Identification of a Novel P190-Derived Breakpoint Peptide Suitable for Peptide Vaccine Therapeutic Approach in Ph+ Acute Lymphoblastic Leukemia Patients

نویسندگان

  • Micaela Ippoliti
  • Marzia Defina
  • Antonella Gozzini
  • Claudia Baratè
  • Lara Aprile
  • Alice Pietrini
  • Alessandro Gozzetti
  • Donatella Raspadori
  • Francesco Lauria
  • Monica Bocchia
چکیده

Ph+ acute lymphoblastic leukemia (Ph+ ALL) is a high-risk acute leukemia with poor prognosis, in which the specific t(9;22)(q34;q11) translocation results in a chimeric bcr-abl (e1a2 breakpoint) and in a 190 KD protein (p190) with constitutive tyrosine kinase activity. The advent of first- and second-generation tyrosine kinase inhibitors (TKIs) improved the short-term outcome of Ph+ ALL patients not eligible for allo-SCT; yet disease recurrence is almost inevitable. Peptides derived from p190-breakpoint area are leukemia-specific antigens that may mediate an antitumor response toward p190+ leukemia cells. We identified one peptide named p190-13 able to induce in vitro peptide-specific CD4+ T cell proliferation in Ph+ ALL patients in complete remission during TKIs. Thus this peptide appears a good candidate for developing an immune target vaccine strategy possibly synergizing with TKIs for remission maintenance.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The Identification of a Novel Peptide Derived from Lactoferrin Isolated from Camel Milk with Potential Antimicrobial Activity

Background and Objective: Antimicrobial peptides have attracted significant attention in recent decades because of their properties, such as rapid bactericidal effects, having a wide spectrum of activity, and a rare development of drug resistance. The purpose of this study was to examine the antibacterial activity of a peptide derived from the lactoferrin isolated from camel milk against Staphy...

متن کامل

The targetable role of herpes virus-associated ubiquitin-specific protease (HAUSP) in p190 BCR-ABL leukemia

Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) is driven by the p190 breakpoint cluster region (BCR)-ABL isoform. Although effectively targeted by BCR-ABL tyrosine kinase inhibitors (TKIs), ALL is associated with a less effective response to TKIs compared with chronic myeloid leukemia. Therefore, the identification of additional genes required for ALL maintenance may ...

متن کامل

Variant breakpoint positions on chromosome 22 in Ph'-positive chronic myelogenous leukemias.

As a consequence of the molecular events associated with the presence of a Philadelphia (Ph') chromosome, two different types of abnormal c-abl proteins, termed P210 and P190 according to their molecular weight, have been found in Ph' positive leukemic cells [1, 2]. P210, expressed in almost all chronic myelogenous leukemias (CML) and in approximately half of the Ph' positive acute lymphoblasti...

متن کامل

Optimization of a Method to Prepare Liposomes Containing HER2/Neu-Derived Peptide as a Vaccine Delivery System for Breast Cancer

The purpose of this study was to optimize a method for the encapsulation of P5 peptide, a new designed peptide containing MHC class I epitopes from rat HER2/neu protein, into liposomes as an approach for breast cancer vaccine formulation. The efficiency of liposomal encapsulation of peptides is generally low and development of an optimized method to increase encapsulation efficiency is a big ch...

متن کامل

Rearrangement of the breakpoint cluster region and expression of P210 BCR-ABL in a "masked" Philadelphia chromosome-positive acute myeloid leukemia.

The Philadelphia (Ph) translocation t(9;22)(q34;q11) occurs frequently in chronic myeloid leukemia (CML) but is less common in acute lymphoblastic leukemia (ALL) and rare in acute myeloid leukemia (AML). In most cases of CML and some cases of Ph+ ALL the protooncogene ABL from 9q34 is translocated to the breakpoint cluster region (bcr) of the BCR gene at 22q11 to form a chimeric gene encoding a...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 2012  شماره 

صفحات  -

تاریخ انتشار 2012