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Related Concept Videos

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...
Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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...
Tumor Progression02:07

Tumor Progression

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Related Experiment Video

Updated: May 9, 2026

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
10:04

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis

Published on: May 1, 2015

Inherited predisposition to multiple myeloma.

Divya T Koura1, Amelia A Langston

  • 1The Winship Cancer Institute of Emory University, Atlanta, GA, USA.

Therapeutic Advances in Hematology
|August 9, 2013
PubMed
Summary
This summary is machine-generated.

Genetic factors may predispose individuals to multiple myeloma (MM), a blood cancer. Research is exploring inherited genetic variations and specific protein targets, like hyperphosphorylated paratarg-7 (pP-7), which may explain disease disparities.

Keywords:
Waldenström macroglobulinemia/geneticsautoantigens/geneticsgenetic predisposition to diseasemonoclonal gammopathy of undetermined significance/geneticsmultiple myeloma/epidemiologymultiple myeloma/geneticsparaproteins/geneticsphosphorylation/physiologyrisk factors

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Published on: January 7, 2019

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Last Updated: May 9, 2026

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
10:04

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis

Published on: May 1, 2015

Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice
05:32

Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice

Published on: January 7, 2019

Area of Science:

  • Hematologic Malignancies
  • Cancer Genetics
  • Immunology

Background:

  • Multiple myeloma (MM) is the second leading hematologic malignancy in the U.S.
  • Evidence suggests a potential inherited predisposition to MM, supported by family studies and racial incidence disparities.
  • Genome-wide association studies (GWASs) are investigating genetic susceptibility loci in MM.

Purpose of the Study:

  • To review current data on inherited predisposition to multiple myeloma.
  • To highlight potential genetic targets and mechanisms in MM development.
  • To explore the role of specific protein targets in MM pathogenesis and disparities.

Main Methods:

  • Review of existing literature on genetic predisposition in MM.
  • Analysis of findings from genome-wide association studies (GWASs).
  • Examination of identified paraprotein targets (paratargs) and their inherited mechanisms.

Main Results:

  • GWASs have identified potential MM susceptibility regions on chromosomes 3p22, 7p15.3, 8q24, and 2p23.3.
  • Hyperphosphorylation of paratarg proteins, inherited in an autosomal dominant manner, is a common antigenic mechanism.
  • Hyperphosphorylated paratarg-7 (pP-7) is a frequent target in MM patients and in high-risk families, potentially explaining racial disparities in incidence.

Conclusions:

  • Inherited factors play a significant role in multiple myeloma development.
  • Specific protein targets, such as pP-7, represent promising areas for future research in MM.
  • Understanding genetic predispositions and antigenic targets may help elucidate MM pathogenesis and inform targeted therapies.