Abstract
Normal mast cells can be propagated in culture when medium is supplemented with interleukin-3 (IL-3). We demonstrate that Abelson-MuLV (Ab-MuLV) infection of mast cells eliminates dependence on IL-3 for growth. By contrast, Harvey, BALB, and Moloney MSV, which also productively infect mast cells, are unable to relieve IL-3 dependence. Ab-MuLV induced IL-3-independent lines express the v-abl-specific transforming protein and have phenotypic characteristics of mast cells. These cells also possess high loning efficiencies in soft agarose and are tumorigenic in nude mice. In addition, Ab-MuLV induces transplantable mastocytomas in pristane-primed adult mice resistant to lymphoid transformation, defining a new hematopoietic target for malignant transformation by this virus. None of the Ab-MuLV-derived transformants express or secrete detectable levels of IL-3 nor is their growth inhibited by anti-IL-3 serum. These results argue that Ab-MuLV abrogation of the IL-3 requirement is not due to an autocrine mechanism.
| Original language | English |
|---|---|
| Pages (from-to) | 685-693 |
| Number of pages | 9 |
| Journal | Cell |
| Volume | 41 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 1985 |
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ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
- Medicine(all)
Cite this
Neoplastic transformation of mast cells by Abelson-MuLV : abrogation of IL-3 dependence by a nonautocrine mechanism. / Pierce, Jacalyn H.; Paolo Di Fiore, Pier; Aaronson, Stuart A.; Potter, Michael; Pumphrey, Janet; Scott, Allen; Ihle, James N.
In: Cell, Vol. 41, No. 3, 1985, p. 685-693.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Neoplastic transformation of mast cells by Abelson-MuLV
T2 - abrogation of IL-3 dependence by a nonautocrine mechanism
AU - Pierce, Jacalyn H.
AU - Paolo Di Fiore, Pier
AU - Aaronson, Stuart A.
AU - Potter, Michael
AU - Pumphrey, Janet
AU - Scott, Allen
AU - Ihle, James N.
PY - 1985
Y1 - 1985
N2 - Normal mast cells can be propagated in culture when medium is supplemented with interleukin-3 (IL-3). We demonstrate that Abelson-MuLV (Ab-MuLV) infection of mast cells eliminates dependence on IL-3 for growth. By contrast, Harvey, BALB, and Moloney MSV, which also productively infect mast cells, are unable to relieve IL-3 dependence. Ab-MuLV induced IL-3-independent lines express the v-abl-specific transforming protein and have phenotypic characteristics of mast cells. These cells also possess high loning efficiencies in soft agarose and are tumorigenic in nude mice. In addition, Ab-MuLV induces transplantable mastocytomas in pristane-primed adult mice resistant to lymphoid transformation, defining a new hematopoietic target for malignant transformation by this virus. None of the Ab-MuLV-derived transformants express or secrete detectable levels of IL-3 nor is their growth inhibited by anti-IL-3 serum. These results argue that Ab-MuLV abrogation of the IL-3 requirement is not due to an autocrine mechanism.
AB - Normal mast cells can be propagated in culture when medium is supplemented with interleukin-3 (IL-3). We demonstrate that Abelson-MuLV (Ab-MuLV) infection of mast cells eliminates dependence on IL-3 for growth. By contrast, Harvey, BALB, and Moloney MSV, which also productively infect mast cells, are unable to relieve IL-3 dependence. Ab-MuLV induced IL-3-independent lines express the v-abl-specific transforming protein and have phenotypic characteristics of mast cells. These cells also possess high loning efficiencies in soft agarose and are tumorigenic in nude mice. In addition, Ab-MuLV induces transplantable mastocytomas in pristane-primed adult mice resistant to lymphoid transformation, defining a new hematopoietic target for malignant transformation by this virus. None of the Ab-MuLV-derived transformants express or secrete detectable levels of IL-3 nor is their growth inhibited by anti-IL-3 serum. These results argue that Ab-MuLV abrogation of the IL-3 requirement is not due to an autocrine mechanism.
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UR - http://www.scopus.com/inward/citedby.url?scp=0022006791&partnerID=8YFLogxK
U2 - 10.1016/S0092-8674(85)80049-0
DO - 10.1016/S0092-8674(85)80049-0
M3 - Article
C2 - 2988783
AN - SCOPUS:0022006791
VL - 41
SP - 685
EP - 693
JO - Cell
JF - Cell
SN - 0092-8674
IS - 3
ER -