Tests of blood, saliva, or tears can look for specific
leukemia proteins.
Not exact matches
In turn, these modifications are caused by two specific
proteins of the so - called chromatin regulator group, on which
leukemia cells are dependent.
«
Protein isolated from baker's yeast shows potential against
leukemia cells: Researchers performed in vitro trials to test the effect of L - asparaginase on acute lymphoblastic
leukemia cells and published the results in Scientific Reports.»
A
protein domain once considered of little importance may be key to helping patients who are fighting acute myeloid
leukemia (AML) avoid a relapse.
«New clue to halting
leukemia relapse found: Molecule created that attacks chemo - inhibiting
protein.»
This clinical trial sponsored by Juno Therapeutics is testing JCAR017, which targets the CD19
protein expressed on most B - cell
leukemias and lymphomas.
However, in some patients, the
leukemia recurred without the CD19 target and expressed a
protein that the CAR T cells were unable to recognize — CD22.
In PLAT - 02, the CAR T cells are reprogrammed to recognize and target the CD19
protein that is expressed by most precursor B acute lymphoblastic
leukemia cells.
The team started by analyzing bone marrow samples from children with B - ALL and cataloging every
protein present in the
leukemia cells.
«Further research is needed to characterize how we can potentially remove or block this
protein to stop the proliferation of
leukemia cells.»
They will examine the safety and feasibility of administering cancer - fighting chimeric antigen receptor (CAR) T cells that have been reprogrammed to target the CD22
protein expressed by some
leukemia cells.
UCLA scientists have uncovered how a cellular
protein contributes to an aggressive form of
leukemia prevalent in young children.
With the PLAT - 04 trial, researchers will now be able to reprogram CAR T cells to detect and destroy
leukemia cells that express the CD22
protein.
The researchers also found that removing the IGF2BP3
protein from
leukemia cells led to decreases in
leukemia - promoting messages, which in turn killed the
leukemia cells.
They discovered that IGF2BP3 binds to and stabilizes hundreds of
leukemia - promoting RNA messages and consequently increases how much
protein is made, resulting in an environment that is conducive to
leukemia cell growth.
The gene (E2A) that codes for
proteins with the properties of immunoglobulin enhancer binding factors E12 / E47 was mapped to chromosome region 19p13.2 - p 13.3, a site associated with nonrandom translocations in acute lymphoblastic
leukemias.
If so, says Grover Bagby, a hematologist who directs the Oregon Cancer Center at the Oregon Health Sciences University in Portland, further work to decipher the
protein's exact function could shed light on how to treat a much larger population of patients with
leukemia, certain other forms of cancer, and aplastic anemia.
The lack of the normal
protein or a mutated version may play a role in how anemia patients acquire
leukemia.
Although insufficient on its own to trigger
leukemia, f - circM9 appears to work together with other cancer - promoting signals (such as the MLL - AF9 fusion
protein) to cause disease.
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.
Rhesus monkey TRIM5α protects against HIV - 1, but the only modern virus that the human
protein has any effect on is one that causes
leukemia in mice — which happens to be closely related to PtERV1.
The findings are particularly noteworthy because drugs that act on the newly discovered target, a
protein known as PIM1, are already in clinical trials for
leukemia and multiple myeloma.
Scientists at Sylvester Comprehensive Cancer Center at the University of Miami Miller School of Medicine have shown that p300, a
protein that increases gene expression by attaching acetyl molecules to DNA, may stop myelodysplastic syndrome (MDS) from developing into acute myeloid
leukemia (AML).
While p300 apparently plays a critical role in MDS progressing to
leukemia, this function is highly contextual as the
protein has no obvious effect on healthy stem cells.
To overcome this hurdle, researchers genetically engineered human T cells to produce a CAR
protein that recognizes a glycopeptide found on various cancer cells but not normal cells, and then demonstrated its effectiveness in mice with
leukemia and pancreatic cancer.
The engineered cells contain an antibody - like
protein known as a chimeric antigen receptor (CAR), which is designed to bind to a
protein called CD19 found on the surface of B cells, including the cancerous B cells that characterize several types of
leukemia.
The vaccine sets off an immune response using a piece of a
protein, called PR1 peptide, found on the surface of
leukemia cells.
Dr Xu showed that for BET inhibitors to successfully kill lymphoma and myeloid
leukemia cells the presence of a
protein called BIM, which brings on apoptosis, was critical.
The modified T cells contain a
protein known as a chimeric antigen receptor (CAR), which is designed to target the CD19
protein found on the surface of B cells, including the cancerous B cells that characterize several types of
leukemia and lymphoma.
«Role of RNA binding
protein in driving cancer,
leukemia study reveals: Abnormally expressed in cancer cells, the
protein was found to promote the proliferation of B cells in B - cell acute lymphoblastic
leukemia.»
This allowed them to the see entire complement of
proteins regulated by TRAF6 in
leukemia cells.
In the case of IGF2BP3 and B - cell
leukemia, the overall effect of the RNA binding
protein is to promote the proliferation of B cells by shifting the expression of a large number of genes, Sanford said.
A study of gene expression in
leukemia cells has identified an RNA binding
protein that plays an important role in driving the development of cancer.
When investigators treated the
leukemia cells with a JQ1 - and - phthalimide «conjugate» called dBET1, the BRD4
protein within the cells was degraded in less than an hour.
Focusing on two
proteins known as transcription factors, the researchers showed that genetically removing the two transcription factors, Tcf1 and Lef1, in mice is sufficient to prevent
leukemia stem cells from persisting.
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.
ANAHEIM, CALIFORNIA — Chronic myeloid
leukemia (CML) cells invade the bone marrow and spleen by destroying healthy cells with a toxic
protein, according to a new study.
A class of therapeutic drugs known as
protein kinase inhibitors has in the past decade become a powerful weapon in the fight against various life - threatening diseases, including certain types of
leukemia, lung cancer, kidney cancer and squamous cell cancer of the head and neck.
By analogy to the gag / abl fusion
protein of Abelson murine
leukemia virus, the replacement of amino terminal c - abl sequences by bcr sequences in P210 may create a transforming
protein involved in CML.
In cancer, a state marked by increased
protein translation and biomass expansion, HSF1 is activated and binds to numerous genes throughout the genome, as seen in the heat map of HSF1 ChIP - Seq read density in M0 - 91acute myeloid
leukemia cells (DMSO, far left).
The symbol ABL is derived from Abelson, the name of a
leukemia virus which carries a similar
protein.
A CAR is a
protein composed of an antibody that can bind to a known target — in our model we picked the CD19 antigen found on B cell
leukemias.
An exciting development in rational anticancer drug design is Gleevac, a drug that acts on a
protein unique to the defective white blood cells in chronic myelogenous
leukemia and on a related
protein in a rare form of gastrointestinal cancer.
Activation of both
protein kinase A (PKA) type I and PKA type II isozymes is required for retinoid - induced maturation of acute promyelocytic
leukemia cells.
Characterization of a nuclear export signal within the human T cell
leukemia virus type I transactivator
protein Tax.
«It may be that the normal TEL allele successfully suppresses the function of the aberrant TEL - AML1
protein resulting from the fusion, so full - blown
leukemia doesn't occur,» said the lead author of the study, Joseph Wiemels, PhD, now a UCSF assistant research molecular epidemiologist.
Secretion of the human T cell
leukemia virus type I transactivator
protein tax.
The synthetic peptide PFWT disrupts AF4 — AF9
protein complexes and induces apoptosis in t (4; 11)
leukemia cells.
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 fact, mutations in a human
protein highly related to the yeast histone methyltransferase Set1, called MLL, are involved in
leukemia.