Related Experiment Video

Updated: Oct 22, 2025

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.6K

Involvement of Alarmins in the Pathogenesis and Progression of Multiple Myeloma

Giuseppe Murdaca1, Alessandro Allegra2, Francesca Paladin1

  • 1Department of Internal Medicine, University of Genoa, Ospedale Policlinico San Martino IRCCS, 20132 Genoa, Italy.

International Journal of Molecular Sciences
|August 27, 2021
PubMed
Abstract

Insights

Alarmins like HMGB1 and S100 proteins drive cancer growth in Multiple Myeloma (MM). Targeting these alarmins and inhibiting new blood vessel formation may offer new treatments for MM and reduce relapse risk.

Area of Science:

  • Hematology
  • Immunology
  • Oncology

Background:

  • Multiple Myeloma (MM) is a plasma cell malignancy characterized by bone erosion.
  • MM progresses through stages, from monoclonal gammopathy of undetermined significance (MGUS) to overt disease.
  • Bone lesions in MM often persist even after disease remission.

Purpose of the Study:

  • To investigate the role of alarmins in the pathogenesis of Multiple Myeloma.
  • To identify molecular targets for improved MM treatment strategies.

Main Methods:

  • Literature search on PubMed using keywords: alarmins, MGUS, MM, and immune system.
  • Analysis of scientific publications focusing on the relationship between alarmins, MGUS, and MM.

Main Results:

  • Alarmins, including high-mobility group box-1 (HMGB1), heat shock proteins, and S100 proteins, are crucial for neoangiogenesis.
  • Neoangiogenesis is a key event in the progression of MM and other cancers.
  • These molecules contribute to the negative evolution of hematological and non-hematological tumors.

Conclusions:

  • Modulating the host immune system is a potential therapeutic strategy for MM.
  • Inhibiting neoangiogenesis may improve survival rates in MM patients.
  • Targeting alarmins and neoangiogenesis could reduce the risk of relapsed/refractory MM (RRMM).
Keywords:
alarminscytokinesmultiple myeloma

More Related Videos

Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice05:32

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

Published on: January 7, 2019

7.0K
Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis10:04

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

Published on: May 1, 2015

13.2K

Related Concept Videos

Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.7K
Differentiation of Common Myeloid Progenitor Cells01:15

Differentiation of Common Myeloid Progenitor Cells

Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
3.6K
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...
4.7K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.6K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
7.1K