Myc Rearrangements

EBV is associated with malignant tumors, in particular: Burkitt’s lymphoma, which is especially prevalent in immunocompromised individuals. EBV has the ability to immortalize B-lymphocytes by hindering apoptosis signals within the cell. The virally encoded cells, therefore, proliferate to high numbers in the body leading to malignancies. EBV can then change the B-lymphocytes to lymphoblastoid cell lines. Individuals who carry the virus in most cases do not go on to have Burkitt’s Lymphoma because the immune system can recognize the transformed cells and destroy them before they cause malignancies. The immune system in immunocompromised patients, however, is not typically able to destroy these cells, making the individual at risk for malignancies

Although research opinions vary on the cause of lymphomas, it is known that T-cell lymphomas are very rare. Lymphomas are thought to be caused by the damaged genes that control the development of the body’s blood cells ( B and T Cell Lymphomas, n.d.) The B- cells and T-cells play different roles in the body. T-cells can be helper cells, suppressor cells or killer cells (Story, 2012). It is the

The normal process of cell division is altered in cancerous cells typically by mutations in the genes involved in the regulation of cellular division. The number of mutations normally will begin to spread because when the genes that make DNA repairing proteins become mutated, this causes the DNA that they would be repairing to become mutated as well. Some changes allow the damaged cells to divide more quickly than normal and to invade other tissues. The cancers cells can divide even where there are signals and normal cells meant to prevent the cell growth.

(1) PMBL considered a distinct entity and has unique clinical, pathologic, and genetic features. Primary mediastinal large b cell lymphoma is acknowledged as a subtype of diffuse large B-cell lymphoma, but shares characteristics with classic Hodgkin lymphoma, and are likely to contain unique characteristics that are infrequent. Research suggests that recurrent aberrations can occur while in the process of the pathogenesis of PMBL. Additionally, physicians observed protein-altering rearrangements thought to emerge from alterations in certain genes; in which contribute to the genesis of PMBL through tumor microenvironment interactions which affirm B-cell growth. Moreover, due to the rarity and peculiarity of the disease, there has been much dispute as to what treatment should patients diagnosed with PMBL should be given. (6) The etiology of primary mediastinal large b cell lymphoma is ambiguous. However, PMBL acts as the misplaced link between the entities, including Hodgkin Lymphoma and

Method: Patients with locally advanced or metastatic cancer harboring genetic alterations in ALK were eligible. In patients with NSCLC, the demonstration of ALK rearrangement was required

If there are mutations of the oncogene, then there will be uncontrolled cell division and therefore tumour formation will occur. However, the chances of the tumour developing into a benign tumour is unlikely as the tumours must break free and invade nearby tissue and this is life threatening. The chances of this happening is slim, however, due to the increased longevity of humans in the recent century, the chances of cancer will therefore increase. The signs of growth are practical abilities that permit malignancy cells to survive, duplicate and spread. Harm to cell DNA is included in mutagenesis and the improvement of malignancy. The DNA in a human cell experiences a few thousand to a million harming occasions for every day, created by both outside (exogenous) and inside metabolic (endogenous) forms. Changes to the phone genome can produce blunders in the interpretation of DNA and resulting interpretation into proteins

Over the years, evidence has proven that any mutations on chromosomes whether they are broken, missing or repositioned is not just a side effect of cancer, but can be an increasing factor for

As said before, despite extensive research and advances, many of leukemia patients undergo relapse and eventually die. The application of intensified therapeutic protocol in order to prevent from relapse leads to the long-term side effects. A virtually simple solution for these problems is full identifying of the effective and suitable prognostic factors. Some of the suggested prognostic factors are immunophenotype of disease, gender, the presence of certain translocations, and epigenetic. In the two next sections, these factors are described.

Chronic Lymphocytic Leukaemia (CLL) is the most common type of leukaemia in adults1, with 20,000 new diagnoses estimated per year in the United States2. It is a type of haematological caner (cancer of the blood). Like most cancers, the cause is thought to be a result of many accumulated mutations: in CLL these can include the presence of large chromosomal mutations, alterations in the expression of microRNA (a small non-coding RNA molecule that has functions in regulating gene expression), mutations in immunoglobulin chains and other genetic damage1. Specifically, deletions can occur in a region of chromosome 17 (named the 17p deletion): this type of

This causes the genomic instability. When both arms are exchanged it causes bcl2 to be overexpressed due to the reading frame being under the control of the promoter. The overexpression of bcl-2 occurs in the B-celll lymphoma cells. Cancer cells want an increase in bcl-2 to allow to keep proliferating and evade apoptosis.

1) The Philadelphia chromosome is chromosome 22, which has undergone a reciprocal translocation with chromosome 9, such that the long arm of chromosome 22 has been replaced with the long arm of chromosome 9. This chromosome is relevant to cancer because the long arm of chromosome 9 contains human c-abl oncogene, which becomes fused to the breakpoint cluster region (bcr) in the Philadelphia chromosome, following translocation. Presence of this bcr-abl gene fusion produces a poorly regulated tyrosine kinase, which results in a much higher level of cell proliferation. The action of this tyrosine kinase results in chronic myelogenous leukemia (CML) symptoms, such as overproduction of white blood cells.

There are four types of chromosome structure changes each one can cause a disease or syndrome depending on which chromosome is affected and the type of change that occurs. When portions of the DNA segment are deleted, such as chromosome 7 losing a tiny end piece, the result is Williams Syndrome. Such is the case with Cri du chat syndrome when an end piece of chromosome 5 is deleted. Translocations, where a segment of DNA detaches from one chromosome and reattaches to another, can be responsible for some cancer formations. Translocation of a part of chromosome 22 to chromosome 9 causes chronic myelogenous leukemia whereas translocation of a part of chromosome 8 to 14 causes Burkitt lymphoma. Inversion where a segment of DNA is rotated 180° usually

Diffuse large B cell lymphoma (DLBCL) is the most prevalent form of non-Hodgkin lymphomas (NHL) and constitutes 30-40% of NHL with a crude incidence of 3–4/100.000/year in the European Union [1]. Classification of DLBCL based on gene expression profiling (GEP) identifies three subgroups, namely germinal-centre B-cell-like (GCB) DLBCL, activated B-cell-like (ABC) DLBCL, and primary mediastinal B-cell lymphoma (PMBCL) [3, 4]. DLBCL is a highly aggressive disease representing a clinically, morphologically, and genetically heterogeneous group with variable clinical outcome. Nowadays, the diagnosis of DLBCL is built on a clinical findings, morphology, histology, immunophenotyping, cytogenetics and molecular genetic assessments. [1] First-line treatment

Mixed lineage leukemia is characterized by the presence of MLL fusion proteins that are the result of chromosomal translocations affecting the MLL gene at 11q23 (Slany et al, 2009). The MLL complex promotes methylation. H3K4 methylation is universally introduced around the transcription at start site of all transcribed genes, and next to MLL1 several other confirmed or putative H3K4 methyltransferases (MLL2, MLL3, MLL5, MLL6 SET1A, SET1B, and ASH1L) have been identified in mammalian cells (Slany et al, 2009). Genes found to be activated in the presence of Mll1, code for factors involved in differentiation pathways, entirely in the development of mesodermal and ectodermal tissues or organogenesis cleotide pyrophosphatase, collagen type VI alpha 3(COL6A3), as well as, several hox genes

Kai et al IkB Kinase β (IKBKB) mutations in lymphomas that constitutively activate canonical nuclear factor kB (NFkB) signalling. 2014, J Biol Chem 289(38)26960-72.