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Related Concept Videos

Mutations01:39

Mutations

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Overview
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Mutations01:35

Mutations

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Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Related Experiment Video

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Enhancing Tumor Content through Tumor Macrodissection
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Germline mutations predisposing to diffuse large B-cell lymphoma.

O C Leeksma1,2, N F de Miranda3, H Veelken2

  • 1Department of Hematology/Medical Oncology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands.

Blood Cancer Journal
|February 18, 2017
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Summary
This summary is machine-generated.

Germline mutations in DNA repair and immune genes are increasingly found in diffuse large B-cell lymphoma (DLBCL). Further research is needed to determine if these genetic alterations predispose individuals to DLBCL.

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Area of Science:

  • Genetics
  • Oncology
  • Immunology

Background:

  • Diffuse large B-cell lymphoma (DLBCL) research has identified somatic mutations and germline alterations.
  • Germline alterations often impact DNA repair and immune function genes, potentially predisposing to other conditions.
  • Understanding these mutations can inform preventative strategies and future DLBCL therapies.

Purpose of the Study:

  • To review the role of germline mutations in DLBCL.
  • To explore the overlap between somatically mutated genes in DLBCL and genes with known germline alterations.
  • To investigate the potential hereditary predisposition to DLBCL.

Main Methods:

  • Review of genetic studies on DLBCL.
  • Analysis of germline alterations in DLBCL patients.
  • Comparison of somatically mutated genes with known germline mutation genes.

Main Results:

  • Over one-third of genes somatically mutated in DLBCL have described germline mutations.
  • Germline mutations in these genes are associated with diverse inherited syndromes, including immunodeficiencies and other malignancies.
  • The direct predisposition conferred by these germline mutations to DLBCL remains an open question.

Conclusions:

  • Germline alterations in DNA repair and immune genes are relevant to DLBCL.
  • Further genomic interrogation of DLBCL patients is expected to identify additional hereditary predisposition genes.
  • Inherited or de novo genetic alterations are implicated in the development of DLBCL.