Genome Damage in Oropharyngeal Cancer Patients Treated by Radiotherapy

Gamulin, Marija; Kopjar, Nevenka; Grgić, Mislav; Ramić, Snježana; Bišof, Vesna; Garaj‐Vrhovac, Vera

doi:10.3325/cmj.2008.4.515

Cited by 18 publications

(27 citation statements)

References 38 publications

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“…On this, data in the literature are inconclusive. Whereas some authors observed that induced damage with chemotherapy or radiotherapy returned to pretreatment values in a short term (27,28), other reports show the persistence of the injury in the lymphocytes (28,29). Very few publications show long followup periods.…”

Section: Discussionmentioning

confidence: 97%

Differential Genetic and Functional Markers of Second Neoplasias in Hodgkin's Disease Patients

Lorenzo

Provencio

Lombardía

et al. 2009

Clinical Cancer Research

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Purpose: The mechanisms involved in the appearance of a second neoplasia in patients with Hodgkin's disease (HD) are probably related to the genomic damage induced by the treatments administered and its repair. Here, we searched for some constitutive molecular mechanisms that in a basal manner may influence the behavior of HD patients. Experimental Design: We aimed to evaluate with the Comet Assay whether baseline, induced, and unrepaired DNA damage differ between HD patients who did not develop a second neoplasia (HD-NST), HD patients who developed a second tumor (HD-ST), and healthy individuals; and to identify, through cDNA microarray hybridization, an expression signature of genes that could discriminate between the three groups. Results: Baseline, induced, and unrepaired DNA damage was higher in HD-ST than in HD-NST and higher in the second group than in healthy donors. The genomic approach revealed two sets of genes that discriminated between healthy subjects and patients and between the three sets of individuals. Hsp40, RAD50, TPMT, Rap2a, E2F2, EPHX2, TBX21, and BATF were validated by reverse transcription-PCR. Conclusions: Functional and genomic techniques revealed that alterations in cell cycle, repair, detoxification, and stress response pathways could be involved in the development of HD and in the occurrence of a primary second neoplasia in these patients. Both approaches may be useful as biological markers in the clinical setting.

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Section: Discussionmentioning

confidence: 97%

Differential Genetic and Functional Markers of Second Neoplasias in Hodgkin's Disease Patients

Lorenzo

Provencio

Lombardía

et al. 2009

Clinical Cancer Research

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“…It is suggested that genetic instability, which takes the form of delayed reproductive death (DRD), can participate in late side effects in patients treated with radiotherapy, because of damage, increased cell loss and longer recovery (Hendry, 2001). Increased level of chromosome aberrations and micronuclei was detected in the head and neck cancer patients undergoing radiotherapy within a year post treatment (Gamulin et al, 2008). DRD phenomenon associated with the presence of an increased percentage of stable and unstable chromosome aberrations in lymphocytes was detected in patients irradiated because of ankylosing spondylitis even several years after radiotherapy.…”

Section: The Potential Clinical Consequences Of Radiation Induced Bysmentioning

confidence: 97%

Intercellular Communication in Response to Radiation Induced Stress: Bystander Effects in Vitro and in Vivo and Their Possible Clinical Implications

Wideł¹

2011

Radioisotopes - Applications in Physical Sciences

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“…Peripheral human lymphocytes, which were proved to be sensitive to IR and previously established as suitable markers, demonstrate a DNA damage response following the exposure to IR . Real‐time PCR analysis showed that GRP78, ATG5, LC3, ATF4,XBP1, and GADD153 genes expression were elevated with increasing dose in the samples of radiotherapy patients, which are detailed graphically in Figure .…”

Section: Resultsmentioning

confidence: 89%

Assessment of ER Stress and Autophagy Induced by Ionizing Radiation in Both Radiotherapy Patients and Ex Vivo Irradiated Samples

Saglar

Ünlü

Babalıoglu

et al. 2014

J Biochem & Molecular Tox

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Acute radiation leads to several toxic clinical states and triggers some molecular pathways. To shed light on molecular mechanisms triggered by ionizing radiation (IR), we examined the expression profiles of endoplasmic reticulum (ER) stress and autophagy-related genes in individuals who were exposed to IR. Blood samples were collected from 50 cancer patients before radiotherapy and on the 5th, 15th, and 25th days of the treatment. Peripheral blood samples from 10 healthy volunteers were also obtained for ex vivo irradiation, divided into five and irradiated at a rate of 373 kGy/h to 0, 0.1, 0.5, 1, and 3Gy γ-rays using a constant gamma source. GRP78, ATG5, LC3, ATF4, XBP1, and GADD153 genes were analyzed by quantitative real-time polymerase chain reaction (QRT-PCR) using beta 2 microglobulin (B2M) and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as references. In both groups, expressions of the selected genes have increased. It can be concluded that IR induces ER stress and related authophagy pathway in the peripheral lymphocyte cells proportionally by dose.

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Genome Damage in Oropharyngeal Cancer Patients Treated by Radiotherapy

Cited by 18 publications

References 38 publications

Differential Genetic and Functional Markers of Second Neoplasias in Hodgkin's Disease Patients

Differential Genetic and Functional Markers of Second Neoplasias in Hodgkin's Disease Patients

Intercellular Communication in Response to Radiation Induced Stress: Bystander Effects in Vitro and in Vivo and Their Possible Clinical Implications

Assessment of ER Stress and Autophagy Induced by Ionizing Radiation in Both Radiotherapy Patients and Ex Vivo Irradiated Samples

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