Search Videos by Topic or Participant
Browse by Series:

Targeting CD30 in Hodgkin Lymphoma

Insight from: John Sweetenham, MD, Huntsman; Robert W. Chen, MD, City of Hope;and Anas Younes, MD, MSK 
Published: Saturday, Mar 21, 2015
For High-Definition, Click
According to John Sweetenham, MD, it has been well known for a number of years that there is cell communication within the Hodgkin lymphoma lymph node that is important to cell survival, particularly between Reed-Sternberg cells and inflammatory background infiltrate. Now, new data suggest that Reed-Sternberg cells form a network of cells that are linked by CD30-bearing protrusions. Cross talk mechnisms may exist between the Reed-Sternberg cells and the protrusions that express CD30, making CD30 an even better target for therapy, Sweetenham suggests.

Until the approval of the antibody-drug conjugate brentuximab vedotin, CD30 remained an elusive target. Brentuximab vedotin binds to CD30 and internalizes, causing the release of the anti-tubulin cytotoxic MMAE within the cancer cell. MMAE works to disrupts the microtubule network, causing cell cycle arrest and apoptosis. Targeting tubulin helps break down the protrusions and membrane-bound vesicles, resulting in a loss of cell communication and reduced survival of Reed-Sternberg cells.
Slider Left
Slider Right
For High-Definition, Click
According to John Sweetenham, MD, it has been well known for a number of years that there is cell communication within the Hodgkin lymphoma lymph node that is important to cell survival, particularly between Reed-Sternberg cells and inflammatory background infiltrate. Now, new data suggest that Reed-Sternberg cells form a network of cells that are linked by CD30-bearing protrusions. Cross talk mechnisms may exist between the Reed-Sternberg cells and the protrusions that express CD30, making CD30 an even better target for therapy, Sweetenham suggests.

Until the approval of the antibody-drug conjugate brentuximab vedotin, CD30 remained an elusive target. Brentuximab vedotin binds to CD30 and internalizes, causing the release of the anti-tubulin cytotoxic MMAE within the cancer cell. MMAE works to disrupts the microtubule network, causing cell cycle arrest and apoptosis. Targeting tubulin helps break down the protrusions and membrane-bound vesicles, resulting in a loss of cell communication and reduced survival of Reed-Sternberg cells.
View Conference Coverage
Online CME Activities
TitleExpiration DateCME Credits
Community Practice Connections™: 18th Annual International Lung Cancer Congress®Oct 31, 20181.5
Provider and Caregiver Connection™: Addressing Patient Concerns While Managing Chemotherapy Induced Nausea and VomitingOct 31, 20182.0
Publication Bottom Border
Border Publication
x