scholarly journals Effect of pseudotype on Abelson virus and Kirsten sarcoma virus-induced leukemia.

1978 ◽  
Vol 147 (4) ◽  
pp. 1044-1053 ◽  
Author(s):  
C D Scher
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Cell Transformation ◽  
Leukemia Virus ◽  
Helper Virus ◽  
Lymphoid Cells ◽  
Lymphoid Leukemia ◽  
Sarcoma Virus ◽  
Marrow Cells

Nonproducer cells transformed by Kirsten sarcoma virus (KiSV) or Abelson murine leukemia virus (A-MuLV) were infected with N- or NB-tropic helper viruses to rescue the defective transforming virus. The titer of the transforming viruses was determined on NIH/3T3 fibroblast-like cells and cell-free filtrates of virus stock were inoculated into newborn Fv-1nn mice. Friend, Moloney, and Rauscher group of MuLV (FMR) pseudotypes of KiSV induced an erythroid leukemia efficiently, while an endogenous helper (N35-MuLV) pseudotype of KiSV did not. FMR pseudotypes of A-MuLV induced the Abelson lymphoid leukemia, while the N35-MuLV or a Kirsten leukemia virus (Ki-MuLV) pseudotype did not. Pseudotypes of A-MuLV were used to infect bone marrow cells of Fv-1nn mice in vitro. The FMR pseudotypes transformed bone marrow cells at 40-100-fold higher frequency than the N35-MuLV or Ki-MuLV pseudotypes. Mixing experiments demonstrated that the addition of an effective helper, such as M-MuLV did not enhance lymphoid transformation by ineffective A-MuLV (N35-MuLV). The A-MuLV genome is responsible for hematopoietic cell transformation because a nonproducer clone of lymphoid cells, free of helper virus, was isolated. The data indicates that the pseudotype of A-MuLV determines its ability to transform hematopoietic cells.

scholarly journals The effect of helper virus on Abelson virus-induced transformation of lymphoid cells.

1978 ◽  
Vol 147 (4) ◽  
pp. 1126-1141 ◽  
Author(s):  
N Rosenberg ◽  
D Baltimore
Keyword(s):  
Bone Marrow Cells ◽  
Cell Transformation ◽  
Leukemia Virus ◽  
Fibroblast Cell ◽  
Helper Virus ◽  
Lymphoid Cells ◽  
Mouse Bone Marrow ◽  
Abelson Virus

Abelson murine leukemia virus (A-MuLV)-transformed fibroblast nonproducer cells were used to prepare A-MuLV stocks containing a number of different helper viruses. The oncogenicity of the A-MuLV stocks was tested by animal inoculation and their ability to transform normal mouse bone marrow cells was measured in vitro. All of the A-MuLV stocks transformed fibroblast cells efficiently. However, only A-MuLV stocks prepared with helper viruses that are highly oncogenic were efficient in vivo and in vitro in hematopoietic cell transformation. In addition, inefficient helpers did not establish a stable infection in lymphoid nonproducer cells. Thus, helper virus has a more central role in lymphoid cell transformation than in fibroblast cell transformation.

scholarly journals Oncogene cooperation in lymphocyte transformation: malignant conversion of E mu-myc transgenic pre-B cells in vitro is enhanced by v-H-ras or v-raf but not v-abl.

1989 ◽  
Vol 9 (1) ◽  
pp. 67-73 ◽  
Author(s):  
W S Alexander ◽  
J M Adams ◽  
S Cory
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Bone Marrow Cells ◽  
Lymphocyte Transformation ◽  
Lymphoid Cells ◽  
B Lineage ◽  
B Lymphoid ◽  
Marrow Cells ◽  
B Lineage Cells

Although transgenic mice bearing a c-myc gene controlled by the immunoglobulin heavy-chain enhancer (E mu) eventually develop B-lymphoid tumors, B-lineage cells from preneoplastic bone marrow express the transgene but do not grow autonomously or produce tumors in mice. To determine whether other oncogenes can cooperate with myc to transform B-lineage cells, we compared the in vitro growth and tumorigenicity of normal and E mu-myc bone marrow cells infected with retroviruses bearing the v-H-ras, v-raf, or v-abl oncogene. The v-H-ras and v-raf viruses both generated a rapid polyclonal expansion of E mu-myc pre-B bone marrow cells in liquid culture and 10- to 100-fold more pre-B lymphoid colonies than normal in soft agar. The infected transgenic cells were autonomous, cloned efficiently in agar, and grew as tumors in nude mice. While many pre-B cells from normal marrow could also be induced to proliferate by the v-raf virus, these cells required a stromal feeder layer, did not clone in agar, and were not malignant. Most normal cells stimulated to grow by v-H-ras also cloned poorly in agar, and only rare cells were tumorigenic. With the v-abl virus, no more cells were transformed from E mu-myc than normal marrow and the proportion of tumorigenic pre-B clones was not elevated. These results suggest that both v-H-ras and v-raf, but apparently not v-abl, collaborate with constitutive myc expression to promote autonomous proliferation and tumorigenicity of pre-B lymphoid cells.

Oncogene cooperation in lymphocyte transformation: malignant conversion of E mu-myc transgenic pre-B cells in vitro is enhanced by v-H-ras or v-raf but not v-abl

1989 ◽  
Vol 9 (1) ◽  
pp. 67-73
Author(s):  
W S Alexander ◽  
J M Adams ◽  
S Cory
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Bone Marrow Cells ◽  
Lymphocyte Transformation ◽  
Lymphoid Cells ◽  
B Lineage ◽  
B Lymphoid ◽  
Marrow Cells ◽  
B Lineage Cells

Although transgenic mice bearing a c-myc gene controlled by the immunoglobulin heavy-chain enhancer (E mu) eventually develop B-lymphoid tumors, B-lineage cells from preneoplastic bone marrow express the transgene but do not grow autonomously or produce tumors in mice. To determine whether other oncogenes can cooperate with myc to transform B-lineage cells, we compared the in vitro growth and tumorigenicity of normal and E mu-myc bone marrow cells infected with retroviruses bearing the v-H-ras, v-raf, or v-abl oncogene. The v-H-ras and v-raf viruses both generated a rapid polyclonal expansion of E mu-myc pre-B bone marrow cells in liquid culture and 10- to 100-fold more pre-B lymphoid colonies than normal in soft agar. The infected transgenic cells were autonomous, cloned efficiently in agar, and grew as tumors in nude mice. While many pre-B cells from normal marrow could also be induced to proliferate by the v-raf virus, these cells required a stromal feeder layer, did not clone in agar, and were not malignant. Most normal cells stimulated to grow by v-H-ras also cloned poorly in agar, and only rare cells were tumorigenic. With the v-abl virus, no more cells were transformed from E mu-myc than normal marrow and the proportion of tumorigenic pre-B clones was not elevated. These results suggest that both v-H-ras and v-raf, but apparently not v-abl, collaborate with constitutive myc expression to promote autonomous proliferation and tumorigenicity of pre-B lymphoid cells.

scholarly journals A quantitative assay for transformation of bone marrow cells by Abelson murine leukemia virus.

1976 ◽  
Vol 143 (6) ◽  
pp. 1453-1463 ◽  
Author(s):  
N Rosenberg ◽  
D Baltimore
Keyword(s):  
Bone Marrow ◽  
Lymphoid Cell ◽  
Murine Leukemia Virus ◽  
Bone Marrow Cells ◽  
Cell Transformation ◽  
Leukemia Virus ◽  
Broad Band ◽  
Abelson Murine Leukemia Virus ◽  
Murine Leukemia ◽  
Marrow Cells

A quantitative Abelson murine leukemia virus (A-MuLV) lymphoid cell transformation assay has been developed using a semisolid agarose culture system. Under these conditions lymphoid cell transformation was shown to vary linearly with the dose of A-MuLV used. The susceptibility of bone marrow cells from different strains of mice to A-MuLV-induced transformation can be estimated using the agarose assay. Strains with bone marrow cells of high, medium, and low susceptibility to A-MuLV can be identified. The assay has been used to study the susceptibility of cells from lymphoid organs of fetal and adult mice to A-MuLV. Cell suspensions from fetal liver, adult bone marrow, and adult spleen are susceptible to A-MuLV, while thymocytes are resistant to A-MuLV-induced transformation. Bovine serum albumin gradient fractionation of bone marrow cells before infection with A-MuLV demonstrates that the majority of A-MuLV-sensitive cells are recovered in a broad band partially overlapping the majority of the nucleated cells. The agarose assay system allows study of A-MuLV-lymphoid cell interaction at the level of single cell-single virus particle interaction.

scholarly journals Colony formation in vitro by leukemic cells in acute lymphoblastic leukemia (ALL)

Blood ◽  
1978 ◽  
Vol 52 (4) ◽  
pp. 712-718 ◽  
Author(s):  
SD Smith ◽  
EM Uyeki ◽  
JT Lowman
Keyword(s):  
Bone Marrow ◽  
Acute Lymphoblastic Leukemia ◽  
Bone Marrow Cells ◽  
Lymphoblastic Leukemia ◽  
Lymphoid Cells ◽  
Assay System ◽  
Leukemic Cells ◽  
Specific Cell ◽  
Specific Cell Surface

Abstract An assay system in vitro for the growth of malignant lymphoblastic colony-forming cells (CFC) was established. Growth of malignant myeloblastic CFC has been previously reported, but this is the first report of growth of malignant lymphoblastic CFC. Established assay systems in vitro have been very helpful in elucidating the control of growth and differentiation of both normal and malignant bone marrow cells. Lymphoblastic CFC were grown from the bone marrow aspirates of 20 children with acute lymphoblastic leukemia. Growth of these colonies was established on an agar assay system and maintained in the relative hypoxia (7% oxygen) of a Stulberg chamber. The criteria for malignancy of these colonies was based upon cellular cytochemical staining characteristics, the presence of specific cell surface markers, and the ability of these lymphoid cells to grow without the addition of a lymphoid mitogen. With this technique, specific nutritional requirements and drug sensitivities can be established in vitro, and these data may permit tailoring of individual antileukemic therapy.

scholarly journals Interleukin-3 is significantly more effective than other colony- stimulating factors in long-term maintenance of human bone marrow- derived colony-forming cells in vitro

Blood ◽  
1989 ◽  
Vol 73 (7) ◽  
pp. 1836-1841 ◽  
Author(s):  
M Kobayashi ◽  
BH Van Leeuwen ◽  
S Elsbury ◽  
ME Martinson ◽  
IG Young ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cultured Cells ◽  
Bone Marrow Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Interleukin 3 ◽  
Gm Csf ◽  
Factor G ◽  
Marrow Cells

Abstract Human bone marrow cells cultured for 21 days in the presence of recombinant human interleukin-3 (IL-3) produced up to 28 times more colony-forming cells (CFC) than could be obtained from cultures stimulated with granulocyte colony stimulating factor (G-CSF) or granulocyte-macrophage CSF (GM-CSF). IL-3-cultured cells retained a multipotent response to IL-3 in colony assays but were restricted to formation of granulocyte colonies in G-CSF and granulocyte or macrophage colonies in GM-CSF. Culture of bone marrow cells in IL-3 also led to accumulation of large numbers of eosinophils and basophils. These data contrast with the effects of G-CSF, GM-CSF, and IL-3 in seven-day cultures. Here both GM-CSF and IL-3 amplified total CFC that had similar multipotential colony-forming capability in either factor. G-CSF, on the other hand, depleted IL-3-responsive colony-forming cells dramatically, apparently by causing these cells to mature into granulocytes. The data suggest that a large proportion of IL-3- responsive cells in human bone marrow express receptors for G-CSF and can respond to this factor, the majority becoming neutrophils. Furthermore, the CFC maintained for 21 days in IL-3 may be a functionally distinct population from that produced after seven days culture of bone marrow cells in either IL-3 or GM-CSF.

scholarly journals Antioxidant Fusion Protein SOD1-Tat Increases the Engraftment Efficiency of Total Bone Marrow Cells in Irradiated Mice

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3395
Author(s):  
Ting Bei ◽  
Xusong Cao ◽  
Yun Liu ◽  
Jinmei Li ◽  
Haihua Luo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Fusion Protein ◽  
Bone Marrow Cells ◽  
Standard Procedure ◽  
Severe Infection ◽  
Copper Zinc Superoxide Dismutase ◽  
Donor Cells ◽  
Total Bone Marrow ◽  
Marrow Cells

Total body irradiation is a standard procedure of bone marrow transplantation (BMT) which causes a rapid increase in reactive oxygen species (ROS) in the bone marrow microenvironment during BMT. The increase in ROS reduces the engraftment ability of donor cells, thereby affecting the bone marrow recovery of recipients after BMT. In the early weeks following transplantation, recipients are at high risk of severe infection due to weakened hematopoiesis. Thus, it is imperative to improve engraftment capacity and accelerate bone marrow recovery in BMT recipients. In this study, we constructed recombinant copper/zinc superoxide dismutase 1 (SOD1) fused with the cell-penetrating peptide (CPP), the trans-activator of transcription (Tat), and showed that this fusion protein has penetrating ability and antioxidant activity in both RAW264.7 cells and bone marrow cells in vitro. Furthermore, irradiated mice transplanted with SOD1-Tat-treated total bone marrow donor cells showed an increase in total bone marrow engraftment capacity two weeks after transplantation. This study explored an innovative method for enhancing engraftment efficiency and highlights the potential of CPP-SOD1 in ROS manipulation during BMT.

In vitro proliferative advantage of bone marrow cells with tetrasomy 8 in Ewing sarcoma

1996 ◽  
Vol 90 (2) ◽  
pp. 176-178 ◽  
Author(s):  
Luba Trakhtenbrot ◽  
Yoram Neumann ◽  
Matilda Mandel ◽  
Amos Toren ◽  
Nelly Gipsh ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Ewing Sarcoma ◽  
Bone Marrow Cells ◽  
Tetrasomy 8 ◽  
Proliferative Advantage ◽  
Marrow Cells
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