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PubMed1998

Impact of adduct determination on the assessment of cancer susceptibility.

The characterization of genetic determinants for cancer susceptibility is important for understanding disease pathogenesis and for preventive measures. There is growing evidence that a group of predisposing polymorphic genes exists, such as those involved in carcinogen metabolism and repair, which may increase cancer in certain environmentally exposed subjects, even those exposed only to low levels of carcinogens. In developing preventive strategies, it is therefore necessary to identify these vulnerable members in our society, particularly those suffering from an unfortunate combination of high carcinogen exposure, cancer-predisposing genes and lack of protective (dietary) factors. Thus, molecular epidemiology faces the difficult task of analyzing carcinogen-exposed individuals for a combination of genotypes associated with cancer susceptibility. Once identified, combinations of cancer-predisposing genes can then be used as intermediate risk markers rather than taking cancer as an endpoint. In case-control studies, simultaneous measurements were carried out in each subject to determine exposure/early effect markers, e.g. polycyclic aromatic hydrocarbons (PAH)-DNA adducts, and susceptibility markers, e.g. genetic polymorphism, in drug-metabolizing enzymes related to cytochrome P450 1A1 (CYP1A1) and glutathione S-transferase (GSTM1) genes. The genotype dependence of human lung (+)-anti-benzo[a]pyrene diol-epoxide (BPDE)-DNA adducts in lung cancer patients was examined. BPDE-DNA adduct levels in bronchial tissue of smokers with high pulmonary CYP1A1 inducibility (by immunohistochemistry) and GSTM1 inactive were approximately 100-fold higher than in subjects with an active GSTM1 at similar smoking dose. Further genetic analyses confirmed that the combination of CYP1A1 homozygous mutants and GSTM1 inactive leads to high levels of BPDE-DNA adducts in human lung of smokers and white blood cells of PAH-exposed coke oven workers. Thus, BPDE-DNA adduct levels resulting from the "at risk" genotype combinations may serve as markers to identify high-risk subjects among smokers and individuals occupationally and/or environmentally exposed to PAH.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed2006

Heart failure induced by non-cardiac drugs.

Although heart failure is predominantly caused by cardiovascular conditions such as hypertension, coronary heart disease and valvular heart disease, it can also be an adverse reaction induced by drug therapy. In addition, some drugs have the propensity to adversely affect haemodynamic mechanisms in patients with an already existing heart condition. In this article, non-cardiac drugs known to be associated with the development or worsening of heart failure are reviewed. Moreover, drugs that may adversely affect the heart as a pump without causing symptoms or signs of heart failure are also included. The drugs discussed include anticancer agents such as anthracyclines, mitoxantrone, cyclophosphamide, fluorouracil, capecitabine and trastuzumab; immunomodulating drugs such as interferon-alpha-2, interleukin-2, infliximab and etanercept; antidiabetic drugs such as rosiglitazone, pioglitazone and troglitazone; antimigraine drugs such as ergotamine and methysergide; appetite suppressants such as fenfulramine, dexfenfluramine and phentermine; tricyclic antidepressants; antipsychotic drugs such as clozapine; antiparkinsonian drugs such as pergolide and cabergoline; glucocorticoids; and antifungal drugs such as itraconazole and amphotericin B. NSAIDs, including selective cyclo-oxygenase (COX)-2 inhibitors, are included as a result of their ability to cause heart disease, particularly in patients with an already existing cardiorenal dysfunction. Two drug groups are of particular concern. Anthracyclines and their derivatives may cause cardiomyopathy in a disturbingly high number of exposed individuals, who may develop symptoms of insidious onset several years after drug therapy. The risk seems to encompass all exposed individuals, but data suggest that children are particularly vulnerable. Thus, a high degree of awareness towards this particular problem is warranted in cancer survivors subjected to anthracycline-based chemotherapy. A second group of problematic drugs are the NSAIDs, including the selective COX-2 inhibitors. These drugs may cause renal dysfunction and elevated blood pressure, which in turn may precipitate heart failure in vulnerable individuals. Although NSAID-related cardiotoxicity is relatively rare and most commonly seen in elderly individuals with concomitant disease, the widespread long-term use of these drugs in risk groups is potentially hazardous. Pending comprehensive safety analyses, the use of NSAIDs in high-risk patients should be discouraged. In addition, there is an urgent need to resolve the safety issues related to the use of COX-2 inhibitors. As numerous drugs from various drug classes may precipitate or worsen heart failure, a detailed history of drug exposure in patients with signs or symptoms of heart failure is mandatory.

Clinical Trials as Topic↗
PubMed2002

Apoptosis of immune cells in the tumor microenvironment and peripheral circulation of patients with cancer: implications for immunotherapy.

Rapid turnover of lymphocytes observed in patients with cancer appears to be driven by increased apoptosis of T lymphocytes or insufficient thymic output of recent thymic emigrants (RTE). Using multicolor flow cytometry and apoptosis assays, we found that CD8+CD95+Annexin+ T cells are dying at a rate that is significantly higher in patients with cancer than in normal controls (NC). CD8+ effector subsets of T cells were particularly vulnerable to apoptosis. Thymic excision circle (TREC) analysis of peripheral blood lymphocytes showed a decreased number of RTE in these patients. Together, the data suggest that a high rate of T-cell turnover might contribute to immunologic imbalance in patients with cancer and have unfavorable effects on immunotherapy, including therapeutic antitumor vaccines.

Apoptosis↗
PubMed1985

Coping with cancer: psychological dimensions.

Cancer has a profound psychological impact upon the patient and his family, and the psychological responses, primarily of the patient himself, the close family, physician and nursing personnel, but also of the extended family, and society in general, become a complex interrelationship. Some of the most important psychological aspects of cancer are reviewed. These include the psychological responses of the patient, such as denial, vulnerability, coping strategies, hope, depression, suicide, reaction to diagnosis, and the management of the family, and the psychological responses and attitudes of the physician and nursing personnel. Based on the above psychological analysis some guidelines are offered to help in coping with cancer.

Adaptation, Psychological↗
PubMed1992

A model for predicting the risk of cancer consequent to retroviral gene therapy.

Theoretical estimates of the risk of cancer resulting from accidental insertion of retroviral gene therapy vectors into oncogenically vulnerable genomic sites may prove an important supplement to experimentally derived data in estimating risk/benefit ratios for future gene therapy trials. We have approached risk assessment by considering either a single vector insertion event or a single natural mutation to be potentially oncogenic, should either occur in a cell that would otherwise end with one less than the total number of mutations required for frank neoplasia. Estimates of the relative probabilities of these two phenomena yield a relative risk assessment, which in conjunction with epidemiologic data on natural cancer frequencies can be converted into an assessment of absolute risk. This approach yields an estimated range of relative risk over 10 years of about 1.00000026 to 25 for cells bearing single copies of inserted vectors; the upper limit is higher for multiple copies. These estimates, if accurate, imply that small experimental human or animal gene therapy cohorts will rarely, if ever, manifest vector-related cancers and that more precise future risk assessments will require additional data on natural and vector-induced mutation rates.

Animals↗
PubMed2026

A machine learning-derived and functionally validated circadian rhythm signature predicts clinical outcomes and in silico drug sensitivity in colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) displays considerable heterogeneity in clinical outcomes, highlighting the need for reliable prognostic biomarkers. While the aberrant expression of circadian rhythm-related genes has been implicated in cancer pathogenesis, its comprehensive role in CRC progression and predicted therapeutic vulnerabilities remains inadequately characterized. METHODS: Bulk and single-cell RNA-sequencing data were integrated from multiple CRC cohorts. A circadian rhythm signature (CRS) was developed through machine learning algorithms and validated for prognostic value. Comprehensive analyses of tumor microenvironment, genomic alterations, and drug sensitivity were performed. Furthermore, the biological function of the core gene, BHLHE40, was validated in CRC cell lines through CCK-8, EdU, and wound healing assays. RESULTS: Single-cell analysis demonstrated an elevated expression signature of circadian rhythm-related genes in dendritic cells. The optimized CRS, comprising 14 circadian rhythm-related genes, successfully categorized patients into high- and low-risk groups. Patients with a high CRS showed markedly poorer overall survival and computationally inferred immunosuppressive features, including reduced CD8+ T cell infiltration and increased M2 macrophage polarization. Genomic analysis revealed enhanced mutation burden in TP53 and alterations in RTK-RAS/WNT pathways. Notably, in vitro assays confirmed that BHLHE40 is significantly overexpressed in CRC cells. Knockdown of BHLHE40 markedly inhibited tumor cell proliferation and migration. Drug sensitivity profiling identified bexarotene and SMER-3 as potential therapeutic options for high-CRS patients. A nomogram integrating CRS with clinical parameters demonstrated superior predictive accuracy for 1-, 3-, and 5-year survival. CONCLUSIONS: The CRS represents a promising prognostic biomarker that reflects tumor immune status and genomic features, providing valuable insights for personalized treatment strategies in CRC.

Circadian rhythm↗
PubMed1988

Cancer development and its natural history. A cancer prevention perspective.

In the design of new approaches to cancer prevention, it is important to realize that most cancers develop stepwise over a long period of time with nonmalignant precursor lesions that only slowly evolve toward cancer. With many chemicals and some radiations, as well as some viruses (DNA and some retroviruses), cancer development can be divided into 3 major stages or periods, initiation, promotion and progression. Initiation is frequently associated with a more or less permanent change in the phenotype of a rare target cell, presumably due to a change in base composition in DNA or to gene rearrangements. During promotion, these rare cells expand by proliferation to generate focal proliferations that resemble benign neoplasms. These in turn exercise at least one of two options, regression to normal appearing tissue or slow evolution to cancer. Progression is self generating but can be modulated by dietary manipulations or by other drugs or xenobiotics. The prolonged nature of the promotion-progression stages in most tissues and its modulatability indicate that these stages are vulnerable sites for the development of dietary and other ways to prevent the progression to cancer. This overall pattern is known to occur in the liver, skin and urinary bladder and is probable in several other tissues or organs including the colon, breast and pancreas. What we know about the human suggests that the patterns may be very similar for cancer development in many sites. The best worked out is melanoma. The phenotypic pattern of the precursor lesions in the experimental animals is remarkably similar in any single organ. For example, the hepatocyte nodules are very similar to each other with many different carcinogens and promoting environments even though the ultimate cancers are quite heterogeneous and diverse. The diversity and heterogeneity appears to be an acquisition that is quite late in the step-by-step development of cancer. Although its exact step has not been delineated as yet, it appears to be acquired as malignancy is. Unlike the cancers, the commonality or homogeneity in the precursor lesions offers many opportunities for interrupting the process and thus in preventing cancer. The experience to date in experimental systems with some hormones, drugs and dietary manipulations indicates that inhibition of the development of cancer may be most readily achieved by affecting the promotion and progression sequences in carcinogenesis.

Humans↗
PubMed1998

Case-control study of the D2 dopamine receptor gene and smoking status in lung cancer patients.

BACKGROUND: Interindividual differences in the structure and expression of the dopamine receptor genes affect dopamine availability and may be the genetic basis for variation in vulnerability to tobacco smoking. In this study, prevalences of polymorphisms in the TaqIA allele (A1 and A2) and the TaqIB allele (B1 and B2) of the D2 dopamine receptor gene in 157 lung cancer case patients and 126 control subjects were determined to assess whether individuals homozygous or heterozygous for the less common A1 and B1 alleles are more vulnerable to nicotine addiction. METHODS: Case and control subjects were accrued from an ongoing epidemiologic study. Blood samples were collected from them and subjected to molecular genetic analyses. Subjects were interviewed to obtain relevant information. Current and former smokers were administered a questionnaire to quantify their addiction to nicotine. RESULTS: The combined B1B2 genotypes appeared to be more prevalent in ever smokers than in never smokers among case patients (30.3% versus 13.3%; two-sided P = .233) and among control subjects (30.9% and 0%; two-sided P = .02); statistically significant differences were not observed among those with A1 genotypes. Statistically significant correlations between the presence of the A1 and B1 alleles were observed (r = .73 for case subjects and r = .76 for control subjects; two-sided P<.001). Individuals with rarer genotypes reported having been substantially younger at the time of smoking initiation (statistically significant for both A1 and B1) and having attempted to quit smoking fewer times (statistically significant for only A1). CONCLUSION: Variant alleles of the D2 dopamine receptor gene may play a role in determining nicotine addiction, although the associations between the at-risk genotypes and measures of nicotine addiction were not entirely consistent.

Aged↗
PubMed1999

Impact of therapeutic research on informed consent and the ethics of clinical trials: a medical oncology perspective.

PURPOSE: To create a more meaningful understanding of the informed consent process as it has come to be practiced and regulated in clinical trials, this discussion uses the experience gained from the conduct of therapeutic research that involves cancer patients. DESIGN: After an introduction of the ethical tenets of the consent process in clinical research that involves potentially vulnerable patients as research subjects, background that details the use of written consent documents and of the term "informed consent" is provided. Studies from the cancer setting that examine the inadequacies of written consent documents, and the outcome of the consent process itself, are reviewed. Two ethically challenging areas of cancer clinical research, the phase I trial and the randomized controlled trial, are discussed briefly as a means of highlighting many dilemmas present in clinical trials. Before concluding, areas for future research are discussed. RESULTS: Through an exclusive cancer research perspective, many current deficiencies in the informed consent process for therapeutic clinical trials can be critically examined. Also, new directions for improvements and areas of further research can be outlined and discussed objectively. The goals of such improvements and research should be prevention of further misguided or ineffective efforts to regulate the informed consent process. CONCLUSION: To ignore this rich and interesting perspective potentially contributes to continued misunderstanding and apathy toward fulfilling the regulatory and ethically obligatory requirements involved in an essential communication process between a clinician-investigator and a potentially vulnerable patient who is considering clinical trial participation.

Clinical Trials as Topic↗
PubMed2004

Improving the selectivity of cancer treatments by interfering with cell response pathways.

The cellular response to the stress induced by treatment with anticancer agents is a key determinant of drug activity. A pivotal role in this response is played by checkpoint proteins that control the normal passage of cells through the cell cycle. There is evidence that cancer cells often have defects in one checkpoint control that makes them more vulnerable to inhibition of a second checkpoint, thereby enhancing the overall response to treatment. The G1 and G2 checkpoints are particularly crucial for the decision of a cell to arrest in the cell cycle after damage. The checkpoints are used to try to allow the repair of any damage, or to activate the apoptotic (programmed cell death) machinery. Inhibition of both G1 and G2 checkpoints in cancer cells is therefore likely to result in an induction of the death response in cancer cells. Similarly, an increasing knowledge of the molecular mechanisms that form the basis of apoptotic pathways has helped to define why cancer cells have a reduced propensity to undergo apoptosis following the activation of apoptotic inhibitory pathways or the inhibition of pro-apoptotic pathways. Therefore, the possibility to modulate these pathways is likely to result not only in the increased activity of anticancer agents, but also in an increase in their specificity.

Antineoplastic Agents↗
PubMed2006

Quality of life of husbands of women with breast cancer.

The life-threatening nature of breast cancer, along with the side effects of treatment, place great strain on patients and their families. Husbands may be especially vulnerable as the main source of support to patients. The present study compared the quality of life (QOL) of husbands of patients with breast cancer (HBC; n=79) to spouses of healthy wives (n=79). Additionally, associations between QOL and caregiver burden, social support, and coping were examined. HBC scored lower on general health, vitality, role-emotional, and mental health subscales of the Medical Outcomes Study (MOS) SF-36 than comparison group participants. No differences were found between groups on the physical functioning, role-physical, bodily pain, or social functioning subscales. Higher QOL in HBC was associated with less caregiver burden as evidenced by lower burden on the Illness Impact Form, lower use of emotion-focused coping on the Ways of Coping Questionnaire, and higher social support on the Interpersonal Support Evaluation List. Wife illness characteristics such as stage of disease and time since diagnosis were not related to QOL in husbands. These findings illuminate the need to support HBC, whose QOL suffers during the breast cancer experience.

Adaptation, Psychological↗
PubMed2004

Self-concept in adult survivors of childhood acute lymphoblastic leukemia: a cooperative Children's Cancer Group and National Institutes of Health study.

BACKGROUND: Self-concept was compared between adult survivors of childhood acute lymphoblastic leukemia (ALL) and sibling controls. Adult survivor subgroups at greatest risk for negative self-concept were identified. PROCEDURE: Survivors (n = 578) aged > or =18 years, treated before age 20 years on Children's Cancer Group (CCG) ALL protocols, and 396 sibling controls completed a telephone interview and the Harter Adult Self-Perception Profile (ASPP). RESULTS: Survivors global self-worth scores were significantly lower than sibling controls (mean 3.09 vs. 3.18; P = 0.022). Unemployed survivors reported lower global self-worth scores than employed (mean 2.77 vs. 3.12; P = 0.0001), whereas employment status was not associated with self-worth in controls. Among survivors, predictors of negative self-concept included unemployment (odds ratio (OR) = 2.87; 95% CI: 1.50-5.50), and believing that cancer treatment limited employability (OR = 3.17; 95% CI: 1.79-5.62). Unemployment increased the odds for negative self-concept among survivors who received combinations of central nervous system (CNS) irradiation (CRT) and intrathecal methotrexate (IT-MTX), except high CRT with no or low dose IT-MTX. Employed survivors who perceived that treatment limited their employability showed increased odds of negative self-concept for all treatment groups compared to those who did not. Minority ethnic group membership was a borderline significant predictor of negative self-concept (OR = 1.79; 95% CI: 0.94-3.33). CONCLUSIONS: Global self-worth was significantly lower in ALL survivors than sibling controls, however, 81% of survivors had positive self-concept. Survivor subgroups most vulnerable to negative self-concept were the unemployed survivors, believing that cancer treatment affected employability, and ethnic minority group members. Targeted intervention may have greater clinical relevance for these subgroups.

Adolescent↗
PubMed2006

Understanding treatment decision making: contexts, commonalities, complexities, and challenges.

BACKGROUND: The diagnosis of cancer sets off a cascade of complex decisions at a time when patients feel vulnerable and distressed. Although clinical decisions used to follow one standard, many guidelines now outline several options and include explicit recognition of the need to incorporate patients' preferences to determine the most appropriate treatment. PURPOSE: The purpose of this article is to provide a brief overview of empirical studies about cancer patients' treatment-related decision making, to highlight the areas of congruence and divergence in that empirical literature, and then to generate a framework that points to future interventions and research. METHODS: Through a group discussion with a range of experts in the field, we generated a framework for the critical treatment decisions and key issues within those decisions. Then, we reviewed the literature describing the experiences of cancer patients and evaluating interventions designed to improve the quality of treatment decisions. RESULTS: We identified four major differences that influence decision making across cancers and across individuals with the same diagnosis. We also identified four common themes across situations and people. There is considerable evidence that decision aids can improve the quality of decisions across a range of diseases, although the data for cancer treatment decision making are limited. Other interventions such as navigation-skill training are promising but have little evidence of benefit for cancer decisions. CONCLUSIONS: There are many opportunities for behavioral research to extend and contribute to the understanding and improvement of cancer treatment decision making. Some key areas in need of research include developing taxonomies of disease and patient characteristics and increasing understanding of the lived experiences of cancer survivors, of the influence of time and timing, of the relationship of information and preferences, and of participation in randomized clinical trials.

Comprehension↗
PubMed2005

Oncolytic viruses for cancer therapy I. Cell-external factors: virus entry and receptor interaction.

After being recognized for their anti-neoplastic properties at the beginning of the last century, viruses are again being considered for use as therapeutic agents against cancer. Certain virus species have a propensity to replicate within transformed cells, which are commonly rendered vulnerable due to tumor-specific defects in their defense against viral infection. Other viruses have been modified to subject them to tumor-specific growth conditions. Oncolytic viruses carry the promise to efficiently target cancer cells for destruction and spread throughout tumor tissue to reach distant neoplastic loci without causing collateral damage to healthy tissues. In contrast to conventional cancer chemotherapy, viral anti-neoplastic agents require complex interactions with the host organism to reach their target and to unfold their oncolytic activity. Recent progress in the elucidation of the molecular mechanisms of viral pathogenesis has opened up new opportunities to manipulate virus-host interactions, generating effective anti-tumor strategies. On the other hand, significant obstacles towards the application of safe and efficacious viral therapies have become apparent. These frequently relate to the lack of cell culture and animal tumor models that accurately reflect the characteristics of cancerous tissues in patients. Throughout the past century, viral therapeutics against cancer have evolved into a new class of treatment strategies characterized by unique opportunities and challenges. A growing number of oncolytic viruses has entered clinical investigation or is scheduled to do so in the near future. Great efforts are being undertaken to rekindle an old idea and, with the help of new technologies, to realize its promise of new treatment facilities for cancer.

Genetic Therapy↗
PubMed1996

Helping children cope when a family member has cancer.

A cancer diagnosis impacts the entire family unit, but children are especially vulnerable. In the past, families and professionals did not share information or allow for children to express their feelings or to be involved. Children have the right to know and the need to know the truth. Interventions should be based on both the developmental stage of the child and the stage of the illness. Approaches by disease phase and developmental stage are discussed. Goals include maintaining family stability, preparing children for what may happen, allowing for flexible communication, and preventing serious psychosocial sequelae.

Adaptation, Psychological↗
PubMed2004

Current concepts in Bcl-2 family member regulation of female germ cell development and survival.

Since the cloning of the bcl-2 gene in 1985, considerable progress has been made in elucidating the function of Bcl-2 and related proteins in controlling apoptosis. Although much of this work initially relied on the ectopic expression of bcl-2 gene family members in cell lines in vitro, a number of genetically manipulated mice have been generated to better understand the in vivo significance of specific family members to organ development and homeostasis. Of the many tissues that exhibit apoptosis at some point during fetal or postnatal life, the female gonads arguably possess one of the highest and most protracted incidences of apoptosis, associated with development and maturation of the germ line. Moreover, female germ cells (oocytes) are, for as-yet poorly understood reasons, extremely vulnerable to a host of pathological insults, such as anti-cancer therapies, that ultimately cause premature ovarian failure and infertility due to accelerated oocyte death. Accordingly, efforts to understand the occurrence and regulation of apoptosis in the ovary are of considerable importance from both biological and clinical perspectives. This review will highlight what is known of apoptosis in the female gonads, and the role that Bcl-2 family members play in regulating this process.

Animals↗
PubMed2006

How many and which items of activities of daily living (ADL) and instrumental activities of daily living (IADL) are necessary for screening.

Geriatric assessment (GA) in elderly cancer patients serves as screening instrument to identify patients who are vulnerable or frail. To reduce the diagnostic burden for patients and caregivers, we asked how many and which items of ADL and IADL questionnaires are necessary to identify those patients with limitations in the sum score of ADL or IADL. Data of 327 elderly patients (age>or=60 years), of whom 27.9% had limitations in ADL and 36.0% in IADL score, were entered in a forward selection model. Four out of ten items of ADL identified 95.3% of patients with limitations in ADL. Two out of eight items of IADL identified 97.4% of patients with limitations in IADL. The combined use of these items recognised 98.5% of patients with limitations in ADL or IADL score. If ADL and IADL scores are used for screening, we recommend an abbreviated version with 6 instead of 18 items.

Activities of Daily Living↗
PubMed1989

Controlled prospective longitudinal study of women with cancer: II. Psychological outcomes.

The incidence and etiology of major life difficulties for women with survivable cancer were studied. Women with early stage cancer (n = 65) were assessed after their diagnosis but prior to treatment and then reassessed at 4, 8, and 12 months posttreatment. Two matched comparison groups, women diagnosed and treated for benign disease (n = 22) and healthy women (n = 60), were also assessed longitudinally. Results for four life areas are reported: (a) The emotional response to the life-threatening diagnosis and anticipation of treatment was characterized by depressed, anxious, and confused moods, whereas the response for women with benign disease was anxious only. In both cases, these responses were transitory and resolved posttreatment. (b) There was no evidence for a higher incidence of relationship dissolution of poorer marital adjustment; however, 30% of the women treated for disease reported that their sexual partners may have had some difficulty in reaching orgasm (i.e., delayed ejaculation) after the subjects' treatment. (c) There was no evidence for impaired social adjustment. (d) Women treated for cancer retained their employment and their occupations; however, their involvement (e.g., hours worked per week) was significantly reduced during recovery. These data and those in a companion report (Andersen, Anderson, & deProsse, 1989) suggest "islands" of significant life disruption following cancer; however, these difficulties do not appear to portend global adjustment vulnerability.

Adult↗