Neoplastic B cells

Vitetta, E.S., and Thorpe, P.E. (1985) Immunotoxins containing ricin A or B chains with modified carbohydrate residues act synergistically in killing neoplastic B cells in vitro. Cancer Drug Deliv. 2, 191. 

The benefit of the immunoperoxidase technique is best exhibited by the ability to detect neoplastic B cells. By demonstrating the presence of k or X (but not both) in lymphoid or plasma cells, one can establish a diagnosis of lymphoma or plasmacytoma. Unfortunately, in routinely processed tissue, only immunoglobulins in the cytoplasm and not on the cell surface membrane can be detected. 

Several effects of forskolin on B-lymphocytes, the cells of the immune system responsible for the production of immunoglobulins, have further been reported. This diterpene was found to inhibit cellular proliferation of B cells stimulated either by antibodies to surface immunoglobulins (anti-mu), and an antibody to CD20 antigen or 12-O-tetradecanoyl phorbol 13-acetate [219]. There was also a clear inhibition of G1 entry and DNA synthesis, and forskolin maintained its inhibitory effect even when added later after anti-mu stimulation. Additionally, no differences were found in the inhibitory effect of forskolin on neoplastic B cells, as compared to the responses of normal cells. Growth inhibition associated with an accumulation of cells in G1 was later found when cells of the B-lymphoid precursor cell line Reh were incubated with forskolin [220]. In that study, a delay of cells in G2/M prior to G1 arrest was observed, suggesting that important restriction points located in the G1 and G2 phases of the cell cycle may be controlled by forskolin (due to cAMP levels elevation). In a subsequent study [221], it was found that the arrest of Reh cells was accompanied by rapid dephosphorylation of retinoblastoma protein, which was suggested to be a prerequisite for the forskolin mediated arrest of these cells in Gl. 

Kinashi, T., Godal, T., Noma, Y., Ling, N.R., Yaoita, Y., Honjo, T. (1987). Human neoplastic B cells express more than two isotypes of immunoglobulins without deletion of heavy-chain constant-region genes. Genes Dev. 1, 465-470. 

Krolick KA, Villemez C, Isakson P, Uhr JW, Vitetta ES. Selective killing of normal or neoplastic B cells by antibodies coupled to the A chain of ricin. Proc Natl Acad Sci USA 1980 77 5419-23. 

The benefit of the immunoperoxidase technique is best exhibited by the ability to detect neoplastic B-cells. By demonstrating the presence of... 

Tsujimoto Y, Finger LR, Yunis J et al (1984) Cloning of the chromosomal breakpoint of neoplastic B cells with the t(14 18) chromosome translocation. Science 226 1097-1099... 

A. Evolution of Immunophenotypic Profile of Non-Neoplastic B-Cells at Different Stages of Differentiation... 

Bone marrow and bone tissue microenvironment plays a key role in normal and neoplastic HSC changes. Differentiation to B-lineage isn t changed and is associated with B-cell compartment growth. 

Lymphoid neoplasms are divided into three main categories B cell neoplasms, T/NK cell neoplasms, and Hodgkin lymphoma. The B and T/NK cell neoplasms are further divided into precursor B and mature B cell neoplasms and into precursor T and mature T/NK cell neoplasms, respectively. The mature B cell and T/NK neoplasms consist of a variety of different neoplastic lymphoid entities, which can be grouped based on primary clinical presentation or based on median survivals without treatment reflecting biologic behavior. However, due to the large number of separate entities, only the more common lesions will be discussed. For information concerning the entities not discussed here or for more in-depth information, the... 

There are four major morphologic subtypes of this form of HL lymphocyte-rich cHL, nodular sclerosis HL, mixed cellularity HL, and lymphocyte-depleted HL. The tumor cells in cHL are mononuclear Hodgkin cells and multinucleated Reed-Sternberg cells (HRS). Similar to the neoplastic cells in NLPHL, the HRS cells have been found to be derived from germinal center B cells (K33, M9). 

G8. Grogran, T. M., and Spier, C. M., B-cell immunoproliferative disorders, including multiple myeloma and amyloidosis. In Neoplastic Hematopathology (D. M. Knowles, ed.), pp. 1557-1587. Lippincott Williams Wilkins, Philadelphia, PA, 2001. 

Onizuka, T., Moriyama, M., Yamochi, T., Kuroda, T., Kazama, A., Kanazawa, N., Sato, K., Kato, T., Ota, H., and Mori, S., BCL-6 gene product, a 92- to 98-kD nuclear phosphoprotein, is highly expressed in germinal center B cells and their neoplastic counterparts. Blood 86, 28-37 (1995). 

Said, J. W., Stoll, P. N., Shintaku, P., Bindl, J. M., Butmarc, J. R., and Pinkus, G. S., Leu-22 A preferential marker for T-lymphocytes in paraffin sections. Staining profile in T- and B-cell lymphomas, Hodgkin s disease, other lymphoproliferative disorders, myeloproliferative diseases, and various neoplastic processes. Am. J. Clin. Pathol. 91, 542-549 (1989). 

Kane, C. D.,Coe, N. R., Vanlandingham, B., Krieg, P., Bernlohr, D. A. (1996). Expression purification, and ligandbinding analysis of recombinant keratinocyte lipid-binding protein (MAL-1), an intracellular lipid-binding found overexpressed in neoplastic skin cells. Biochemistry 35, 2894-2900. 

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