Claim: Genes offer predictions on leukemia
Verdict: REFUTES

Retrieved passages:
title: Breast cancer classification
text: commercial-stage 80-gene panel marketed by Agendia, either as a standalone test, or combined with the MammaPrint gene profile. The choice of established chemotherapy medications, if chemotherapy is needed, may also be affected by DNA assays that predict relative resistance or sensitivity. Topoisomerase II (TOP2A) expression predicts whether doxorubicin is relatively useful. Expression of genes that regulate tubulin may help predict the activity of taxanes. Various molecular pathway targets and DNA results are being incorporated in the design of clinical trials of new medicines. Specific genes such as p53, NME1, BRCA and PIK3CA/Akt may be associated with responsiveness of the cancer

title: David Baltimore
text: as a model for the study of disease. They suggested that "control of lg gene rearrangement might be the only mechanism that determines the specificity of heavy chain gene expression within the lymphoid cell lineage." in 1987, they created transgenic mice with the fused gene that developed fatal leukemia. David G. Schatz and Marjorie Oettinger, as students in Baltimore's research group in 1988 and 1989, identified the protein pair that rearranges immunoglobulin genes, the recombination-activating gene RAG-1 and RAG-2. this was a key discovery in determining how the immune system can have specificity for a given molecule out of many

title: Chronic myelomonocytic leukemia
text: mutations in genes such as ASXL1 and EZH2 are associated with poor prognosis. CMML has a 20-30% chance of transformation to AML, a lower rate than other similar diseases. The CMML-2 subtype is associated with increased risk of transformation and ASXL1 and RUNX1 mutations also increase the risk of transition to AML. The International Prognostic Scoring System (IPSS) was developed in the mid-1990s to assess the prognosis of MDS patients. This system stratifies cases into 2 groups; a lower-risk group (sub divided into low and intermediate-1) and a higher risk (subdivided into intermediate-2 and high). It uses the blast percentage,

title: Acute lymphoblastic leukemia
text: lead to the creation of a leukemic lymphoblast. These changes include chromosomal translocations, intrachromosomal rearrangements, changes in the number of chromosomes in leukemic cells, and additional mutations in individual genes. Chromosomal translocations involve moving a large region of DNA from one chromosome to another. This move can result in placing a gene from one chromosome that promotes cell division to a more actively transcribed area on another chromosome. The result is a cell that divides more often. An example of this includes the translocation of "C-MYC", a gene that encodes a transcription factor that leads to increased cell division, next

title: Acute megakaryoblastic leukemia
text: to suppress the expression of various genes that are involved in the maturation of platelet, myeloid and lymphocyte precursor cells. In consequence, the RBM15-MLK1 fusion protein acts in an unregulated fashion to suppress MLK1 targeted genes while stimulating RPBJ target genes. This causes an over-active Notch signaling pathway and, among other abnormalities, expansion of fetal hematopoiesis and development of AMKL in a small percentage of adult mice. It is assumed that these events must be accompanied by other, as yet undefined, oncogenic (i.e., cancer causing) events to explain the development of human non-Down AMLK. A large number of other genetic

title: Leukemia
text: twin studies. The affected people may have a single gene or multiple genes in common. In some cases, families tend to develop the same kinds of leukemia as other members; in other families, affected people may develop different forms of leukemia or related blood cancers. In addition to these genetic issues, people with chromosomal abnormalities or certain other genetic conditions have a greater risk of leukemia. For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia. Mutation

title: MECOM
text: leukemia (AML), myelodysplastic syndrome (MDS) and chronic myelogenous leukemia (CML), and more recently has been shown as a poor prognostic indicator. Its function in these cells may be regulated by phosphorylation of serine196, in its N-terminal DNA binding domain. All of these involve erratic cellular development and differentiation in the bone marrow leading to dramatic alterations in the normal population of blood cells. EVI1 has also been found to play a role in solid ovarian and colon tumors, although it is not yet well characterized in this context. It has been hypothesized that it acts as a survival factor in

title: BAALC
text: Weber et al. where no difference in mutations in IDH1 and IDH2 where seen depending on expression of BAALC. IGFBP7 is another gene involved in leukemia, this was found conducting gene expression profiles (GEP) with BAALC. This gene has BAALC characteristics and, unlike BAALC, may have a role in drug resistance and the mechanism of leukemogenesis. It has been found that treatment for some acute leukemias failed due to BAALC and this suggests BAALC to be a potential surrogate marker. The use of BAALC expression in acute leukemia prognosis is unclear and being studied.Prognosis of patients with AML and BAALC

title: Pier Paolo Pandolfi
text: mechanisms and genetics underlying the pathogenesis of leukemias, lymphomas and solid tumors, and modeled these cancers in the mouse. His basic and translational research has led to the development of many experimental trials. He has also presented a new theory describing how messenger RNAs and non-coding RNAs exert their biological functions with profound implications for human genetics, cell biology and cancer biology. While a medical student, Pandolfi cloned and characterized PML-RARa (retinoic acid receptor alpha), the product of the long-sought after t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL) and its normal counterpart promyelocytic leukemia protein (PML). Later, Pandolfi's lab

title: Hairy cell leukemia
text: hairy cells, such as trisomy 5 had been found. The expression of genes is also dysregulated in a complex and specific pattern. The cells under express 3p24, 3p21, 3q13.3-q22, 4p16, 11q23, 14q22-q24, 15q21-q22, 15q24-q25, and 17q22-q24 and overexpress 13q31 and Xq13.3-q21. It has not yet been demonstrated that any of these changes have any practical significance to the patient. The diagnosis of HCL may be suggested by abnormal results on a complete blood count (CBC), but additional testing is necessary to confirm the diagnosis. A CBC normally shows low counts for white blood cells, red blood cells, and platelets in

title: Acute megakaryoblastic leukemia
text: (also termed MRTFA) on chromosome 22 to create a RBM15-MLK1 fusion gene. Studies in mice indicate that the "Mkl1" gene (only the first letter of a mouse gene is capitalized) product, MLK1, interacts with the transcription factor SRF to stimulate the expression of various genes. MLKl is required for the maturation of mouse megakaryoblasts: in its absence, megakaryoblasts and promegakaryocytes proliferate abnormally while megakaryocytes are few in number and have an abnormal morphology. Mouse studies also indicate that the product of Rbm15, RMB15, interacts with Nuclear receptor co-repressor 1, Nuclear receptor co-repressor 2 (also termed SMRT), and RBPJ nuclear proteins

title: Cancer biomarker
text: When these two chromosomes combine they create a cancer-causing gene known as BCR-ABL. In such patients, this gene acts as the principle initial point in all of the physiological manifestations of the leukemia. For many years, the BCR-ABL was simply used as a biomarker to stratify a certain subtype of leukemia. However, drug developers were eventually able to develop imatinib, a powerful drug that effectively inhibited this protein and significantly decreased production of cells containing the Philadelphia chromosome. Another promising area of biomarker application is in the area of surrogate endpoints. In this application, biomarkers act as stand-ins for the

title: FIP1L1
text: nuclear retinoic acid receptor alpha (RARA) protein. The RARA protein, when ligand-bound, regulates the expression of genes that are implicated in the control of development, differentiation, apoptosis, myelopoiesis, and the transcription of transcription factors which in turn regulate the transcription of clock genes. Translocations between this 17q21.2 locus and several other loci have been associated with acute promyelocytic leukemia. Three case reports have found that chromosome translocations between "FIP1L1" and "RARA" gene loci are associated with two cases of acute promyelocytic leukemia and one case of juvenile myelomonocytic leukemia. Relatively little is known about function of or therapy for these

title: Promyelocytic leukemia protein
text: dysregulation of these processes, has been implicated in a variety of cancers. PML was poorly understood until described in the findings of Grignani "et al" in their 1996 study of patients with acute promylocytic leukemia (APL). It was found that the karyotype of 90% of APL patients included a reciprocal translocation, resulting in the fusion of the Retinoic Acid Receptor (RARalpha) gene of chromosome 17 and the PML gene of chromosome 15, which had not previously been characterized. The resultant PML/RARalpha oncofusion gene was shown to disturb normal PML and RARalpha function, thus inhibiting the terminal differentiation of blood precursor

title: Cancer epigenetics
text: studied, including 5/5 TERT, 1/4 DAPK1, 2/5 RARB, MAL, and CADM1. Furthermore, 1/3 of CpG sites in mitochondrial DNA were associated with increased methylation in CIN3+. Thus, a correlation exists between CIN3+ and increased methylation of CpG sites in the HPV16 L1 open reading frame. This could be a potential biomarker for future screens of cancerous and precancerous cervical disease. Recent studies have shown that the mixed-lineage leukemia (MLL) gene causes leukemia by rearranging and fusing with other genes in different chromosomes, which is a process under epigenetic control. There are about 15,000 new cases of sarcoma in the US

title: Acute lymphoblastic leukemia
text: "RUNX1" gene, encoding a protein involved in transcriptional control of hemopoiesis, has been translocated and repressed by the "ETV6"-"RUNX1" fusion protein. Below is a table with the frequencies of some cytogenetic translocations and molecular genetic abnormalities in ALL. French-American-British Historically, prior to 2008, ALL was classified morphologically using the French-American-British (FAB) system that heavily relied on morphological assessment. The FAB system takes into account information on size, cytoplasm, nucleoli, basophilia (color of cytoplasm), and vacuolation (bubble-like properties). While some clinicians still use the FAB scheme to describe tumor cell appearance, much of this classification has been abandoned because of limited

title: Acute biphenotypic leukaemia
text: The hybrid gene product ABL/BCR is an oncogene which could lead several types of leukemia including BAL. ABL/BCR could active several molecular pathways: MLL gene encode Histone-lysine N-methyltransferase (HRX), which is a histone methyltransferase. It is a positive regulator for gene transcription. It has been shown that associates with Host cell facor C1, CREB binding protein, WDR5, CTBP, MEN1, etc. The rearrangement of MLL are related with different kinds of aggressive acute leukemias. Most of biphenotypic leukemia in children is due to the rearrangement of MLL Besides them, other gene abnormalities has been reported. Such as t(8;21), t(15;17), del(6q), del(12p),

title: Variant of uncertain significance
text: gene are involved in the development of breast cancer because of the publicity surrounding Angelina Jolie's preventative treatment. Few people are aware of the immense number of other genetic variants in and around BRCA1 and other genes that may predispose to hereditary breast and ovarian cancer. A recent study of the genes ATM, BRCA1, BRCA2, CDH1, CHEK2, PALB2, and TP53 found 15,311 DNA sequence variants in only 102 patients. Many of those 15,311 variants have no significant phenotypic effect. That is, a difference can be seen in the DNA sequence, but the differences have no effect on the growth or

title: X-linked severe combined immunodeficiency
text: such as the retrovirus, that incorporate the gene into the genome result in long-term effects. This, coupled with the bone marrow stem cells, has been successful in treating individuals with X-SCID. In one particular trial by Cavazzana-Calvo et al., ten children were treated with gene therapy at infancy for X-SCID. Nine of the ten were cured of X-SCID. However, about three years after treatment, two of the children developed T-cell leukemia due to insertion of the IL2RG gene near the LMO2 gene and thereby activating the LMO2 gene (a known oncogene). A third child developed leukemia within two years of

title: HK3
text: leukemia (AML) blast cells and acute promyelocytic leukemia (APL) patients. The transcription factor PU.1 is known to directly activate transcription of the antiapoptotic "BCL2A1" gene or inhibit transcription of the p53 tumor suppressor to promote cell survival, and is proposed to also directly activate "HK3" transcription during neutrophil differentiation to support short-term cell survival of mature neutrophils. Regulators repressing HK3 expression in AML include PML-RARA and CEBPA. Regarding acute lymphoblastic leukemia (ALL), functional enrichment analysis revealed "HK3" as a key gene and suggests that HK3 shares antiapoptotic function with HK1 and HK2. The "HK3" promoter is known to interact with