Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PLASMACYTOMA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources
PubMedDate not supplied

Solitary plasmacytoma of bone: clinical features, treatment and survival.

Eleven patients with solitary plasmacytoma of bone were seen between 1978 and 1991. A retrospective review of the clinical features, treatment and survival of these patients was made with the aim of helping to define those at risk for early development of myeloma. Nine patients (82 per cent) had paraparoteinemia at diagnosis. Treatment consisted of local irradiation plus or minus surgery (nine patients) and surgery alone (two patients). No patient received adjuvant chemotherapy. One patient had evidence of both generalized osteopenia and immunoparesis, and progressed to myeloma within six months. Four patients (36 per cent) progressed to myeloma. All of these had paraprotein levels which continued to rise following initial treatment. Three patients died of myeloma at 12, 81 and 144 months and the other patient is alive with myeloma at 76 months. Patients without paraproteinemia at presentation or whose paraprotein decreased after treatment did not progress to myeloma. Three patients have been followed for 8, 11 and 19 years with no evidence of myeloma. Failure of paraprotein to clear after local treatment suggests occult disseminated disease and is predictive of later development of overt myeloma.

Adult↗
PubMed2002

Isotype switch-mediated CH deletions are a recurrent feature of Myc/CH translocations in peritoneal plasmacytomas in mice.

Oncogene activating chromosomal translocations that interrupt IGH switch (S) regions at 14q32 are thought to be caused by misguided IGH isotype switching in postgerminal center B-cell lymphomas and plasma cell myelomas in humans. Aberrant switching also seems to be involved in altering the fine structure of the translocation in some of these tumors, but the significance of these changes is not known. Here we report on 3 cases of IL-6 transgenic mouse plasmacytomas (PCT) that harbor T(12;15) translocations that had been modified by frustrated switch attempts that result in C(H) deletions. When considered together with 6 similar cases of PCT described previously, our observations suggest that secondary deletions in C(H) are a regular feature in the molecular evolution of T(12;15) translocations and, thereby, in the progression of PCT. We propose that the T(12;15)(+) mouse PCT offers a uniquely valuable model system for elucidating the dual role of abnormal isotype switching in causation and 'remodeling' of chromosomal translocations.

Animals↗
PubMed1987

Suppression of transformed phenotypes in intraspecific somatic cell hybrid clones between the c-myc activating mouse plasmacytoma line and normal cells.

The role of normal-cell-derived chromosome 15 in suppressing transformed phenotypes was studied in intraspecific hybrid clones between the c-myc oncogene activating BALB/c mouse plasmacytoma (S194) cells and normal spleen cells or fibroblasts from CBA/H-T6 mice. All the hybrid clones between S194 and normal spleen cells grew very rapidly in suspension and formed colonies in soft agar. In contrast, the hybrid clones between S194 and normal fibroblasts grew slowly in an attached form. They were divided into 2 groups on the basis of their morphology and growth properties: most clones showed flat type morphology, and no colony formation was seen in soft agar, while some clones grew in a piled-up fashion and formed colonies in soft agar. The hybrid clones between S194 and normal spleen cells lost some normal-cell-derived chromosomes but retained most tumor-derived marker chromosomes including the t(12;15) chromosome which carried the activated c-myc oncogene. On the other hand, hybrid clones between S194 cells and normal fibroblasts retained almost all chromosomes from both parental cells. With respect to retention of normal-cell-derived chromosome 15, both the flat and piled-up type clones retained 2 copies each of the t(14;15) and T6 marker chromosomes, the normal counterparts of the t(12;15) chromosomes. Our results suggest that the transformed phenotypes of the hybrid clones between S194 cells and normal fibroblasts are negatively modulated by normal-cell-derived chromosomes but not by normal-cell-derived chromosome 15 alone.

Animals↗
PubMed1988

An atypical t(12;15) translocation of chromosomes found in murine plasmacytomas and activation of the c-myc oncogene.

Cells from murine plasmacytomas (MPC) consistently exhibit either the 12;15 or the 6;15 translocation. Recently, we found that cells from 2 MPC (ABPC 45 and ABPC 26) did not exhibit any known translocation. However, these MPC contained one chromosome 15 (15q-) that was shorter than its normal homologue and one 12 (12q+) that was longer than its normal 12 counterpart. Chromosome 15q- contained only one thin D band, corresponding in size to either D1 or D3 band. A minor light band D2 was apparently deleted. Chromosome 12q+ contained a light F1 band that was longer than the normal 12F1. In ABPC 45, the c-myc gene was assigned by in situ hybridization to the F1 region of 12q+ as well as to its original site of 15D2. Moreover, the in situ hybridization experiment assigned the S alpha gene to the F1 regions of both chromosomes 12 and 12q+. These findings indicate that a minor light band D2 of chromosome 15 carrying the c-myc gene was translocated into the major light band F1 of 12, resulting in a longer chromosome 12q+ and a correspondingly shorter chromosome 15q-. This type of chromosomal translocation suggests that ABPC 45 developed through a cytogenetic mechanism different from that of MPC with the typical t(12;15) translocation.

Animals↗
PubMed1989

Plasmacytoma induction in radiochimeras.

We have induced plasmacytomas (MPC) in BALB/c radiochimeras (RCh) repopulated with syngeneic hemopoietic cells carrying distinctive chromosomal markers. A group of 38 RCh that received 0.5 ml pristane, followed by Abelson virus infection 2-3 weeks later, developed 7 tumors (18.5%) of donor origin after a relatively short latency period (X = 83 +/- 8.3 days). In contrast, only 3 (2%) MPCs were observed in 149 RChs that received 0.5 ml pristane 3 times at monthly intervals. Two of them originated from host cells. Pristane-treated RChs developed a less extensive oil granuloma (OG), compared with pristane-treated intact mice. This may explain the low incidence of MPC in the former. Our findings also suggest that Abelson virus can overcome the postulated deficiency of OG. MPC induction in the pristane + Abelson-virus-treated RCh system will facilitate the further characterization of the MPC precursor cell and the localization of genetic resistance vs. susceptibility factors at the donor vs. host level.

Animals↗
PubMed1989

The accelerating role of Abelson murine leukemia virus in murine plasmacytoma development: in vitro infection of spleen cells generates donor-type tumors after transfer to pristane-treated BALB/c mice.

The role of Abelson murine leukemia virus (A-MuLV) in the accelerated development of murine plasmacytomas (PCs) (Potter et al., 1973: Science, 132, 592-594) was studied in a new experimental system. Spleen cells from pristane-treated or untreated BALB/c mice carrying Robertsonian 6;15 fusion chromosomes were infected in vitro with helper-free A-MuLV overnight and subsequently transplanted into the peritoneal cavity of pristane-treated or untreated BALB/c mice. Donor-derived PCs developed in 4 out of 76 pristane-treated recipients [latent periods: 38-82 (mean 51) days] that had received spleen cells from pristane-treated donors, and also in 2 out of 41 pristane-treated recipients that had received untreated donor-derived spleen cells (latent periods: 65 and 120 days). Three of the PCs in the former and both PCs in the latter group were tested for integration and expression of the v-abl gene, with positive results. This indicates that the spleen contains PC-precursor cells that can be activated by A-MuLV even before the impact of pristane. All 6 donor-origin PCs carried a translocation involving chromosome 15, band D2/3. Four of these corresponded to a typical 12;15 translocation, one was a variant 6;15 translocation and the 6th may represent a previously unidentified translocation between chromosome 15 and the lambda gene-carrying chromosome 16. No PCs developed among 29 pristane-untreated recipients that had received pristane-treated donor-derived spleen cells. In addition to PCs, monocytic tumors developed in 37 (26%) of all recipients. Their development was independent of pristane treatment of recipients but was particularly frequent in those who had received spleen cells from pristane-treated donors.

Abelson murine leukemia virus↗
PubMed1990

A synthetic thymic hormone, THF-gamma 2, repairs immunodeficiency of mice cured of plasmacytoma by melphalan.

BALB/c mice cured of large MOPC-315 plasmacytomas by melphalan remain deficient in their spleen T-cell functions. This was manifested by impairment of the allogeneic and the antibody responses in vitro to SRBC and in decreased numbers of T-cells including their subsets CD4 and CD8. IL-2 production and specific cytotoxicity against MOPC-315 tumor cells were, on the other hand, maintained. Treatment of these cured mice by in-vivo administration of THF-gamma 2, an octapeptide from calf thymus, repaired these deficits. This was evidenced by in vitro tests with spleen cells which manifested an increased allogeneic response and elevated generation of primary antibody response, restoration of T-cell subpopulations to normal and an enhanced IL-2 production above normal levels. The potential use of THF-gamma 2 as supportive therapy in cancer treatment is suggested.

Animals↗
PubMed1991

Therapeutic effectiveness against MOPC-315 plasmacytoma of low or high doses of the synthetic thymic hormone THF-gamma 2 in combination with an "immunomodulating" or a "non-immunomodulating" drug.

We reported previously that treatment of mice bearing MOPC-315 plasmacytoma with the drugs L-PAM (phenylalanine mustard) or 5-FU (5-fluorouracil), in combination with low doses of THF-gamma 2, was more effective in increasing their survival time than treatment with the drug alone. We show here that in the combined treatment using a single injection of 5-FU followed by multiple (8-15) injections of THF-gamma 2, the megadoses were more effective than the low doses in increasing the survival time of MOPC-315 tumor-bearing mice. On the other hand, in combination with L-PAM, both low and high doses of THF-gamma 2 were equally effective. The need for high doses of THF-gamma 2, when used in combination with 5-FU, could be due to the fact that 5-FU acts as a "non-immunomodulating" drug and has to be used at a high, immunosuppressive dose.

Animals↗
PubMed1991

v-abl does not abolish IL-6 requirement by murine plasmacytoma cells.

Activation of c-myc by juxtaposition to an immunoglobulin locus and introduction of the v-abl oncogene act synergistically in generating a mouse plasmacytoma (PC). The question arose whether the effect of v-abl could be attributed to a deregulation of interleukin-6 (IL-6) production or responsiveness, in view of the fact that IL-6 exerts potent growth-stimulatory activity on PC cells. We studied the effect of IL-6 on the in vitro growth of primary PCs induced by pristane alone (TEPCs) or by pristane + A-MuLV (ABPCs). Five of 13 TEPCs and 3 of 7 ABPCs responded to IL-6. Macrophage supernatants prepared from both TEPCs and ABPCs had similar stimulatory effects on PC cells. From 30 primary PCs (including both TEPCs and ABPCs), we established 9 in vitro lines, 2 of which expressed v-abl. All were able to grow on macrophage feeder layers. Three types of behavior could be distinguished on the basis of growth in feeder-free cultures in the presence and absence of IL-6. Group I contained 4 IL-6-dependent lines. Group II contained 2 IL-6-independent lines (one v-abl expressor) that grew faster in the presence of IL-6. Group III consisted of 3 feeder-dependent lines (one v-abl expressor) that were not significantly stimulated by IL-6. These findings indicate that v-abl expression does not influence IL-6 dependence or responsiveness by itself. The supernatant of one line in group II was able to stimulate PC cells. All 6 lines of Groups I and II carried a typical (12;15) translocation, while all 3 lines in group III had a variant (6;15) or (15;16) translocation.

Abelson murine leukemia virus↗
PubMed1994

Molecular requirements for rapid plasmacytoma and pre-B lymphoma induction by Abelson murine leukemia virus in myc-transgenic mice.

Mutants and fusion products of the c-abl gene were used to define some of the molecular requirements for rapid plasmacytoma (PC) and pre-B-lymphoma induction in pristane-treated N-myc transgenic BALB/c mice. A-MuLV induced PCs in 21 of 25 mice with a mean post-pristane latency period of 46 +/- 9 days, compared to 134 +/- 25 days in controls exposed to pristane alone. delta XB, a mutant of type IV c-abl with a deletion of the SH3 domain, was equally effective in inducing PCs in 7 of 7 mice with a latency period of 49 +/- 7 days, indicating that gag sequences are not required for rapid PC induction. The delta XB delta Nar mutant that carried a large C-terminal deletion in addition showed only a negligible activity, if any, suggesting that PC acceleration requires the C-terminal domain in the same way as lymphoid transformation and in contrast to fibroblast transformation. BCR-ABL fusion constructs encoding an 185-kDa protein as in acute leukemia, or a 210-kDa protein as in chronic myelocytic leukemia (CML), did not accelerate pristane-induced PC development in the N-myc transgenic mice, in contrast to their known ability to immortalize lymphoid cells in vitro. Only one of 14 non-transgenic littermates developed a pre-B lymphoma after A-MuLV infection, and none of 10 normal littermates infected with delta XB virus developed a construct-carrying tumor. This result suggests that PC acceleration is due to co-operative interaction of the N-myc transgene and activated abl. Infection of N-myc transgenic bone marrow or spleen cells with A-MuLV in vitro led to the outgrowth of pre-B lymphomas after transplantation to pristane-treated BALB/c recipients. The lymphoma-inducing activity of A-MuLV depends on its high titer, since diluted A-MuLV or the lower-titered delta XB induced only PCs under the same conditions. The v-abl, delta XB and BCR-ABL-carrying viruses generated immortalized lymphoblastoid lines in vitro, regardless of the presence of the N-myc transgene, suggesting that lymphoid transformation is a direct function of appropriate abl sequences in contrast to PC acceleration.

Animals↗
PubMed1985

Characterization of immunoglobulin enhancer deletions in murine plasmacytomas.

We have analyzed enhancer deletions found in murine plasmacytomas by DNA cloning. This analysis revealed that the deletions occurred between the JH region and the switch region, removing the Ig heavy chain enhancer. The loss of the enhancer did not significantly affect the level of heavy chain expression as determined by RNA blots. Nucleotide sequence analysis revealed that there are no characteristic or homologous sequences around the recombination site. Extra nucleotides were found at the recombination sites, in a manner analogous to Ig and T-cell receptor V-D-J joining. The germline JH and switch sequences involved in the deletion were analyzed by the in vitro DNA cleavage system with an endonucleolytic activity purified from mouse fetal liver nuclear extracts. It was found that the germline JH DNA was strongly cleaved at the deletion recombination site.

Alleles↗
PubMed1995

Okadaic acid Co-induces vimentin expression and cell cycle arrest in MPC-11 mouse plasmacytoma cells.

The effect of the tumor promoter okadaic acid on cell cycle progression and on vimentin expression in MPC-11 mouse plasmacytoma cells was compared with that of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Cell cycle progression of asynchronously grown MPC-11 cells was inhibited by both agents, but, in contrast to the G1 phase arrest caused by TPA, okadaic acid gave rise to G2/M phase and S phase arrest. This effect of okadaic acid was delayed significantly compared to the TPA-caused arrest. Furthermore, okadaic acid was able to induce vimentin expression to an extent comparable to the TPA response. However, vimentin expression was markedly delayed in okadaic acid-treated relative to TPA-treated cells. Another protein phosphatase inhibitor, calyculin A, also induced cell cycle changes and vimentin expression at concentrations at or above 1 x 10(-9) M. Based on these observations, we suggest an involvement of protein phosphatase 1 (possibly also phosphatase 2A and/or other phosphatases) in both the G2/M cell cycle block and the induction of vimentin expression in MPC-11 cells by okadaic acid.

Animals↗
PubMed1983

Pancoast syndrome caused by extramedullary plasmacytoma.

A 61-year-old patient had the clinical findings of Pancoast syndrome with shoulder pain, weakness and atrophy of band muscles, and an opacified area in the apical lung field. Unlike most cases with Pancoast syndrome in which the tumors are primary carcinomas of the lung, the present case was shown to have a plasmacytoma involving the apical parietal pleura and the adjacent chest wall. The need for histologic diagnosis before treating patients with Pancoast syndrome is emphasized.

Humans↗
PubMed1985

Plasmacytoma of the parotid gland.

Extramedullary plasmacytoma of the parotid gland is an extremely rare lesion of which there have been only four other reported cases. The importance of these lesions rests in the possibility of their being a harbinger of multiple myeloma or their subsequent transformation to multiple myeloma. Because of its extreme rarity, the proper management remains unclear.

Adult↗
PubMed1986

Localized thyroid plasmacytoma.

Two cases of localized thyroid plasmacytoma are described and the literature is reviewed. In most cases the tumors arise in thyroid glands with lymphocytic thyroiditis. Thyroidectomy with regional lymph node biopsy seems to be the initial treatment of choice. Postoperative irradiation appears to be indicated in cases with residual thyroid tissue remaining and in those with documented regional nodal involvement.

Aged↗
PubMed1978

Plasmacytomas and mesothelioma.

A patient is reported who developed five plasmacytomas over a four-year period and developed a pleural mesothelioma 12 years later. The relationship of these two entities is discussed and the question of a common environmental carcinogen is raised.

Asbestos↗
PubMed1977

Atypical glycogen deposits in a plasmacytoma: an ultrastructural study.

A solitary, benign plasmacytoma, arising from the gum of the lower jaw of a dog, was studied by light and electron microscopy. Some of the tumour cell nuclei showed the characteristic clockface or cartwheel pattern of heterochromatin distribution similar to that found in normal plasma cells. Like normal plasma cells the tumour cells were endowed with rough endoplasmic reticulum but this was invariably dilated or visiculated. Glycogen deposits were found within mitochondria and within the dilated and vesiculated rough endoplasmic reticulum. The idea that these deposits were derived secondarily from glycogen deposits in the cytoplasm seems untenable because no glycogen particles were found in the cytoplasmic matrix. It would therefore appear that most, perhaps all, stages of glycogen synthesis occurred within the mitochondria and rough endoplasmic reticulum of some of these tumour cells.

Animals↗
PubMed1993

Cytoplasmic poly(ADP-ribose)polymerase from mouse plasmacytoma free messenger ribonucleoprotein particles: purification and characterization.

A cytoplasmic poly(ADP-ribose)polymerase (PARP) was purified from mouse plasmacytoma free messenger ribonucleoprotein particles using chromatography on 3-aminobenzamide affigel-10. The purified protein showed one band at 116 kDa on SDS-polyacrylamide gel electrophoresis and shared similar antigenic sites to the nuclear PARP. An apparent Km for NAD of 100.5 +/- 6.3 microM and a Vmax of 174 +/- 40 nmoles of ADP-ribose incorporated/min/mg protein were observed. RNA was detected in the enzyme preparation and the enzymatic activity was not DNA dependent.

Animals↗