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1/25. The risks of treating keloids with radiotherapy.

    The risk of carcinogenesis from radiation exposure is well known. It has been questioned for some time therefore, whether it is wise to treat benign disease with radiotherapy. We report a case of a patient who developed bilateral breast carcinomas almost 30 years after treatment of chest wall keloids with radiotherapy. There are only anecdotal reports in the literature of malignancies following treatment of keloids with radiotherapy. We review these reports and discuss the safety of this approach to the management of keloid scars.
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ranking = 1
keywords = carcinogenesis
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2/25. Colorectal adenocarcinoma as a second malignant neoplasm following rhabdomyosarcoma of the urinary bladder: a case report.

    Following improvements in therapy for childhood malignancies, the striking increase in survival rate over the past 30 years has led to the increase risk of developing second malignant neoplasms (SMNs). We report a case of colorectal carcinoma as a SMN, following treatment for rhabdomyosarcoma. The patient was diagnosed with rhabdomyosarcoma of the urinary bladder at his age of three years, and developed adenocarcinoma in the colon 13 years later. Histologic examination of the surgical specimen revealed adenocarcinoma involving the rectosigmoid area with radiation colitis in its background. The tumor cells showed strong immunoreactivity for p53 protein, suggesting the role of irradiation and p53 mutation in carcinogenesis. This case emphasizes the need for dose observation in survivors of early childhood malignancies treated with radiation and multiagent chemotherapy.
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ranking = 1
keywords = carcinogenesis
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3/25. radiation-induced esophageal squamous cell carcinoma in situ.

    A report of radiation-induced squamous cell carcinoma in situ of the esophagus is presented. This report indicates that the patient developed the carcinoma in situ many years after chest wall irradiation for breast cancer treatment. A review of the literature with respect to carcinogenesis after radiotherapy is included and recommendations for the follow-up of patients having mediastinal radiation are suggested.
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ranking = 1
keywords = carcinogenesis
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4/25. osteosarcoma following retinoblastoma: age at onset and latency period.

    In order to assess the role of genetic predisposition in the induction of radiation-induced tumors, we performed statistical analysis on data from the literature and from our own Institute with regard to the age at onset and the latency period of osteosarcoma as the second primary tumor for retinoblastoma with or without subsequent radiotherapy. In retinoblastoma survivors who subsequently developed osteosarcoma, the age at onset of retinoblastoma was young (average of 12 months) in both unilateral and bilateral forms. This suggests that all or almost all of the patients were genetically predisposed by a mutation of one allele of the RB1 gene. For retinoblastoma patients, osteosarcomas occurred 1.2 years earlier inside than outside the radiation field. The latency period between radiotherapy and osteosarcoma onset was 1.3 years shorter inside than outside the radiation field. Interestingly, a bimodal distribution of latency periods was observed for osteosarcomas arising inside, but not outside the radiation field: 40% occurred after a short latency, while the latency of the remaining 60% was comparable to that of osteosarcoma occurring outside the radiation field. This suggests that different mechanisms may be involved in radiocarcinogenesis. A radiation-induced mutation of the second RB1 allele may be the cause of osteosarcomas occurring after a short delay, while other genes may be affected in those occurring after a longer delay.
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ranking = 1
keywords = carcinogenesis
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5/25. Two metachronous tumors in the radiotherapy fields of a patient with Li-Fraumeni syndrome.

    A woman with a family history of brain tumors in her daughter and sister presented with a breast cancer. She subsequently developed two metachronous primary tumors: a small-cell lung cancer and a colon carcinoma. These tumors arose within the internal mammary radiotherapy field and within the field irradiated for ovariolysis. The p53 gene was analyzed in whole blood lymphocytes using a functional assay developed in yeast saccharomyces cerevisiae, which tests the transcriptional competence of p53. dna from the colon cancer cells was analyzed by polymerase chain reaction and sequencing. The patient had a germline-inactivating p53 mutation, confirming the diagnosis of li-fraumeni syndrome (LFS). The colon tumor and the lung tumor both conserved the mutant p53 allele but had lost the wild-type allele. This observation and the experimental data suggest an abnormal sensitivity of LFS patients to radiogenic carcinogenesis. The indications and extent of radiotherapy in patients with a clinical or molecular diagnosis of LFS should be discussed individually and should take into account the risk of secondary neoplasms arising in the radiation fields.
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ranking = 1
keywords = carcinogenesis
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6/25. Postradiation prostatic sarcoma: de novo carcinogenesis or dedifferentiation of prostatic adenocarcinoma?

    Postradiation sarcoma (PRS) of the prostate is rare. We describe the second case associated with brachytherapy for adenocarcinoma and review the literature on prior cases of PRS as well as carcinosarcoma, a dedifferentiated form ofadenocarcinoma that may be confused with true prostate sarcoma. It is clear that radiation to the prostate confers a significantly increased risk for subsequent sarcoma, although not within the prostate. Because many of the reported cases of PRS were admixed with adenocarcinoma and had relatively short latency periods, we conclude that these cases of PRS ofthe prostate are, in fact, carcinosarcoma. Therefore, with only one case reported following therapeutic irradiation, PRS of the prostate is extremely rare.
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ranking = 4
keywords = carcinogenesis
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7/25. radiation-induced cancers of the pharynx and larynx: a study of five clinical cases.

    radiation-induced cancer, a rare clinical entity, is often difficult to diagnose and manage. This study reports a series of five cases of radiocarcinogenesis of the pharynx and/or larynx that developed after external radiotherapy. The primary lesion was diagnosed at a mean age of 50 years ( /-12.9) and the radiation-induced cancer at a mean age of 59 years ( /-13.1), giving a latent period of 9 years ( /-3.7). Analysis of gammagraphic records indicated that four of the patients had developed a secondary tumour in the penumbra of irradiation fields. In these zones, the delivered dose was between 20 and 80% of the prescribed dose, corresponding to an estimated cumulative mean dose of 14.1-56.3 Gy. These results are compared with data in the literature to determine the diagnostic criteria for radiation-induced cancer, possible predisposition (genetic or acquired) and the dose effect.
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ranking = 1
keywords = carcinogenesis
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8/25. radiation carcinogenesis.

    Accidental or therapeutic exposure to radiation may induce tumors of various histologic types in human beings as well as in animals. Two tumors in this report arose in the organs which had been included in the field of radiation 32 and 8 years before, respectively. The author briefly reviews the literature, which abounds with references to radiation carcinogenesis.
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ranking = 5
keywords = carcinogenesis
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9/25. Genetic analysis of radiation-associated rectal cancer.

    Genetic aberrations in radiation-associated colorectal cancer have not been studied in detail. We analyzed genetic aberrations in five rectal cancers that developed long after radiotherapy had been performed for cervical cancer. microsatellite instability (MSI) in tumors was examined at five loci: D2S123, D3S966, TP53, DCC, and BAT26. mutation of simple repeat sequences within the hMSH3, BAX, and transforming growth factor beta type II receptor ( TGFBetaRII) genes was examined by polymerase chain reaction and single-strand conformation polymorphism (PCR-SSCP). mutation of p53 exons 5-8 was examined by PCR-SSP and direct sequencing. Mutations of the K- ras gene were analyzed by two-step PCR. No MSI was found in tumor specimens at any of the loci examined, and no mutations in the target genes were observed. K- ras mutation was detected in two carcinomas, but not in their irradiated normal mucosa, while p53 mutation was observed in another two carcinomas, but not in their irradiated normal mucosa. Our results suggest that the radiation-associated rectal carcinomas examined in this study did not develop through the mutator phenotype pathway; rather, tumorigenesis was probably mediated through the multistep carcinogenesis pathway.
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ranking = 1
keywords = carcinogenesis
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10/25. Calculated risk of breast cancer following mantle irradiation determined by measured dose.

    Tumor registry data indicate a two- to fourfold increased incidence of breast cancer following mantle irradiation, but cumulative risk is unknown. radiation exposure to the breasts underlying the mantle block ranges from 4 to 40 Gy and is dependent on relative positions of the breasts and mantle block. Unshielded outer breast quadrants near axillary nodal regions receive 36 to 40 Gy, while central breast quadrants under the lung blocks receive approximately 4 Gy as determined by dose volume histogram analysis. Relative dose risk analysis for breast cancer following mantle irradiation was performed and indicated an overall excess risk of 1.5 for the upper outer quadrant (total dose 40 Gy), 1.3 for the upper and lower inner, and central quadrants (total dose 15 to 20 Gy), and 1.2 for the lower outer quadrant (total dose 4 Gy). Linear and cell-kill carcinogenesis models demonstrated similar relative risk assessments in the low-dose regions, defined as < 15 Gy. Predicted risk for breast cancer in the high-dose regions (> or = 15 Gy) varied considerably according to the model evaluated. The linear model predicted a three to ten times greater risk above baseline breast cancer incidence for the high-dose regions. In contrast, the cell-kill model predicted no excess cases of breast cancer, assuming cell death at these higher dose levels. The greatest relative predicted risk is observed in women < 20 years of age at the time of irradiation; however, women older than 20 years continue to have a 50% higher than baseline risk for subsequent breast cancer development. All women treated for Hodgkin's lymphoma should undergo dose volume histogram evaluation. Prospective clinical and mammographic evaluations should be performed in all female patients following mantle irradiation to better define the risk for secondary breast carcinogenesis.
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ranking = 2
keywords = carcinogenesis
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