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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Cancer02:18

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: Jul 6, 2026

Enhancing Tumor Content through Tumor Macrodissection
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Enhancing Tumor Content through Tumor Macrodissection

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Oncogenic CARD11 mutations in human diffuse large B cell lymphoma.

Georg Lenz1, R Eric Davis, Vu N Ngo

  • 1Metabolism Branch, Division of Cancer Treatment and Diagnosis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.

Science (New York, N.Y.)
|March 8, 2008
PubMed
Summary

Mutations in the CARD11 gene promote the growth of Diffuse Large B cell Lymphoma (DLBCL) by activating the NF-kappaB pathway. Targeting CARD11 offers a new therapeutic strategy for this aggressive B cell cancer.

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Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation
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Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation

Published on: August 23, 2024

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Diffuse Large B cell Lymphoma (DLBCL) is the most common non-Hodgkin's lymphoma.
  • The ABC subtype of DLBCL relies on the nuclear factor-kappaB (NF-kappaB) pathway for malignant cell survival.
  • CARD11 is essential for NF-kappaB activation in normal B cells via antigen receptor signaling.

Purpose of the Study:

  • To investigate the role of CARD11 mutations in DLBCL tumorigenesis.
  • To determine if CARD11 acts as an oncogene in DLBCL.

Main Methods:

  • Sequencing of the CARD11 gene in human DLBCL tumor samples.
  • Experimental introduction of CARD11 mutants into lymphoma cell lines.
  • Assessing NF-kappaB pathway activation in response to CARD11 mutations.

Main Results:

  • Missense mutations in the CARD11 coiled-coil domain were identified in 9.6% of ABC DLBCL biopsies.
  • Engineered CARD11 mutants led to constitutive NF-kappaB activation.
  • Mutant CARD11 enhanced NF-kappaB activity upon antigen receptor stimulation.

Conclusions:

  • CARD11 functions as a bona fide oncogene in DLBCL.
  • These findings provide a genetic basis for developing CARD11 pathway inhibitors for DLBCL treatment.