Skip to content

The Aesthetic Surgery Education and Research Foundation

Newsroom
Genomic Profiling to Understand the Pathogenesis of BIA-ALCL Print

The ASERF Scientific Research Committee and Board of Directors are pleased to announce the following grant award:

Researcher: Nandu Nairn, MD

Grant Award: ASERF Interim Grant

Amount Awarded: $ 10,000

Project Name: Genomic Profiling to Understand the Pathogenesis of BIA-ALCL

Project Summary:

Hypothesis:
We hypothesize that micro and nano-silica nanoparticles with polyurethane may differentially affect the induction of new biomarkers that can potentially influence the pathogenesis of BIA-ALCL.

Accordingly, we propose following specific aim:  

Specific Aim:
To study the comparative effect of nano, micro, and macro silica gel in combination with the polyurethane on global mRNA profiling in T-Cell. Hypothesis: a) silica and polyurethane is the basic implant materials; b) comparison of different sizes will reveal their physiological implications; c) The mRNA profiling will reveal novel yet unidentified molecular factors associated with the implant materials; d) identification of novel molecular markers specific to implant constituents may lead to better treatment approach in BIA-ALCL.

Significance:
Currently more than 11 million women worldwide have breast implants and this number is continuously increasing. Recent reports of BIA-ALCL can be a significant health concern for women with implants. As such, examination of the molecular basis of BIA-ALCL may reveal specific biomarkers leading to better therapeutic approach.

 
Pathogenesis of BIA-ALCL Print

The ASERF Scientific Research Committee and Board of Directors are pleased to announce the following grant award:

Researcher: Marshall Kadin, MD

Grant Award: ASERF Interim Grant

Amount Awarded: $ 193,110

Project Name: Pathogenesis  of BIA-ALCL

Project Summary: Hypothesis: Anaplastic cells in BIA-ALCL produce cytokines that shape the tumor microenvironment (Figure 1). Our preliminary results indicate that anaplastic cells in culture produce IL-13 which induces immunoglobulin heavy chain class switch of plasma cells to produce IgE. We found IgE bound to the surface of mast cells and antigen presenting cells (APC) within involved tissues. Mast cells produce prostaglandin D2 (PGD2) which recruits Th2 cells and eosinophils prominent in BIA-ALCL lesions. A possible source of IgE is plasma cells in tumors and regional lymph nodes. Neither IL-13, IgE nor PGD2 has been quantified in malignant seromas before nor after treatment or compared to benign seromas. Whether IgE binds to bacteria or tumor associated antigens also has not been explored. IL-13 can be produced by effector T cells and innate lymphoid cells (ILCs) which will be addressed in this proposal. We hypothesize there will be different clinical presentations according to the cellular origin and functional polarization of anaplastic cells, specifically the Th1/ILC1 phenotype may associated with clinically indolent behavior and the Th3/ILC3 phenotype with invasive tumors.

To address our hypothesis our specific aims are:

Aim 1- Determine the significance of cytokine, prostaglandin D2 and IgE levels in benign and malignant seroma fluids and blood at clinical presentation and after treatment.

Aim 2- Determine if anaplastic cells are derived from effector T cells or innate lymphoid cells.

   Subaim 1- Determine which subset anaplastic cells belong to- Th1/1LC1, Th2/ILC2, or Th3/ILC3.

   Subaim 2- Is there a difference in subsets between in situ and invasive disease?

   Subaim 3- Can Th3/ILC3 anaplastic cells be repolarized to Th1/ILC1?

Aim 3- Identify precursors of BIA-ALCL with a similar phenotype in capsules, seroma fluids and regional lymph nodes.

AIM 4- Determine if IgE binds to bacterial and/or tumor associated antigens

 
<< Start < Prev 1 2 3 4 5 6 7 8 9 10 Next > End >>

Page 10 of 28


Copyright © 2009-2018 ASERF. 11262 Monarch St., Garden Grove, CA 92841-1441 P: 800-364-2147 F: 562-799-1098