Malignant B cells and antigenic receptor

Necessity or habit?

Bogoljub Ciric, Larry R Pease

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

B-cell malignancies account for the majority of lymphoid tissue neoplasia. Similar to normal B cells, malignant B cells in most Hodgkin's and non-Hodgkin's types of lymphomas express B-cell receptor (BCR) on their membrane. Since neoplastic B cells retain the capacity to respond to microenvironmental signals, and in many respects still behave as normal B cells, it does not seem bizarre that the BCR, which dominates the biology of normal B cells, can remain equally important for some malignant B cells. Indirect evidence suggests that retained BCR expression, and in certain cases coupled with stimulation by antigen (Ag), may be necessary for the viability of some B-cell tumors. The aim of this review is to consider the evidence regarding the role of the BCR in tumorigenesis of B-cell lymphomas, and discuss different approaches used in evaluating this role in the persistence and progression of these malignancies. The diversity in B-cell lymphomas prevents easy classification of these cancers based on their dependence on BCR expression. It seems likely that some malignant B cells need BCR expression, or additionally, stimulation by Ag in order to survive. However, through accumulation of additional genetic changes, the original tumor can give rise to a clone that no longer requires signals from the BCR to survive. Thus, most B-cell lymphomas may initially retain dependence on BCR expression that governs normal B-cell physiology and may lose it only at later stages of tumor progression, through the accumulation of additional transforming events.

Original languageEnglish (US)
Pages (from-to)1383-1390
Number of pages8
JournalLeukemia and Lymphoma
Volume43
Issue number7
DOIs
StatePublished - 2002

Fingerprint

Habits
B-Lymphocytes
B-Cell Lymphoma
Neoplasms
Antigens
Cell Physiological Phenomena
Lymphoid Tissue
Hodgkin Disease
Non-Hodgkin's Lymphoma
Carcinogenesis

Keywords

  • B cell
  • B-cell receptor
  • Clonal evolution
  • Malignancy

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

Cite this

Malignant B cells and antigenic receptor : Necessity or habit? / Ciric, Bogoljub; Pease, Larry R.

In: Leukemia and Lymphoma, Vol. 43, No. 7, 2002, p. 1383-1390.

Research output: Contribution to journalArticle

@article{3fe88d117a884046a997022f006b4fe3,
title = "Malignant B cells and antigenic receptor: Necessity or habit?",
abstract = "B-cell malignancies account for the majority of lymphoid tissue neoplasia. Similar to normal B cells, malignant B cells in most Hodgkin's and non-Hodgkin's types of lymphomas express B-cell receptor (BCR) on their membrane. Since neoplastic B cells retain the capacity to respond to microenvironmental signals, and in many respects still behave as normal B cells, it does not seem bizarre that the BCR, which dominates the biology of normal B cells, can remain equally important for some malignant B cells. Indirect evidence suggests that retained BCR expression, and in certain cases coupled with stimulation by antigen (Ag), may be necessary for the viability of some B-cell tumors. The aim of this review is to consider the evidence regarding the role of the BCR in tumorigenesis of B-cell lymphomas, and discuss different approaches used in evaluating this role in the persistence and progression of these malignancies. The diversity in B-cell lymphomas prevents easy classification of these cancers based on their dependence on BCR expression. It seems likely that some malignant B cells need BCR expression, or additionally, stimulation by Ag in order to survive. However, through accumulation of additional genetic changes, the original tumor can give rise to a clone that no longer requires signals from the BCR to survive. Thus, most B-cell lymphomas may initially retain dependence on BCR expression that governs normal B-cell physiology and may lose it only at later stages of tumor progression, through the accumulation of additional transforming events.",
keywords = "B cell, B-cell receptor, Clonal evolution, Malignancy",
author = "Bogoljub Ciric and Pease, {Larry R}",
year = "2002",
doi = "10.1080/10428190290033314",
language = "English (US)",
volume = "43",
pages = "1383--1390",
journal = "Leukemia and Lymphoma",
issn = "1042-8194",
publisher = "Informa Healthcare",
number = "7",

}

TY - JOUR

T1 - Malignant B cells and antigenic receptor

T2 - Necessity or habit?

AU - Ciric, Bogoljub

AU - Pease, Larry R

PY - 2002

Y1 - 2002

N2 - B-cell malignancies account for the majority of lymphoid tissue neoplasia. Similar to normal B cells, malignant B cells in most Hodgkin's and non-Hodgkin's types of lymphomas express B-cell receptor (BCR) on their membrane. Since neoplastic B cells retain the capacity to respond to microenvironmental signals, and in many respects still behave as normal B cells, it does not seem bizarre that the BCR, which dominates the biology of normal B cells, can remain equally important for some malignant B cells. Indirect evidence suggests that retained BCR expression, and in certain cases coupled with stimulation by antigen (Ag), may be necessary for the viability of some B-cell tumors. The aim of this review is to consider the evidence regarding the role of the BCR in tumorigenesis of B-cell lymphomas, and discuss different approaches used in evaluating this role in the persistence and progression of these malignancies. The diversity in B-cell lymphomas prevents easy classification of these cancers based on their dependence on BCR expression. It seems likely that some malignant B cells need BCR expression, or additionally, stimulation by Ag in order to survive. However, through accumulation of additional genetic changes, the original tumor can give rise to a clone that no longer requires signals from the BCR to survive. Thus, most B-cell lymphomas may initially retain dependence on BCR expression that governs normal B-cell physiology and may lose it only at later stages of tumor progression, through the accumulation of additional transforming events.

AB - B-cell malignancies account for the majority of lymphoid tissue neoplasia. Similar to normal B cells, malignant B cells in most Hodgkin's and non-Hodgkin's types of lymphomas express B-cell receptor (BCR) on their membrane. Since neoplastic B cells retain the capacity to respond to microenvironmental signals, and in many respects still behave as normal B cells, it does not seem bizarre that the BCR, which dominates the biology of normal B cells, can remain equally important for some malignant B cells. Indirect evidence suggests that retained BCR expression, and in certain cases coupled with stimulation by antigen (Ag), may be necessary for the viability of some B-cell tumors. The aim of this review is to consider the evidence regarding the role of the BCR in tumorigenesis of B-cell lymphomas, and discuss different approaches used in evaluating this role in the persistence and progression of these malignancies. The diversity in B-cell lymphomas prevents easy classification of these cancers based on their dependence on BCR expression. It seems likely that some malignant B cells need BCR expression, or additionally, stimulation by Ag in order to survive. However, through accumulation of additional genetic changes, the original tumor can give rise to a clone that no longer requires signals from the BCR to survive. Thus, most B-cell lymphomas may initially retain dependence on BCR expression that governs normal B-cell physiology and may lose it only at later stages of tumor progression, through the accumulation of additional transforming events.

KW - B cell

KW - B-cell receptor

KW - Clonal evolution

KW - Malignancy

UR - http://www.scopus.com/inward/record.url?scp=0036306360&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036306360&partnerID=8YFLogxK

U2 - 10.1080/10428190290033314

DO - 10.1080/10428190290033314

M3 - Article

VL - 43

SP - 1383

EP - 1390

JO - Leukemia and Lymphoma

JF - Leukemia and Lymphoma

SN - 1042-8194

IS - 7

ER -