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California Medicine Jul 1964
Review
Topics: Antineoplastic Agents; Drug Therapy; Humans; Leukemia; Leukemia, Lymphoid; Leukemia, Myeloid; Leukemia, Radiation-Induced; Neoplasms
PubMed: 14179529
DOI: No ID Found -
Japanese Journal of Clinical Oncology Jul 2012Absorption of energy from ionizing radiation by the genetic material in the cell leads to damage to DNA, which in turn leads to cell death, chromosome aberrations and... (Review)
Review
Absorption of energy from ionizing radiation by the genetic material in the cell leads to damage to DNA, which in turn leads to cell death, chromosome aberrations and gene mutations. While early or deterministic effects result from organ and tissue damage caused by cell killing, latter two are considered to be involved in the initial events that lead to the development of cancer. Epidemiological studies have demonstrated the dose-response relationships for cancer induction and quantitative evaluations of cancer risk following exposure to moderate to high doses of low-linear energy transfer radiation. A linear, no-threshold model has been applied to assessment of the risks resulting from exposure to moderate and high doses of ionizing radiation; however, a statistically significant increase has hardly been described for radiation doses below 100 mSv. This review summarizes our current knowledge of the physical and biological features of low-dose radiation and discusses the possibilities of induction of cancer by low-dose radiation.
Topics: Age Factors; Cell Transformation, Neoplastic; Chernobyl Nuclear Accident; Chromosome Aberrations; DNA Damage; DNA Repair; Dose-Response Relationship, Radiation; Environmental Exposure; Humans; Japan; Leukemia, Radiation-Induced; Linear Energy Transfer; Neoplasms, Radiation-Induced; Nuclear Weapons; Radiation Dosage; Radiation, Ionizing; Radiotherapy; Risk Assessment; Risk Factors; Survivors; Thyroid Gland; Thyroid Neoplasms
PubMed: 22641644
DOI: 10.1093/jjco/hys078 -
Human Genomics Jul 2014The use of radiation therapy is a cornerstone of modern cancer treatment. The number of patients that undergo radiation as a part of their therapy regimen is only... (Review)
Review
The use of radiation therapy is a cornerstone of modern cancer treatment. The number of patients that undergo radiation as a part of their therapy regimen is only increasing every year, but this does not come without cost. As this number increases, so too does the incidence of secondary, radiation-induced neoplasias, creating a need for therapeutic agents targeted specifically towards incidence reduction and treatment of these cancers. Development and efficacy testing of these agents requires not only extensive in vitro testing but also a set of reliable animal models to accurately recreate the complex situations of radiation-induced carcinogenesis. As radiation-induced leukemic progression often involves genomic changes such as rearrangements, deletions, and changes in methylation, the laboratory mouse Mus musculus, with its fully sequenced genome, is a powerful tool in cancer research. This fact, combined with the molecular and physiological similarities it shares with man and its small size and high rate of breeding in captivity, makes it the most relevant model to use in radiation-induced leukemia research. In this work, we review relevant M. musculus inbred and F1 hybrid animal models, as well as methods of induction of radiation-induced myeloid leukemia. Associated molecular pathologies are also included.
Topics: Animals; Carcinogenesis; Humans; Leukemia, Myeloid; Mice; Mice, Inbred Strains; Mice, Transgenic; Radiation Injuries, Experimental; Radiation Tolerance
PubMed: 25062865
DOI: 10.1186/1479-7364-8-13 -
Environmental Health Perspectives Jan 2005The U.S. government recently implemented rules for awarding compensation to individuals with cancer who were exposed to ionizing radiation while working in the nuclear... (Review)
Review
The U.S. government recently implemented rules for awarding compensation to individuals with cancer who were exposed to ionizing radiation while working in the nuclear weapons complex. Under these rules, chronic lymphocytic leukemia (CLL) is considered to be a nonradiogenic form of cancer. In other words, workers who develop CLL automatically have their compensation claim rejected because the compensation rules hold that the risk of radiation-induced CLL is zero. In this article we review molecular, clinical, and epidemiologic evidence regarding the radiogenicity of CLL. We note that current understanding of radiation-induced tumorigenesis and the etiology of lymphatic neoplasia provides a strong mechanistic basis for expecting that ionizing radiation exposure increases CLL risk. The clinical characteristics of CLL, including prolonged latency and morbidity periods and a low case fatality rate, make it relatively difficult to evaluate associations between ionizing radiation and CLL risk via epidemiologic methods. The epidemiologic evidence of association between external exposure to ionizing radiation and CLL is weak. However, epidemiologic findings are consistent with a hypothesis of elevated CLL mortality risk after a latency and morbidity period that spans several decades. Our findings in this review suggest that there is not a persuasive basis for the conclusion that CLL is a nonradiogenic form of cancer.
Topics: Eligibility Determination; Epidemiologic Studies; Humans; Leukemia, Lymphocytic, Chronic, B-Cell; Leukemia, Radiation-Induced; Morbidity; Nuclear Warfare; Public Policy; Risk Factors; Time Factors; United States; Workers' Compensation
PubMed: 15626639
DOI: 10.1289/ehp.7433 -
Journal of Korean Medical Science Dec 2010The purpose of this study was to review the existing studies on lymphohematopoietic (LHP) cancer in Korea, estimate the prevalence of workers exposed to carcinogens, and... (Review)
Review
The purpose of this study was to review the existing studies on lymphohematopoietic (LHP) cancer in Korea, estimate the prevalence of workers exposed to carcinogens, and determine the population attributable fraction (PAF) of leukemia. Two case series and 4 case reports were reviewed. Using official statistics, the prevalence of benzene exposure and ionizing radiation exposure was estimated. Based on the prevalence of exposure and the relative risk, The PAF of leukemia was calculated. Between 1996 and 2005, 51 cases of LHP cancer were reported from the compensation system. Greater than 50% of occupational LHP cancer was leukemia, and the most important cause was benzene. In a cohort study, the standardized incidence ratio was 2.71 (95% CI, 0.56-7.91). The prevalence of exposure was 2.5% and 2.2% in 1995 and 2000, respectively. Using the 1995 prevalence, 3.6-4.8% and 0.1% of cases with leukemia were attributable to benzene and ionizing radiation exposure, respectively, which resulted in 39.7-51.4 cases per year. Benzene is the most important cause of occupational leukemia in Korea. Considering the estimated PAF in this study, the annual number of occupational LHP cancer (51 cases during 10-yr period), might be underreported within the compensation system.
Topics: Adult; Benzene; Cohort Studies; Female; Humans; Incidence; Leukemia; Leukemia, Radiation-Induced; Male; Middle Aged; Occupational Diseases; Occupational Exposure; Prevalence; Radiation, Ionizing; Republic of Korea; Workers' Compensation
PubMed: 21258598
DOI: 10.3346/jkms.2010.25.S.S99 -
Blood Mar 2001
Topics: Humans; Leukemia, Myeloid, Acute; Radioactive Fallout; Translocation, Genetic
PubMed: 11263441
DOI: 10.1182/blood.v97.6.1897 -
International Journal of Molecular... Apr 2023Although the prevalence of leukemia is increasing, the agents responsible for this increase are not definitely known. While ionizing radiation (IR) was classified as a... (Review)
Review
Although the prevalence of leukemia is increasing, the agents responsible for this increase are not definitely known. While ionizing radiation (IR) was classified as a group one carcinogen by the IARC, the IR-induced cancers, including leukemia, are indistinguishable from those that are caused by other factors, so the risk estimation relies on epidemiological data. Several epidemiological studies on atomic bomb survivors and persons undergoing IR exposure during medical investigations or radiotherapy showed an association between radiation and leukemia. IR is also known to induce chromosomal translocations. Specific chromosomal translocations resulting in preleukemic fusion genes (PFGs) are generally accepted to be the first hit in the onset of many leukemias. Several studies indicated that incidence of PFGs in healthy newborns is up to 100-times higher than childhood leukemia with the same chromosomal aberrations. Because of this fact, it has been suggested that PFGs are not able to induce leukemia alone, but secondary mutations are necessary. PFGs also have to occur in specific cell populations of hematopoetic stem cells with higher leukemogenic potential. In this review, we describe the connection between IR, PFGs, and cancer, focusing on recurrent PFGs where an association with IR has been established.
Topics: Infant, Newborn; Humans; Child; Translocation, Genetic; Neoplasms, Radiation-Induced; Leukemia; Chromosome Aberrations; Radiation, Ionizing
PubMed: 37047553
DOI: 10.3390/ijms24076580 -
Blood Oct 1987Radiation-induced leukemia is considered to be similar to the de novo disease. However, following an analysis of clinical and hematological findings in leukemia...
Radiation-induced leukemia is considered to be similar to the de novo disease. However, following an analysis of clinical and hematological findings in leukemia occurring in irradiated cervical cancer patients, adult Japanese atomic-bomb survivors, and spondylitics treated with x-ray, striking differences were noted. Acute leukemias in cervical cancer patients and Japanese survivors were similar in type to acute de novo leukemias in adults. Cell types among spondylitics were very dissimilar; rare forms, eg, acute erythromyelocytic leukemia (AEL) and acute megakaryocytic leukemia, were increased. Pancytopenia occurred in 25 of 35 cases and erythromyelodysplastic disorders were noted in seven of 35 acute cases. The leukemias and myelodysplastic disorders closely resembled those occurring in patients treated with alkylating agents. This similarity suggests a common pathogenesis involving marrow stem cell injury and extra-medullary mediators of hematopoiesis. Investigation of early acute leukemias and myelodysplastic disorders with newer techniques may provide valuable insights into the pathogenesis of leukemia in humans.
Topics: Adult; Aged; Aged, 80 and over; Female; Humans; Leukemia, Myeloid, Acute; Leukemia, Radiation-Induced; Male; Middle Aged; Myelodysplastic Syndromes
PubMed: 3477299
DOI: No ID Found -
Journal of Radiation Research Dec 1991Parental exposure to radiation could induce various kinds of tumors in the next generation. In ICR mice, a large and significant increase of adult types tumor was... (Review)
Review
Parental exposure to radiation could induce various kinds of tumors in the next generation. In ICR mice, a large and significant increase of adult types tumor was observed in the F1 offspring after X-ray exposure at spermatozoa and spermatid stages, and less clear increase was observed after spermatogonial exposure. Mature oocytes were resistant upto 1 Gy, but very sensitive to tumor induction at higher doses. While there was no difference in the tumor incidence between acute and fractionated (0.36 Gy at 2 hr intervals) irradiation at post-gonial stages, a large reduction of tumor incidence was observed after spermatogonial and mature oocyte exposure, suggesting some repairs of X-ray damages in these germ cells. Acute lymphocytic leukemia was not induced in ICR and LT mice after spermatogonial exposure, while a large increase of adult type cancers was observed in F1 offspring. However, 1.9-3.2 fold and 4.5-7.4 fold increases of leukemia incidence were observed in ICR and LT mice, when spermatozoa stage was treated with the X-ray doses of 0.36-5.04 Gy and 3.6-5.04 Gy, respectively, indicating the large difference in the sensitivity of developing germ cells to leukemia induction by radiation in the F1 offspring. In contrast to ICR and LT mice, N5 strain developed about 10 or 18 times higher incidence of leukemia in the offspring after spermatogonial or spermatozoa exposure to 5.04 Gy of X-rays, respectively, showing a marked difference in the sensitivity to the leukemia induction by radiation between mouse strains.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Animals; Fathers; Female; Leukemia, Radiation-Induced; Male; Mice; Mice, Inbred ICR; Radiation Genetics
PubMed: 1823368
DOI: 10.1269/jrr.32.supplement2_64 -
Stem Cell Reports Jun 2022Receptor-interacting protein kinase 3 (Ripk3) is one of the critical mediators of inflammatory cytokine-stimulated signaling. Here we show that Ripk3 signaling...
Receptor-interacting protein kinase 3 (Ripk3) is one of the critical mediators of inflammatory cytokine-stimulated signaling. Here we show that Ripk3 signaling selectively regulates both the number and the function of hematopoietic stem cells (HSCs) during stress conditions. Ripk3 signaling is not required for normal homeostatic hematopoiesis. However, in response to serial transplantation, inactivation of Ripk3 signaling prevents stress-induced HSC exhaustion and functional HSC attenuation, while in response to fractionated low doses of ionizing radiation (IR), inactivation of Ripk3 signaling accelerates leukemia/lymphoma development. In both situations, Ripk3 signaling is primarily stimulated by tumor necrosis factor-α. Activated Ripk3 signaling promotes the elimination of HSCs during serial transplantation and pre-leukemia stem cells (pre-LSCs) during fractionated IR by inducing Mlkl-dependent necroptosis. Activated Ripk3 signaling also attenuates HSC functioning and represses a pre-LSC-to-LSC transformation by promoting Mlkl-independent senescence. Furthermore, we demonstrate that Ripk3 signaling induces senescence in HSCs and pre-LSCs by attenuating ISR-mediated mitochondrial quality control.
Topics: Animals; Hematopoietic Stem Cells; Leukemia, Radiation-Induced; Mice; Necrosis; Protein Kinases; Receptor-Interacting Protein Serine-Threonine Kinases; Signal Transduction
PubMed: 35561683
DOI: 10.1016/j.stemcr.2022.04.009