Tumor dormancy. I. Regression of BCL1 tumor and induction of a dormant tumor state in mice chimeric at the major histocompatibility complex

H. Siu, E. S. Vivetta, R. D. May, J. W. Uhr

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Abstract

The growth of the BCL1 tumor in murine H-2 chimeras was studied. Lethally x-irradiated BALB/c mice were reconstituted with C57BL/6 bone marrow that had been depleted of T cells. When chimerism was established 90 to 120 days later, large doses of BCL1 cells were injected. The tumor grew progressively, reaching a peak level of as many as 109 tumor cells per animal by 40 days after inoculation. After that time, the tumor regressed in all the chimeric animals, and by 100 days after inoculation, virtually all the animals appeared disease free as judged by an absence of BCL1-idiotype-positive cells in the spleen and peripheral blood, a normal spleen size, and absence of an elevated white blood cell count. Such animals were followed for as long as 8 mo after tumor inoculation and remained disease free. However, transfer of graded numbers of splenocytes from these animals into normal BALB/c recipients resulted in development of tumor in recipients receiving 100 or more spleen cells. These results indicate a large tumor burden in the spleen of each donor, namely, 106 to 107 BCL1 cells. The present model should facilitate characterization of the mechanisms underlying tumor dormancy.

Original languageEnglish (US)
Pages (from-to)1376-1382
Number of pages7
JournalJournal of Immunology
Volume137
Issue number4
StatePublished - 1986

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Major Histocompatibility Complex
Spleen
Neoplasms
Animal Diseases
Chimerism
Tumor Burden
Leukocyte Count
Bone Marrow
T-Lymphocytes
Growth

ASJC Scopus subject areas

  • Immunology

Cite this

Tumor dormancy. I. Regression of BCL1 tumor and induction of a dormant tumor state in mice chimeric at the major histocompatibility complex. / Siu, H.; Vivetta, E. S.; May, R. D.; Uhr, J. W.

In: Journal of Immunology, Vol. 137, No. 4, 1986, p. 1376-1382.

Research output: Contribution to journalArticle

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AB - The growth of the BCL1 tumor in murine H-2 chimeras was studied. Lethally x-irradiated BALB/c mice were reconstituted with C57BL/6 bone marrow that had been depleted of T cells. When chimerism was established 90 to 120 days later, large doses of BCL1 cells were injected. The tumor grew progressively, reaching a peak level of as many as 109 tumor cells per animal by 40 days after inoculation. After that time, the tumor regressed in all the chimeric animals, and by 100 days after inoculation, virtually all the animals appeared disease free as judged by an absence of BCL1-idiotype-positive cells in the spleen and peripheral blood, a normal spleen size, and absence of an elevated white blood cell count. Such animals were followed for as long as 8 mo after tumor inoculation and remained disease free. However, transfer of graded numbers of splenocytes from these animals into normal BALB/c recipients resulted in development of tumor in recipients receiving 100 or more spleen cells. These results indicate a large tumor burden in the spleen of each donor, namely, 106 to 107 BCL1 cells. The present model should facilitate characterization of the mechanisms underlying tumor dormancy.

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