Relative Radiosensitivities of the Thymus, Spleen, and Lymphohemopoietic Systems

Maruyama, Yosh; Feola, Jose M.

doi:10.1016/b978-0-12-035412-2.50005-9

Cited by 21 publications

(4 citation statements)

References 320 publications

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“…Similarly, within the germ cell lineage of the rodent testis, rapid-dying transit spermatogonia have a D o of around 0.21 Gy of y-irradiation while spermatogonial stem cells have a Do of around 2 Gy (reviewed in Bianchi 1983) . The ST4 y-ray clonogenic survival data are also very similar to viability data for normal cortical thymocytes (Maruyama and Feola 1987, figure 3) . However, while the aforementioned survival data for normal cells are based on the scoring of tissue cross sections for dying or surviving cells and may require various assumptions, the ST4 data are unencumbered by such problems .…”

Section: Discussionsupporting

confidence: 56%

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Radiation Response of Mouse Lymphoid and Myeloid Cell Lines. Part I. Sensitivity to Killing by Ionizing Radiation, Rate of Loss of Viability, and Cell Type of Origin

Radford

1994

International Journal of Radiation Biology

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The sensitivity of 10 mouse lymphoid or myeloid cell lines to gamma-ray- and DNA-associated 125I-decay-induced clonogenic cell killing have been compared with their rate of loss of viability (membrane integrity) and with their putative cell type of origin. The pseudodiploid haematopoietic cell lines showed D0 values for 125I-induced DNA double-strand breakage (dsb) that ranged from 7.7 +/- 0.7 to 40.8 +/- 2.8 decays. These lines generally appeared to be more sensitive to killing by radiation-induced DNA dsb than are fibroblast-like cell lines. The increased sensitivity of haematopoietic cell lines to killing by DNA dsb may be related to their mode of death (apoptosis versus necrosis). Mode of cell death may thus be an important factor in determining the 'inherent radiosensitivity' of normal cells/tissues. Haematopoietic cell lines that undergo rapid interphase apoptotic death showed extreme sensitivity to DNA dsb. The latter cell lines were found to have derived from immature lymphoid cells, and it is speculated that their high radiosensitivity might reflect the action of a mechanism that normally eliminates cells containing illegitimate V(D)J recombinase-induced DNA dsb.

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Section: Discussionsupporting

confidence: 56%

“…The unusually high radiosensitivity of normal lymphoid tissue, first described by Heineke in 1903, extends to many lymphomas and leukaemias and is a crucial factor in the response of higher organisms to irradiation (reviewed in Anderson andWarner 1976, Maruyama andFeola 1987) .…”

Section: Introductionmentioning

confidence: 98%

Radiation Response of Mouse Lymphoid and Myeloid Cell Lines. Part I. Sensitivity to Killing by Ionizing Radiation, Rate of Loss of Viability, and Cell Type of Origin

Radford

1994

International Journal of Radiation Biology

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“…Although B cell production continues throughout life, proliferation in the precursor compartment is much more extensive in very young animals (Miller & Osmond, 1975). In the T cell system, the thymus atrophies in the post-pubertal period (Clarke & MacLennan, 1986) (Maruyama & Feola, 1987) and are very sensitive to steroid-induced apoptosis (Wyllie, 1981). Lymphocyte progenitor populations may be ultra-sensitive to DNA damage.…”

Section: Curability Of Childhood Leukaemiamentioning

confidence: 99%

Stem cell origins of leukaemia and curability

1993

Br J Cancer

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It is suggested that most childhood acute lymphoblastic leukaemias and some other paediatric cancers are chemo-curable because they arise in stem cell populations that are functionally transient, chemosensitive and programmed for apoptosis. Most adult acute leukaemias are chemo-incurable at least in part because they originate in relatively drug resistant stem cells with extensive self-renewal capacity. The latter property in turn increases the probability of clones evolving with multi-drug resistance. Particular mutations may superimpose additional adverse features on leukaemic cells.

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“…However, the apoptotic cells in case 1 were visualized in the specimen taken 18 months after radiosurgery. If these apoptotic cells were induced by irradiation, this long detection period may be explained by delayed mitotic death with the cells completing several mitoses before dying [14]. It seems unlikely that ischemic-related cell death by obliteration of intratumoral vessels is related to apoptosis in case 1, because apoptotic cells were found among viable-looking tumor cells and were located far from any necrotic area.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis following Gamma Knife Radiosurgery in a Case of Acoustic Schwannoma

Fukuoka

Oka

Seo

et al. 1998

Stereotact Funct Neurosurg

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A 25-year-old woman with a large acoustic schwannoma underwent surgical excision 18 months after Gamma Knife radiosurgery because of transient expansion of the tumor causing ataxia. Histopathologial investigation by the TUNEL method revealed the presence of some apoptotic cells. The findings were compared with findings from a control group of 7 operated cases where radiosurgery had not been used. There was no apoptosis found in any of these cases. In addition, another case which resulted in a regrowing tumor following Gamma Knife treatment also showed no apoptosis. These findings suggest apoptosis may be a possible mechanism in reducing tumor size following Gamma Knife radiosurgery.

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Relative Radiosensitivities of the Thymus, Spleen, and Lymphohemopoietic Systems

Cited by 21 publications

References 320 publications

Radiation Response of Mouse Lymphoid and Myeloid Cell Lines. Part I. Sensitivity to Killing by Ionizing Radiation, Rate of Loss of Viability, and Cell Type of Origin

Radiation Response of Mouse Lymphoid and Myeloid Cell Lines. Part I. Sensitivity to Killing by Ionizing Radiation, Rate of Loss of Viability, and Cell Type of Origin

Stem cell origins of leukaemia and curability

Apoptosis following Gamma Knife Radiosurgery in a Case of Acoustic Schwannoma

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