The present study sought to investigate whether some of the personality characteristics observed among cancer patients in the American and International literature are outcomes of cancer, or whether they, in themselves, constitute factors that may be contributing to cancer development.Twenty-five pre-biopsy subjects who were later diagnosed as having benign tumors (Benign Unaware) and twenty pre-biopsy subjects who were later diagnosed as having malignant tumors (Cancer Unaware) were administered the Eysenck Personality Inventory (EPI) and the Fundamental Interpersonal Relationships Orientation-Behavior (FIRO-B). A third group of subjects with already diagnosed malignant tumors who had been informed of their condition (Cancer Aware) were also administered the same instruments.A multivariate analysis of variance revealed that subjects comprising the Cancer Unaware group scored significantly lower (p.4.001) on the Neuroticism Scale of the EPI than both the Benign Unaware and Cancer Aware groups.The subjects comprising the Cancer Aware group scored significantly lower (P4-05) than both the Benign Unaware and the Cancer Unaware groups on the Control Expressed Scale of the FIRO-B.The observed differences obtained by both instruments did not appear to be affected by either the sex or the age of the subjects.On the basis of these data, conclusions were drawn and speculations were made concerning the utilization of psychological interventions in the prevention and treatment of cancer.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 5 uppsatser.

Thesis (Ph. D.)--Illinois State University, 1981. / Title from title page screen, viewed March 29, 2005. Dissertation Committee: A. Richardson (chair), H. Brockman, F. Schwalm, M. Nadakavukaren, A. Katz. Includes bibliographical references (leaves 138-153) and abstract. Also available in print.

Thesis (M.Sc.) -- Memorial University of Newfoundland, 1984. / Bibliography : leaves 139-147. Also available online.

Thesis (Ph. D.)--West Virginia University, 2009. / Title from document title page. Document formatted into pages; contains xiv, 301 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 193-213).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1969. / Typescript. Vita. Includes bibliographical references.

Restriction enzyme inhibition and lambda exonuclease studies indicate that carcinogen N-acetoxy-N-acetyl-2 aminofluorene (AAAF) binds to sequences on ɸX174 RF and SV40 plasmids DNA that are similar to the eight preferred binding sites previously located on pBR 322. Both DNAs were digested with enzyme Hinf I and resultant fragments 32P end-labeled. Labeled fragments were reacted with the carcinogen to give one to sixteen bound moieties per DNA. Fragments were isolated and restriccion enzyme and lambda exonuclease inhibition assays were performed. Inhibition detected occurred at selected sites and was not specific for a certain enzyme or certain size of recognition sequence. Results of these assays allow mapping of the location of high affinity binding sites of the carcinogen on both DNAs. All sites have common sequence elements: the presence of either the sequence T(G/C)TT(G/C) or the sequence T(G/C) CTT(G/C).

An attempt has been made to demonstrate an association between the carcinogenic activity of a chemical compound and its capacity to induce DNA damage and chromosome aberrations which may result in mutations and/or neoplastic transformation. Twenty-five 4-nitroquinoline 1-oxide (4NQO) derivatives and five related compounds of 4-nitropyridine 1-oxide (4NPO) of varying carcinogenicity were examined. [Formulae omitted] The induction of DNA damage, chromosome aberrations and clone forming capacity were used as end points. Monolayer cultures of embryonal Syrian-hamster cells and an established line of baby hamster kidney cells (BHK-21) were employed in this study. DNA damage, as measured by the unscheduled incorporation of tritiated thymidine (³H-TdR), was assayed by the autoradiographic procedure. To distinguish DNA repair synthesis from DNA replication synthesis at S-phase, cultured embryonal hamster cells were arrested at G₁ by growing them in an arginine deficient medium (ADM) prior to the application of the various carcinogens. The unscheduled uptake of radioisotope was estimated by counting the number of grains per diploid nucleus of carcinogen treated cells. The highly oncogenic derivatives of 4NQO and 4NPO elicited an elevated level of unscheduled ³H-TdR incorporation in treated cells, while the weakly oncogenic compounds induced only a smaller amount of DNA repair synthesis. The non-oncogenic N-oxides failed to provoke any detectable ³H-TdR uptake. Chromosome aberrations were studied in ADM-arrested cells which were exposed to the various compounds and then triggered into division by transferring them into the regular growth medium. A direct proportionality was observed between the degree of carcinogenicity of a compound and the frequency of induced chromosome aberrations. The clone forming ability of treated cells was employed as a means to compare the cytotoxicity of the 4NQO and 4NPO derivatives. Potent carcinogens were highly cytotoxic; weakly carcinogenic compounds showed only a slight lethal effect and non-oncogenic derivatives did not affect cell survival. This study demonstrated the capacity of carcinogens to induce alterations at the chromosome and DNA level. The possible role of DNA repair and chromosome aberrations in neoplastic transformation was discussed. The use of DNA repair synthes as an economic and relevant tool for identifying mutagens and/or carcinogens has been suggested. / Medicine, Faculty of / Medical Genetics, Department of / Graduate

Yes / Objective: The increasing prevalence of malignant disease has been associated with shifts in environmental, socioeconomic, and lifestyle risk factors as well as increased adult lifespan. We examine the relationship between malignant neoplasms affecting bone, age and industrialization. Materials: Pre-existing skeletal data from 11 medieval (1066-1547, n=8,973) and 14 industrial (1700-1890, n=4,748) cemeteries (N=13,721) from England. Methods: Context number, sex, age-at-death, evidence of skeletal malignancy, and diagnosis were collated. The data were compared using chi square, Kolmogorov-Smirnov tests and logistic regression (α=0.01). Results: There was a statistically significant increase in skeletal malignancy from 0.06% in the medieval sample to 0.36) in the industrial sample (p< 0.001). Age had a strong relationship with malignancy (p = 0.003), sex did not (p = 0.464). Logistic regression revealed that time-period (p < 0.001) was a stronger predictor of skeletal malignancy than age-at-death (p = 0.002). Conclusion: Our results confirm that even with the temporal increase in adult human lifespan the increase of malignant neoplasms of bone between the medieval and industrial time periods is still statistically significant. Significance: The augmented exposure to carcinogens and pollution during the Industrial Revolution had a strong effect on an individual’s susceptibility to developing malignant disease of bone. Limitations: This meta-analysis relies upon previously gathered data and diagnosis from a large number of researchers and did not include radiographic or CT screening. Only malignant neoplasms that affected bone could be included. Suggestions for further research: Increasing excavation and analysis of post-medieval cemeteries will provide more data. Multimethod approaches (radiography, CT, Micro-CT and histology) are encouraged.