Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “abscopal effects of radiation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2003

Radiation abscopal antitumor effect is mediated through p53.

The observation that radiation treatment to a local area of the body results in an antitumor effect for tumors distant to the radiation site has been termed the "abscopal effect." To understand the mechanism of this unusual phenomenon, we examined whether the effect was mediated through p53, a protein complex up-regulated in irradiated cells. Non-tumor-bearing legs of C57BL/6 (wild-type p53) and p53 null B6.129S2-Trp53(tm1Tyj) mice were irradiated to determine whether an abscopal effect could be observed against Lewis lung carcinoma (LLC) and T241 (fibrosarcoma) implanted at a distant site. In mice with wild-type p53, both LLC and T241 tumors implanted into the midline dorsum grew at a significantly slower rate when the leg of the animal was exposed to five 10-Gy fractions of radiation compared with sham-irradiated animals, suggesting that the abscopal effect is not tumor specific. When the radiation dose to the leg was reduced (twelve fractions of 2 Gy each), the inhibition of LLC tumor growth was decreased indicating a radiation-dose dependency for the abscopal effect. In contrast, when the legs of p53 null animals or wild-type p53 mice treated with pifithrin-alpha (a p53 blocker) were irradiated (five 10-Gy fractions), tumor growth was not delayed. These data implicate p53 as a key mediator of the radiation-induced abscopal effect and suggest that pathways downstream of p53 are important in eliciting this response.

Animals↗
PubMed2002

The Southern Urals radiation studies. A reappraisal of the current status.

In the late 1940s and early 1950s the nuclear workers of the Mayak Production Association in the Southern Urals were exposed to high doses from gamma-rays and from incorporated plutonium. In addition, the population of the Techa riverside downstream of the plutonium-production sites received continued exposures from external gamma-rays due to fission products released into the river and from the internal radiation due to incorporation of the fission products. Based on two international coordination meetings in 1998 and 2000, a synopsis has been given recently in this journal of the radioepidemiological studies on these exposed populations. This commentary describes the current status of these singular investigations with regard to the dosimetry, the assessment of late health effects, and the risk estimation both for the Mayak nuclear workers and the Techa riverside population. A central issue are newly published reduced estimates of the external dose to the Techa riverside population which imply substantially increased risk coefficients for solid cancer. Unless the new dosimetry system, TRDS-2000, has missed a major dose contribution, there is now conspicuous disagreement with current risk estimates. Unaccounted doses from atmospheric releases of fission products and from radiological screening of the Techa riverside population need to be explored, but underestimation of the short lived fission products released into the river appears to be a more critical factor. It is furthermore argued that even if TRDS-2000 were confirmed it would remain questionable whether risk estimates can be based on organ-specific doses when they are obtained in a population with a much higher bone-marrow exposure that may possibly have caused an 'abscopal' radiation effect.

Female↗
PubMed2004

Ionizing radiation inhibition of distant untreated tumors (abscopal effect) is immune mediated.

PURPOSE: Ionizing radiation can reduce tumor growth outside the field of radiation, known as the abscopal effect. Although it has been reported in multiple malignancies, the abscopal effect remains a rare and poorly understood event. Ionizing radiation generates inflammatory signals and, in principle, could provide both tumor-specific antigens from dying cells and maturation stimuli that are necessary for dendritic cells' activation of tumor-specific T cells. We therefore tested the hypothesis that the abscopal effect elicited by radiation is immune mediated. This was directly tested by enhancing the number of available dendritic cells using the growth factor Flt3-Ligand (Flt3-L). METHODS AND MATERIALS: Mice bearing a syngeneic mammary carcinoma, 67NR, in both flanks were treated with Flt3-L daily for 10 days after local radiation therapy (RT) to only 1 of the 2 tumors at a single dose of 2 or 6 Gy. The second nonirradiated tumor was used as indicator of the abscopal effect. Data were analyzed using repeated measures regression. RESULTS: RT alone led to growth delay exclusively of the irradiated 67NR tumor, as expected. Surprisingly, growth of the nonirradiated tumor was also impaired by the combination of RT and Flt3-L. As control, Flt3-L had no effect without RT. Importantly, the abscopal effect was shown to be tumor specific, because growth of a nonirradiated A20 lymphoma in the same mice containing a treated 67NR tumor was not affected. Moreover, no growth delay of nonirradiated 67NR tumors was observed when T cell deficient (nude) mice were treated with RT plus Flt3-L. CONCLUSIONS: These results demonstrate that the abscopal effect is in part immune mediated and that T cells are required to mediate distant tumor inhibition induced by radiation.

Animals↗
PubMed2005

The controversial abscopal effect.

The abscopal effect is potentially important for tumor control and is mediated through cytokines and/or the immune system, mainly cell-mediated immunity. It results from loss of growth stimulatory and/or immunosuppressive factors from the tumor. Until recently, the abscopal effect referred to the distant effects seen after local radiation therapy. However, the term should now be used interchangeably with distant bystander effect. Through analysis of distant bystander effects of other local therapies, we discuss the poorly understood and researched radiation-induced abscopal effect. Although the abscopal effect has been described in various malignancies, it is a rarely recognized clinical event. The abscopal effect is still extremely controversial with known data that both support and refute the concept.

Animals↗
PubMed2005

Abdominal radiation exposure elicits inflammatory responses and abscopal effects in the lungs of mice.

An inflammatory reaction is a classical feature of radiation exposure and appears to be a key event in the development of the acute radiation syndrome. We have investigated the radiation-induced inflammatory response in C57BL6/J mice after total abdominal or total-body irradiation at a dose of 15 Gy. Our goal was to determine the radiation-induced inflammatory response of the gut and to study the consequences of abdominal irradiation for the intestine and for the lungs as a distant organ. A comparison with total-body irradiation was used to take into account the hematopoietic response in the inflammatory process. For both irradiation regimens, systemic and intestinal responses were evaluated. A systemic inflammatory reaction was found after abdominal and total-body irradiation, concomitant with increased cytokine and chemokine production in the jejunum of irradiated mice. In the lungs, the radiation-induced changes in the production of cytokines and chemokines and in the expression of adhesion molecules after both abdominal and total-body irradiation indicate a possible abscopal effect of radiation in our model. The effects observed in the lungs after irradiation of the abdomino-pelvic region may be caused by circulating inflammatory mediators consequent to the gut inflammatory response.

Abdomen↗
PubMed2025

Radiation Without Borders: Unraveling Bystander and Non-Targeted Effects in Oncology.

Radiotherapy (RT) remains a cornerstone of cancer treatment, offering spatially precise cytotoxicity against malignant cells. However, emerging evidence reveals that ionizing radiation (IR) exerts biological effects beyond the targeted tumor volume, manifesting as radiation bystander effects (BEs) and other non-targeted effects (NTEs). These phenomena challenge the traditional paradigm of RT as a localized intervention, highlighting systemic and long-term consequences in non-irradiated tissues. This comprehensive review synthesizes molecular, cellular, and clinical insights about BEs, elucidating the complex intercellular signaling networks gap junctions, cytokines, extracellular vesicles, and oxidative stress that propagate damage, genomic instability, and inflammation. We explore the role of mitochondrial dysfunction, epigenetic reprogramming, immune modulation, and stem cell niche disruption in shaping BEs outcomes. Clinically, BEs contribute to neurocognitive decline, cardiovascular disease, pulmonary fibrosis, gastrointestinal toxicity, and secondary malignancies, particularly in pediatric and long-term cancer survivors. The review also evaluates countermeasures including antioxidants, COX-2 inhibitors, exosome blockers, and FLASH RT, alongside emerging strategies targeting cfCh, inflammasomes, and senescence-associated secretory phenotypes. We discuss the dual nature of BEs: their potential to both harm and heal, underscoring adaptive responses and immune priming in specific contexts. By integrating mechanistic depth with translational relevance, this work posits that radiation BEs are a modifiable axis of RT biology. Recognizing and mitigating BEs is imperative for optimizing therapeutic efficacy, minimizing collateral damage, and enhancing survivorship outcomes. This review advocates for a paradigm shift in RT planning and post-treatment care, emphasizing precision, personalization, and systemic awareness in modern oncology.

Humans↗
PubMed1987

[Study of abscopal effect and cellular infiltration of tumor nests using less-fractionated, large-dose radiation].

As reported by several authors, abscopal effect and favorable cellular infiltrations into the tumor nest caused by irradiation suggest the existence of cell immunity in the host. In our present study, as first step to elucidate the mechanism of the fact mentioned above, effects of radiation with a single dose irradiation was estimated in terms of the increase of survival rate and the inhibition of pulmonary metastasis, i.e. abscopal effect in the mice of irradiated tumor burden. Therefore, we examined the resected and pulmonary specimen after irradiation histopathologically. We also examined the effects of the administration of immune modulator PSK and OK-432. Results; 1) Increase of survival rate and inhibition of pulmonary metastasis were observed in groups of mice with inoculated tumor and with again inoculated tumor treated by a single dose irradiation, compared to either the control groups. 2) Also administration of immune potentiator with radiation enhanced the survival rate and inhibition of pulmonary metastasis in all experimental protocols. 3) Remarkable cellular infiltrations of tumor nest after irradiation were observed, and these cellular infiltrations suggest participation of immunoreaction. In the group of using immune modulator, the cellular infiltrations were observed more remarkable than the other groups. 4) Optimal radiation dose was proved to be 30 Gy in this study.

Animals↗
PubMed2004

Review of radiation-induced bystander effects.

It is now apparent that the target for the biological effects of ionizing radiation (IR) is not solely the irradiated cell(s), but also includes the surrounding cells/tissue as well. Radiation-induced bystander effects (BSEs) are defined by the presence of the biological effects of radiation in cells that were not themselves in the field of irradiation. Decreased plating efficiency, increased sister chromatid exchanges, oncogenic transformation, among other endpoints have been used to describe the BSE. Two primary means have been established for the transmission of the bystander signal; one is mediated by gap-junction intracellular communication, and the other is initiated through the secretion of factors from irradiated cells. While the basis for these phenomena have been established in cell culture systems, there is also evidence for their presence in vivo. This in vivo effect may contribute to increased tumor cell killing, and may also play a role in the abscopal effects of radiation, where radiation responses are seen in areas separated from the irradiated tissue. Although the precise molecular components and mechanisms remain unknown, their discovery will shed new light on the role of the BSEs in radiation risk assessment, and clinical radiotherapy in the clinic.

Animals↗
PubMed2005

Local irradiation not only induces homing of human mesenchymal stem cells at exposed sites but promotes their widespread engraftment to multiple organs: a study of their quantitative distribution after irradiation damage.

Mesenchymal stem cells (MSCs) have been shown to migrate to various tissues. There is little information on the fate and potential therapeutic efficacy of the reinfusion of MSCs following total body irradiation (TBI). We addressed this question using human MSC (hMSCs) infused to nonobese diabetic/ severe combined immunodeficient (NOD/SCID) mice submitted to TBI. Further, we tested the impact of additional local irradiation (ALI) superimposed to TBI, as a model of accidental irradiation. NOD/SCID mice were transplanted with hM-SCs. Group 1 was not irradiated before receiving hMSC infusion. Group 2 received only TBI at a dose of 3.5 Gy, group 3 received local irradiation to the abdomen at a dose of 4.5 Gy in addition to TBI, and group 4 received local irradiation to the leg at 26.5 Gy in addition to TBI. Fifteen days after irradiation, quantitative and spatial distribution of the hMSCs were studied. Histological analysis of mouse tissues confirmed the presence of radio-induced lesions in the irradiated fields. Following their infusion into nonirradiated animals, hMSCs homed at a very low level to various tissues (lung, bone marrow, and muscles) and no significant engraftment was found in other organs. TBI induced an increase of engraftment levels of hMSCs in the brain, heart, bone marrow, and muscles. Abdominal irradiation (AI) as compared with leg irradiation (LI) increased hMSC engraftment in the exposed area (the gut, liver, and spleen). Hind LI as compared with AI increased hMSC engraftment in the exposed area (skin, quadriceps, and muscles). An increase of hMSC engraftment in organs outside the fields of the ALI was also observed. Conversely, following LI, hMSC engraftment was increased in the brain as compared with AI. This study shows that engraftment of hMSCs in NOD/ SCID mice with significantly increased in response to tissue injuries following TBI with or without ALI. ALI induced an increase of the level of engraftment at sites outside the local irradiation field, thus suggesting a distant (abscopal) effect of radiation damage. This work supports the use of MSCs to repair damaged normal tissues following accidental irradiation and possibly in patients submitted to radiotherapy.

Animals↗
PubMed1990

[Therapeutic efficacy of pre-operative radiotherapy on breast carcinoma: in special reference to its abscopal effect on metastatic lymph-nodes].

UNLABELLED: The abscopal effect is the radiation response in tissue at a distance from the irradiated site invoked by local irradiation. It is reported that the abscopal effect is observed occasionally in the cases of radiotherapy for malignant lymphoma, malignant melanoma and seminoma. However, pathophysiology and mechanism of the abscopal effect have not been well defined. An aim of this study was to investigate the pathophysiology and mechanism of the abscopal effect in patients with breast carcinoma. SUBJECTS AND METHODS: Sixty two patients entered this study. Age distribution was from 29 to 84 years old (mean 54.0 years old) and all cases were females. Their stages were as follows: stage II 12 cases, stage IIIa 16 cases, stage IIIb 22 cases and stage IV 12 cases. They were irradiated pre-operatively using less fractionated large dose irradiation. Then, they underwent mastectomy or tumor resection. RESULTS: The abscopal effect on metastatic lymph nodes was observed in 15 out of 42 cases (35.7%) by palpation. The histopathological abscopal effect was noted in 22 out of 42 cases (52.4%). Incidence of the abscopal effect was significantly higher in patients under 55 years old as compared with that in patients over 56 years old (p less than 0.05). The abscopal effect was highly observed in the cases who had the infiltrating lymphocytes around the degenerated cancer cells in the irradiated primary tumor nests (p less than 0.01). The subsets of the infiltrative lymphocytes were analyzed immunohistologically using monoclonal antibodies. It disclosed that the infiltrative lymphocytes were CD8 and CD4 positive lymphocytes. Those findings suggest that abscopal effect was caused by activated cellular immunity in hosts. The five and ten years survival rates of stage IIIa were 71.4% and 71.4% respectively. Stage IIIb showed 62.5% in 5 years survival rate and 54.7% in 10 years survival rate. The survival rate of the cases with the abscopal effect was higher than that of the cases without the abscopal effect, however it was not statistically significant. No complications such as pneumonia was observed.

Adult↗
PubMed2004

TRAIL induction by radiation in lymphoma patients.

TRAIL/Apo-2 L, a member of the Tumor Necrosis Factor cytokine family, induces apoptosis specifically in malignant cells. A combination of TRAIL and radiation is highly synergistic in in vitro experiments. In addition to this additive effect, we observed that TRAIL is induced by irradiation of certain cell lines. The induction begins approximately 2 hours after irradiation. This might even enhance the antineoplastic effect of ionizing radiation and partially explain the abscopal effect observed in hematopoietic malignancies. TRAIL levels were evaluated in 17 patients treated with radiation for Hodgkin's and non-Hodgkin's lymphoma. We did not observe a specific TRAIL expression pattern that could be correlated with histology, disease status, volume of disease, radiation dose, and other antineoplastic therapies, but a definite pattern observed in a single patient remained constant over time. TRAIL and interferons display a common pattern of gene expression at certain nodal points of interaction between the two physiologic pathways. Our hypothesis is that the radiation-induced changes in TRAIL expression observed in patients undergoing therapeutic radiation may be emblematic of the various physiologic pathways induced or inhibited by ionizing radiation and may even be partially responsible for the "bystander effect" observed in unirradiated cells in close proximity to irradiated cells.

Adult↗
PubMed1986

Evolving perspectives on the biology and mechanisms of carcinogenesis.

From experimental and epidemiological evidence, radiation-induced cancers appear to arise as multistage, monoclonal growths, which are elicited through various mechanisms, depending on the neoplasm in question and the conditions of exposure. At the molecular level, the process of carcinogenesis may involve the activation of oncogenes and/or the inactivation or loss of anti-oncogenes, through chromosomal rearrangements, point mutations, and other effects of radiation on DNA. In contrast to these mechanisms of carcinogenesis, which result from the absorption of radiation by the tumor-forming cells themselves, abscopal effects resulting from irradiation of other cells may contribute to carcinogenesis under certain conditions, e.g. in the induction of tumors of endocrine target cells through radiation-induced disturbances of hormonal balance. Effects of the latter type, which require the killing of substantial numbers of cells, are not elicited at low doses, thus contrasting with effects of the former type, which may be presumed to have no thresholds. Because radiation carcinogenesis may be mediated through a diversity of effects, the relationship between incidence and dose can vary accordingly. The relationship between the incidence of radiation-induced tumors and the time elapsing after irradiation also varies, depending on the type of tumor in question, species, age at irradiation, exposure conditions, and other factors. Although the variations with dose and time are consistent with multistage models of tumor initiation, tumor promotion, and tumor progression, the precise nature of the successive steps that are involved remains to be determined. The tendency for the tumors to resemble their spontaneous counterparts in age-distribution points to interactions between radiation and other carcinogenic risk factors which are as yet poorly understood. Also poorly understood are species- and organ-differences in susceptibility to radiation carcinogenesis, which bear no consistent relationship to corresponding 'spontaneous' cancer rates.

Age Factors↗
PubMed1981

The abscopal effect: demonstration in lymphomatous involvement of kidneys.

A patient with bilateral involvement of the kidneys with diffuse histiocytic lymphoma associated with renal failure is presented. This case report provides an example of the abscopal effect. Although only one kidney received radiation therapy, both kidneys were shown to respond to this treatment.

Acute Kidney Injury↗
PubMed1994

Abscopal depression of G-CSF mobilized peripheral stem cells.

Transient suppression of hematopoietic colony formation from cytokine mobilized PBSC was observed in a patient following local radiation therapy for lymphoma. This effect was seen 2 weeks after completion of radiation and reversed by 6 weeks. The patient successfully engrafted after myeloablative chemotherapy with harvested PBSC. This report documents the first reported case of suppression of PBSC colony formation following radiation and we speculate that this finding may be due to an abscopal effect.

Antigens, CD↗