers identify further causes of leukemia in children.»

We do not understand much about the causes of leukemias, and so more research is needed in this area.»

Acute myeloid leukemia (AML) is the leading cause of leukemia mortality in the United States.1 Curative treatment involves intensive induction chemotherapy, before proceeding to either consolidation chemotherapy or allogeneic stem cell transplantation based on the patient's risk for relapse.2 This approach has been employed for > 4 decades and, although most individuals achieve complete remissions with front - line therapy, 3 the majority of patients ultimately relapse with drug - resistant disease, and overall survival rates remain disappointingly poor.4 The limited ability of many patients to tolerate the intense chemotherapy - based treatments, in particular hematological toxicity, further contributes to the poor outcomes noted in this disease.

The benzenes are petroleum - based, so they're cheap, easy to come by, and, by the way, a known cause of leukemia.

The cause of leukemia in cats is unknown.

Not exact matches

Why not look at all of God's «love», such as what caused this man's disease, or Leprosy, or Childhood Leukemia.

Obviously, a «pro-life» person would support and encourage research designed to find the causes and cures of diseases that strike down young children disproportionately, such as leukemia.

«I am calling upon him to take those donations out of his $ 27 million campaign coffer and donate them to a worthy institution that treats children with life - threatening allergies who can't afford EpiPens or with pediatric cancers like leukemia and Hodgkin's who are suffering because of generic drug shortages that he causes,» Long said in a statement.

In a common subtype of acute myeloid leukemia, this abnormal activation of such self - renewing genes is apparently caused by structural modifications of the DNA packaging.

In turn, these modifications are caused by two specific proteins of the so - called chromatin regulator group, on which leukemia cells are dependent.

MLVs so dependably cause cancer in lab - bred mice — especially leukemia and lymphoma — that a small fraternity of scientists at the NCI and elsewhere has fruitfully studied these viruses since the 1960s in an effort to understand how human cancer begins.

However, a type of cellular signaling caused by the BRAF inhibitors may leave patients susceptible to secondary malignancies, such as squamous cell carcinoma and RAS - mutant leukemia.

The scientists discovered that dinaciclib, by interfering with UPR activation, caused multiple myeloma and myeloid leukemia cells to initiate a form of cell suicide known as apoptosis when exposed to agents that induced ER stress.

Significantly, disabling both anti-apoptotic proteins, Bcl - 2 and Bcl - xL, in conjunction with Mcl - 1, caused profound cell death of leukemia cells in the test tube as well as in animal models of AML.

As part of the new study, the researchers showed that intact axons without Phr1 were protected from the damage caused by vincristine, a chemotherapy drug used to treat leukemia, neuroblastoma, Hodgkin's disease and non-Hodgkin's lymphoma, among other cancers.

There's some disagreement about how much is needed to cause cancer or what kinds of cancer it causes, but there's no debate about whether it's a carcinogen and it's most closely associated with leukemia and lymphoma.

Research carried out at the Division of Genetics at Friedrich - Alexander - Universität Erlangen - Nürnberg (FAU) with support from the Institute for Human Genetics has now discovered another molecular cause for a particularly aggressive type of leukemia in infants.

«Opening the door to the cause of myeloid leukemia: Finding the targets of common mutation.»

«Like Angelina Jolie, study pinpoints genetic cause of increased leukemia risk.»

A year later, Carlo Croce, now director of the Human Cancer Genetics Program at Ohio State University, reported that chronic lymphocytic leukemia (CLL), the most common form of the disease, was caused by deletion of two microRNA genes.

While the cause remains largely unknown, only a small fraction of childhood leukemia is believed to involve an inherited genetic predisposition.

A University of Colorado Cancer Center study published today in the journal Nature Genetics describes a newly - discovered, heritable genetic cause of acute lymphoblastic leukemia (ALL), namely mutation of the gene ETV6.

One, the simian immunodeficiency virus, is the predecessor of HIV; the other is simian T - lymphotropic virus 1, whose descendant in humans, HTLV - 1, can cause leukemia.

With arsenic forcing the production of largely useless telomerase in cell lines that simulate acute promyelocytic leukemia, the chromosomes in cancer cells fuse together, causing the cell death that helps fight the cancer.

Concerned that the therapy itself might have caused leukemia in one of 10 patients they have treated, however, the French group halted its trial in September and urged colleagues using retroviruses to hold off while the risks are assessed.

When tested in laboratory samples of leukemia cells and in animals with human - like leukemia, the approach caused cancer cells to die much more quickly than with conventional targeted therapies.

When Ralph Arlinghaus, a molecular biologist at the University of Texas MD Anderson Cancer Center in Houston, learned that growth factor — starved healthy cells release a protein called 24p3 that causes them to die, he wondered if leukemia cells also use the molecule to kill off their competition.

But following the onset of leukemia in some trials (ScienceNOW, 7 March 2005), scientists began to wonder whether IL2RG or another viral gene was inserting itself in the patients» DNA in a way that disrupted a class of genes called oncogenes, which can cause cancer if mutated.

Beyond LFS, osteosarcoma is the most common type of bone cancer in all children, and after leukemia, the second leading cause of cancer death for them.

So far, only five transmissible cancers have been observed among animals, all of which cause leukemia - like diseases in clams and other shellfish.

Importantly, the fusion of the TEL and AML1 genes is not sufficient to cause development of the disease, known as «common acute lymphoblastic leukemia,» the researchers said.

In 2001 imatinib was approved for the treatment of chronic myeloid leukemia, a disease that is almost universally caused by a single genetic mutation, known as the Philadelphia chromosome, and its resulting mutant protein.

In a 2015 Nature Communications paper, Rao, who heads LJI's Division of Signaling and Gene Expression, reported that TET2 / 3 mutations caused myeloid disease resembling acute myeloid leukemia in mice.

This work raises the possibility that histones can signal to non-histone proteins in human cells, and that deregulation of these events caused by MLL mutations might contribute to leukemia development.

Other DNA repair deficits can cause a range of diseases such as leukemia, breast cancer and hereditary non-polyposis colorectal cancer, a common cause of colon cancer in Western nations.

Gallo and his colleagues then opened and pioneered the field of human retrovirology with the discovery of the first human retrovirus (HTLV - 1) and along with Japanese investigators showed it was a cause of a particular form of human leukemia.

(Chronic myeloid leukemia, a deadly blood cancer, for example, is caused when two chromosomes in white blood cells exchange fragments, resulting in a hapless fusion of genes that are normally kept apart.)

Previous reports have shown that in a genetic abnormality called Philadelphia chromosome, fusion of ABL and BCR genes cause leukemia.

The results of her project will help scientists develop novel therapies to target the regulatory proteins that cause CD47 overproduction in leukemia and other cancer stem cells, with the goal of restoring immunosurveillance and enabling the immune system to recognize and destroy these aberrant cancer cells.

A hallmark of the Notch pathway is its gene dosage sensitivity, such that small differences in the amount of Notch activity can cause aberrant cell fate choices and T - cell leukemia.

Death caused by leukemia was defined by enlargement of the spleen and liver on autopsy, whereas death caused by GVHD was defined as the absence of tumor and the presence of GVHD.

Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias.

The therapeutic potential of bone marrow transplantation (BMT) relies on the graft - versus - leukemia (GVL) effect, which is closely associated with graft - versus - host disease (GVHD), the major cause of morbidity and mortality after BMT (1 — 4).

The researchers found that 10 out of the 20 bioflavonoids tested caused breaks in one small region of a gene known as MLL, which is a key player in about 80 percent of infant leukemias.

A decade has passed since the first of two stem cell transplants cured Brown of both leukemia and HIV, making him the first and so far only person to be cured of the virus that causes AIDS.

Some researchers have argued that the cause may be an infectious agent, but epidemiologic studies have suggested that maternal consumption of foods such as bioflavonoids could lead to an increased risk of infant leukemia.

April 10, 2000 Dietary bioflavonoids induce DNA breaks, may contribute to infant leukemia Ordinarily considered quite beneficial, bioflavonoids — found in many foods including soybeans, fruits, root vegetables and herbs, and in high concentrations in dietary supplements — can cause breaks in DNA that could trigger the development of infant leukemias.

In 2005, the identification of an activating mutation in JAK2 (the V617F mutation) as a STAT5 - activating and disease - causing genetic alteration in a significant proportion of patients with myeloproliferative neoplasms (MPNs) has emphasized the oncogenic role of the JAK tyrosine kinases in hematologic malignancies.2 — 5 JAK2 is a member of the Janus tyrosine kinase family comprising three other mammalian non-receptor tyrosine kinases (JAK1, JAK3 and TYK2) that associate with cytokine receptors lacking intrinsic kinase activity to mediate cytokine - induced signal transduction and activation of STAT transcription factors.6 All JAKs share a similar protein structure and contain a tyrosine kinase domain at the C - terminus flanked by a catalytically inactive pseudokinase domain with kinase - regulatory activity, by an atypical SH2 domain and by a FERM domain that mediates association to the membrane - proximal region of the cytokine receptors.7, 8 Soon after the discovery of JAK2 V617F, we and others described that activating JAK1 mutations are relatively common in adult patients with T - cell acute lymphoblastic leukemia (ALL) and participate in ALL development allowing for constitutive activation of STAT5.9 — 11 Several STAT5 - activating JAK1 mutations were also reported in AML and breast cancer patients.10

Cause of Resistant Leukemia Identified Kimmel Cancer Center investigators identify an FLT3 mutation and link it to a treatment - resistant form of acute myeloid lLeukemia Identified Kimmel Cancer Center investigators identify an FLT3 mutation and link it to a treatment - resistant form of acute myeloid leukemialeukemia.

Changes in an epigenetic mechanism that turns expression of genes on and off may be as important as genetic alterations in causing pediatric acute lymphoblastic leukemia (ALL), according to a study led by scientists at St. Jude Children's Research Hospital and published in the June 10 online edition of the Journal of Clinical Investigation.