Hematopoietic stem cell compartment: Acute and late effects of radiation therapy and chemotherapy

Mauch, Peter; Constine, Louis S.; Greenberger, Joel S.; Knospe, William H.; Sullivan, Jessie; Liesveld, Jane L.; Deeg, H. Joachim

doi:10.1016/0360-3016(94)00430-s

Cited by 442 publications

(328 citation statements)

References 110 publications

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“…[6][7][8][9][10][11][12][13] These transcriptional regulators activate genes for many cytokine regulators and cellular protective gene products. 9,28 Radioresistance of mammalian cells in culture can be induced by the expression of recombinant oncogenes of several categories 47 or by increasing the availability of specific recombinant growth factors. 28 The mechanism of these two forms of radiation resistance may have a common molecular pathway, but the molecular mechanism of radiation protection by either an oncogene or a cytokine is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…9,28 Radioresistance of mammalian cells in culture can be induced by the expression of recombinant oncogenes of several categories 47 or by increasing the availability of specific recombinant growth factors. 28 The mechanism of these two forms of radiation resistance may have a common molecular pathway, but the molecular mechanism of radiation protection by either an oncogene or a cytokine is unknown. There are data to support a common role of MnSOD and metallothionein in the cellular response to chemical-induced or radiation-induced damage.…”

Section: Discussionmentioning

confidence: 99%

“…[17][18][19] In the lung, as in most other organ systems, the acute effects of irradiation exposure have been shown to correlate with elevated levels of cytokines including interleukin-1 (IL-1), tumor necrosis factoralpha (TNF-␣) and transforming growth factor-beta (TGF-␤). [20][21][22][23][24][25][26][27][28] These are humoral regulators common to the response of tissues to other cellular damaging agents including heat, ultraviolet (UV) irradiation, infectious organisms, hyperbaric oxygen and chemical toxins. [20][21][22][23][24][25][26][27][28] Interventional approaches toward modulation of levels of these and other cytokines associated with acute pulmonary irradiation exposure, including the delivery of basic fibroblast growth factor (bFGF) 29,30 or corticosteroids, 24 have been successful in some cases but do not always correlate with prevention of the late effects, which in the rodent model include organizing alveolitis/fibrosis.…”

Section: Introductionmentioning

confidence: 99%

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Prevention of late effects of irradiation lung damage by manganese superoxide dismutase gene therapy

et al. 1998

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prevention of late effects of irradiation lung damage by manganese superoxide dismutase gene therapy

et al. 1998

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“…Unfortunately, these therapies are not tumor-specific. Normal tissues, particularly BM, are extremely vulnerable to cytotoxicity caused by these therapies [25]. An acute and transient myelosuppression is a common side effect of radiotherapy and chemotherapy, which primarily damage the rapidly proliferating hematopoietic progenitors and their more mature progeny.…”

Section: Stem Cell-based Bm Regenerationmentioning

confidence: 99%

Local signals in stem cell-based bone marrow regeneration

Wang

Liu

2006

Cell Res

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The cellular basis of bone marrow (BM) tissue development and regeneration is mediated through hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs). Local interplays between hematopoietic cells and BM stromal cells (BMSCs) determine the reconstitution of hematopoiesis after myelosuppression. Here we review the BM local signals in control of BM regeneration after insults. Hematopoietic growth factors (HGFs) and cytokines produced by BMSCs are primary factors in regulation of BM hematopoiesis. Morphogens which are critical to early embryo development in multiple species have been added to the family of HSCs regulators, including families of Wnt proteins, Notch ligands, BMPs, and Hedgehogs. Global gene expression analysis of HSCs and BMSCs has begun to reveal signature groups of genes for both cell types. More importantly, analysis of global gene expression coupled with biochemical and biological studies of local signals during BM regeneration have strongly suggested that HGFs and cytokines may not be the primary local regulators for BM recovery, rather chemokines (SDF-1, FGF-4) and angiogenic growth factors (VEGF-A, Ang-1) play instructive roles in BM reconstitution after myelosuppression. A new direction of management of BM toxicity is emerging from the identification of BM regenerative regulators.

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“…Hematopoietically active BM (ABM) stem cells are sensitive to ionizing radiation (10). In cervical cancer patients, the pelvic BM and much of the lumbar BM may be included in the radiation field, encompassing up to 50% of the total ABM (11,12). HT is rare in patients who receive solely pelvic radiation therapy (RT) (13), largely as a result of compensatory hematopoiesis in unirradiated BM (12).…”

Section: Introductionmentioning

confidence: 99%

Longitudinal Changes in Active Bone Marrow for Cervical Cancer Patients Treated With Concurrent Chemoradiation Therapy

Noticewala

Williamson

et al. 2017

International Journal of Radiation Oncology*Biology*Physics

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SummaryHematologic toxicity (HT) is a common adverse effect in patients with cervical cancer treated with concurrent chemoradiation therapy. In this study, we used 18 F-fluorodeoxyglucose positron emission tomography to quantify changes in functional bone marrow (BM) in unirradiated (extrapelvic) and irradiated (pelvic) BM in cervical cancer patients treated with concurrent chemotherapy of varying intensities. We found that patients have varying Purpose: To quantify longitudinal changes in active bone marrow (ABM) distributions within unirradiated (extrapelvic) and irradiated (pelvic) bone marrow (BM) in cervical cancer patients treated with concurrent chemoradiation therapy (CRT). Methods and Materials: We sampled 39 cervical cancer patients treated with CRT, of whom 25 were treated with concurrent cisplatin (40 mg/m 2 ) and 14 were treated with cisplatin (40 mg/m 2 ) plus gemcitabine (50-125 mg/m 2 ) (C/G). Patients underwent 18 F-fluorodeoxyglucose positron emission tomographic/computed tomographic imaging at baseline and 1.5 to 6.0 months after treatment. ABM was defined as the subvolume of bone with standardized uptake value (SUV) above the mean SUV of the total bone. The primary aim was to measure the compensatory response, defined as the change in the log of the ratio of extrapelvic versus pelvic ABM percentage from baseline to after treatment. We also quantified the change in the proportion of ABM and mean SUV in pelvic and extrapelvic BM using a 2-sided paired t test. Results: We observed a significant increase in the overall extrapelvic compensatory response after CRT (0.381; 95% confidence interval [CI]: 0.312, 0.449) and separately in patients treated with cisplatin (0.429; 95% CI: 0.340, 0.517) and C/G (0.294; 95% CI: 0.186, 0.402). We observed a trend toward higher compensatory response in patients treated with cisplatin compared with C/G (PZ.057). Pelvic ABM percentage

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Hematopoietic stem cell compartment: Acute and late effects of radiation therapy and chemotherapy

Cited by 442 publications

References 110 publications

Prevention of late effects of irradiation lung damage by manganese superoxide dismutase gene therapy

Prevention of late effects of irradiation lung damage by manganese superoxide dismutase gene therapy

Local signals in stem cell-based bone marrow regeneration

Longitudinal Changes in Active Bone Marrow for Cervical Cancer Patients Treated With Concurrent Chemoradiation Therapy

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