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Breast cancer in younger women: effects on interpersonal and family relations.

Although breast cancer can have a stressful impact on women of all ages, young women may be particularly vulnerable to the negative effects of the disease. Based on a developmental perspective, this article reviews studies on the emotional impact of breast cancer on young women, their spouses, children, and the marital relationship. Studies indicate that younger women experience more emotional distress than older women, although the inverse relationship between age and emotional distress is not consistent across all studies. Although age does not appear to have a direct relationship to husbands' adjustments, younger husbands reported more problems carrying out domestic roles and a greater number of life stresses than older husbands. Studies on the impact of breast cancer on children are limited in number and scope but indicate that the effects of breast cancer vary according to the developmental level of the child. Directions for further research on young women and their families are suggested.

Adaptation, Psychological↗

Concern about aspects of body image and adjustment to early stage breast cancer.

OBJECTIVE: Several authors have suggested that patients adjust more poorly to breast cancer if they are heavily invested in body image as a source of their sense of self-worth. This prospective study examined this possibility, looking at two aspects of concern about body image as predictors of several indices of adjustment over the first postoperative year. METHODS: At diagnosis (and again a year later) 66 women with early stage breast cancer reported how much they valued a) a sense of body integrity (or intactness) and b) a good physical appearance. The day before surgery, a week afterward, and at 3-month, 6-month, and 12-month follow ups, they reported on their mood. At presurgery and at follow ups they also rated their attractiveness and sexual desirability and reported on frequency of sexual interaction. At follow-ups they also indicated how much their illness and treatment were interfering with social and recreational activities. RESULTS: Initial investment in appearance was related to distress across the postsurgical year. In contrast, investment in appearance made women more resilient against deterioration in their perceptions of attractiveness. Concern about body integrity did not strongly predict emotional distress, but it related to adverse impact on social and recreational activities in the follow-up period, to deterioration in feelings of sexual desirability, and to feelings of alienation from the self (feeling "not like yourself anymore"). CONCLUSIONS: Body image is often thought of in terms of physical appearance, but there is also a body image pertaining to integrity, wholeness, and normal functioning. People who are greatly concerned about either aspect of their body image are vulnerable to poorer psychosocial adjustment when confronting treatment for breast cancer. The poorer adjustment takes a different form, however, depending on the nature of the patient's body-image concern.

Adaptation, Psychological↗

Feminist practice and breast cancer: "The patriarchy has claimed my right breast...".

Breast cancer is the leading cause of death of women between the ages of thirty-five and forty-five. Women of color and lesbians are particularly vulnerable populations. In this article, a feminist social worker weaves her personal experience with breast cancer, the literature on social work and breast cancer, and her research on feminist practice to propose some guidelines for services and practice.

Adaptation, Psychological↗

Immunologic status of the cancer patient and the effects of blood transfusion on antitumor responses.

For patients undergoing potentially curative surgery for cancer, the perioperative period is when they appear to be most vulnerable. The antitumor immune response is subjected to a number of iatrogenic insults at this time, not the least of which is the surgery itself. Any improvements that can be made by a further understanding of the pathophysiology of the events in the perioperative period, and the therapeutic interventions to control them, would obviously benefit the patient. Over the past 10 years, the desire for such benefits has led to the intense investigation of "the blood transfusion effect" in cancer surgery, which this article reviews.

Antibodies, Neoplasm↗

Viruses for the treatment of malignant glioma.

Viruses have been considered for use as therapeutic agents against cancer, and malignant glioma in particular. Oncolytic viruses were designed to target malignant cells supporting efficient virus replication, or rendered vulnerable to viral destruction due to tumor-specific defects in their defense against virus infection. Other than conventional cancer chemotherapy, viral antineoplastic agents require complex interactions with the host organism to reach their target and to unleash their oncolytic activity. Recent progress in the design and therapeutic application of oncolytic viruses carries the promise to make these agents available for treatment of malignant glioma.

Cell Death↗

Opportunistic cancers in patients with immunodeficiency syndromes.

Patients with inherited or acquired immunodeficiency disorders are vulnerable to a broad spectrum of opportunistic infectious diseases, but a narrow spectrum of malignancies. These malignancies--B-cell lymphomas, Kaposi's sarcomas, and squamous cell carcinomas--are likely due to failure of immune surveillance to recognize virally transformed target cells. The evidence for this hypothesis is substantial regarding Epstein-Barr virus-induced lymphoproliferative lesions in immunodeficient patients.

Acquired Immunodeficiency Syndrome↗

Rethinking breast cancer risk and the environment: the case for the precautionary principle.

The World Health Organization recently reported that breast cancer has become the most common cancer in women throughout the world. Known risk factors account for less than half of all cases of breast cancer, and inherited germ line mutations occur in at most only 10% of all cases. Cumulative exposure to estradiol and other hormones links many of the established risk factors for breast cancer. This paper reviews epidemiologic and toxicologic evidence on breast cancer risks and presents a comprehensive construct of risk factors intended to focus on the identification of those factors that can be controlled or modified. We attempt to provide a framework for interpreting the etiologic interplay of endogenous metabolic changes and environmental changes in the etiology of breast cancer. The construct we develop distinguishes between those risk factors that are directly causal, such as ionizing radiation and inherited germ cell defects, those vulnerability factors that extend the time period during which the breast undergoes development, and those contributing factors that increase total hormonal stimulation of the breast. Some hormonally active compounds, such as those in soy and broccoli and other phytoestrogen-containing foods, can be protective against breast cancer, while others, such as some environmental contaminants, appear to increase the risk of the disease by increasing levels of harmful hormones. Efforts to explain patterns of breast cancer should distinguish between these different risk factors. Identification of vulnerability and contributing risk factors can foster the development of public policy to reduce the burden of this prevalent cancer. Prudent precautionary principles suggest that reducing exposure to avoidable or modifiable risk factors should receive high priority from the public and private sectors.

Breast Neoplasms↗

Tissue-derived extracellular matrix hydrogels instruct epigenetic adaptation in metastatic colonization.

The extracellular matrix (ECM) plays a central role in regulating tumor progression and metastatic colonization by providing biochemical and mechanical signals that shape cancer cell fate. However, most organoid culture systems rely on basement membrane extracts that fail to reproduce the tissue-specific extracellular environments encountered during metastasis. Here, we develop tissue-derived decellularized matrix hydrogels to reconstruct organ-specific microenvironments and investigate epigenetic adaptation to ECM cues during metastatic colonization. Patient-derived colorectal cancer organoids cultured in colon-derived matrices exhibited enhanced maintenance of stem-like phenotypes and colon-specific chromatin accessibility landscapes compared with cultures grown in basement membrane extracts, demonstrating improved physiological relevance for primary tumor modeling. When exposed to matrices derived from secondary organs, the organoids showed distinct growth phenotypes accompanied by rapid, tissue-dependent chromatin accessibility remodeling, indicating that ECM composition alone can reshape regulatory programs governing metastatic adaptation. Notably, liver-derived matrices selectively activated hepatocyte nuclear factor 4 alpha (HNF4A)-associated transcriptional networks and created a context-specific dependence on c-MET signaling for survival. Functional perturbation of HNF4A or c-MET signaling confirmed that both are required for organoid formation specifically within the liver matrix environment. Together, these findings establish tissue-derived matrix hydrogels as instructive bioactive materials that actively regulate cancer cell epigenetic states and reveal microenvironment-specific therapeutic vulnerabilities during early metastatic colonization.

Journal Article↗

Relating information needs to the cancer experience. 2. Themes from six cancer narratives.

Many different issues may arise for individuals with cancer, where the provision of information can be an effective coping strategy. It is also clear that information needs change over time and vary from person to person. This paper considers six cancer narratives from a study seeking to identify the information needs of people with cancer that emerged out of their cancer experience. Six respondents were invited to tell their story through in-depth interviews and narrative analysis uncovered thematic aspects of the lived experience. Themes emerged which showed that cancer impacts on different aspects of an individual's self-identity, including body image, family, social and work relationships. Cancer was viewed as an intrusion and the illness engendered feelings of vulnerability that impacted on their normal coping mechanisms. This resulted in a decreased ability to process information. While individuals expressed medical information needs, they were less likely to articulate their need for information when it related to other areas of their lives. Individuals reached a turning point during their experience, when the self-acknowledgement that they were living with cancer, enabled them to become more active respondents in the information process. As this stage cannot readily be identified as occurring at a specific point of the cancer trajectory, communication channels need to be kept open regarding information-giving. This raises questions about areas for further study.

Adaptation, Psychological↗

Psychoneuroendocrine influences on immunocompetence and neoplasia.

Emotional, psychosocial, or anxiety-stimulated stress produces increased plasma concentrations of adrenal corticoids and other hormones though well-known neuroendocrine pathways. A direct consequence of these increased corticoid concentrations is injury to elements of the immunological apparatus, which may leve the subject vulnerable to the action of latent oncogenic viruses, newly transformed cancer cells, or other incipient pathological processes that are normally held in check by an intact immunological apparatus. This article describes studies that examine the adverse effects of increased plasma concentrations of adrenal corticoids on the thymus and thymus-dependent T cells, inasmuch as these elements constitute a major defense system against various neoplastic processes and other pathologies. The studies demonstrate that anxiety-stress can be quantitatively induced and the consequences measured through specific biochemical and cellular parameters, providing that authentic quiescent baselines of these conditions are obtained in the experimental animals by the use of low-stress protective housing and handling techniques.

Animals↗

Minimizing cancer risk using molecular techniques: a review.

This review article summarizes molecular markers that can signal enhanced risk of cancer and provide clinicians with these clues in order to attempt the use of natural and synthetic compounds to intervene in the early precancerous stages of carcinogenesis before invasive disease begins. With an aim such as this in mind, we have begun to apply molecular techniques based on many research articles to look for biomarkers capable of signaling a greater risk of cancer. It is possible to attain relatively quick answers by monitoring selected signs and damage in the body which provide the environment for abnormal cell growth and differentiation. These molecular techniques aim to uncover critical precancerous events taking place inside the body and identify measurable biologic flags signaling their occurrence. For years now, scientists have understood that the onset of cancer is a gradual, step-wise process that may unfold over the course of decades, rather than a single, fixed event that can be dated in a pathologist's report. Carcinogenesis usually encompasses the prolonged accumulation of injuries at several different biological levels and includes both genetic and biochemical changes in cells. At each of these levels there is an opportunity for intervention-a chance to prevent, slow or even halt the gradual march of healthy cells toward malignancy. It is estimated that 75% of cancers are induced by chemicals; thus, if exposure to chemicals is avoided, cancer can be prevented. Also, depending on the individual's genetic background, the ability to metabolize chemicals is different among the population. This means that, "you and I can be exposed to exactly the same amount of a chemical," yet our response will differ because we metabolize carcinogens differently due to different rates of deoxyribonucleic acid (DNA) repair, apoptosis, and mitosis or different levels of Phase I and Phase II detoxification enzymes. This, along with a more or less efficient immune system, may promote tumor formation or destroy a cancer cell at its earliest stage of development. Therefore, measurement of the biologic markers such as DNA and protein adducts, DNA damage, programmed cell death, DNA repair system, mitosis, gene activation, levels of antioxidants and efficient immune function described in this chapter and summarized in Figures 2 and 10, are biological clues indicating that the body has been assaulted by toxic (or cancer-causing) agents. This early identification of biomarkers for special vulnerability to the effects of chemicals and detection of selected signs of precancerous damage in the body may culminate preventive measures and the saving of lives.

Apoptosis↗

The sensitivity of children to electromagnetic fields.

In today's world, technologic developments bring social and economic benefits to large sections of society; however, the health consequences of these developments can be difficult to predict and manage. With rapid advances in electromagnetic field (EMF) technologies and communications, children are increasingly exposed to EMFs at earlier and earlier ages. Consistent epidemiologic evidence of an association between childhood leukemia and exposure to extremely low frequency (ELF) magnetic fields has led to their classification by the International Agency for Research on Cancer as a "possible human carcinogen." Concerns about the potential vulnerability of children to radio frequency (RF) fields have been raised because of the potentially greater susceptibility of their developing nervous systems; in addition, their brain tissue is more conductive, RF penetration is greater relative to head size, and they will have a longer lifetime of exposure than adults. To evaluate information relevant to children's sensitivity to both ELF and RF EMFs and to identify research needs, the World Health Organization held an expert workshop in Istanbul, Turkey, in June 2004. This article is based on discussions from the workshop and provides background information on the development of the embryo, fetus, and child, with particular attention to the developing brain; an outline of childhood susceptibility to environmental toxicants and childhood diseases implicated in EMF studies; and a review of childhood exposure to EMFs. It also includes an assessment of the potential susceptibility of children to EMFs and concludes with a recommendation for additional research and the development of precautionary policies in the face of scientific uncertainty.

Brain Neoplasms↗

Lonidamine: an overview.

The attention of pharmaco-therapeutic research is shifting from the cell duplication mechanisms to the oncogene expressions and cofactors that are the actual cause of cancer. This trend corresponds to the appearance of a second generation of anticancer agents that are typically represented by tamoxifen and lonidamine. The first is a hormonal agent with endocrine effect that was developed making use of a rationale and methods already available, although in a different context. The second, an energolytic agent, is a more complicated case. It was discovered when neither a solid knowledge of cancer energy systems nor the related pharmacological methods were available. Both had to be developed along with a basic research in which lonidamine was at the same time target and tool. In this way, the indication was obtained that cancer activates a specialized energy system in the repair phase following exposure to hyperthermia, alkylating agents, and radiations. This system confers cancer cells an advantage over the normal ones, but is vulnerable and appears to be lonidamine's target. The presently available data show that lonidamine, when used in appropriate conditions with respect to its mode of action, increases the disease-free interval and survival in some types of tumours.

Antineoplastic Agents↗

It's ok to say no! A discussion of ethical issues arising from informed consent to chemotherapy.

This article is written in response to anecdotal evidence from patients, reports from nurses, sociological studies, and documentation from oncologists, which all suggest that the process of refusing treatment for chemotherapy is not an easy one. There is substantial evidence to suggest that pressures that are counterproductive to informed consent are having an impact on the decision making of vulnerable individuals coping with the stress of terminal illness through cancer. Informed consent is a basic ethical principle underpinning any medical or nursing intervention (Johnstone M. Bioethics: a nursing perspective. Sydney: Harcourt Brace Jovanovich, 1989). The following focus on informed consent is an attempt to begin to address the present hiatus which exists in the health literature on ethical issues surrounding the modality, chemotherapy (Young D. An ethical approach to chemotherapy in private practice. J Natl Cancer Inst 1992;84:810). Recent research suggests that the holistic orientation of nurses, in comparison to the reductionist stance of physicians, allows them to be emotionally close to their patients and hence, more aware of the difficulties individuals experience in coping with stressful regimens (Uden G, Norberg A, Lindseth A, Marhaug V. Ethical reasoning in nurses' and physicians' stories about care episodes. J Adv Nurs 1992;17:1028-34). Consequently, it is anticipated that ethical issues in relation to chemotherapy, a modality that has been described as distressing and capable of seriously compromising quality of life (Burish T, Tope D. Psychological techniques for controlling the adverse side effects of cancer chemotherapy: findings from a decade of research. J Pain Sympt Man 1992;7:287-301), will have an impact on the working life of many oncology nurses.

Antineoplastic Agents↗

Personal care products that contain estrogens or xenoestrogens may increase breast cancer risk.

Established models of breast cancer risk, such as the Gail model, do not account for patterns of the disease in women under the age of 35, especially in African Americans. With the possible exceptions of ionizing radiation or inheriting a known genetic mutation, most of the known risk factors for breast cancer are related to cumulative lifetime exposure to estrogens. Increased risk of breast cancer has been associated with earlier onset of menses or later age at menopause, nulliparity or late first parity, use of hormonal contraceptives or hormone replacement therapy, shorter lactation history, exposure to light at night, obesity, and regular ingestion of alcohol, all of which increase circulating levels of unbound estradiol. Among African Americans at all ages, use of hormone-containing personal care products (PCPs) is more common than among whites, as is premature appearance of secondary sexual characteristics among infants and toddlers. We hypothesize that the use of estrogen and other hormone-containing PCPs in young African American women accounts, in part, for their increased risk of breast cancer prior to menopause, by subjecting breast buds to elevated estrogen exposure during critical windows of vulnerability in utero and in early life. These early life and continuing exposures to estrogenic and xenoestrogenic agents may also contribute to the increased lethality of breast cancer in young women in general and in African American women of all ages. Public disclosure by manufacturers of proprietary hormonally active ingredients is required for this research to move forward.

Adolescent↗

Quality of life assessment for low literacy Latinos: a new multimedia program for self-administration.

Cancer patients who have limited literacy skills or English language proficiency are particularly vulnerable to receiving sub-optimal care. Outcome measurement in these patients may provide new insight into previously undetected problems. This report describes the development and testing of a Spanish language, multimedia program for quality of life (QOL) assessment. Pilot testing was conducted with 30 Latino cancer patients with a range of education levels and computer experience. Patients found the program easy to use and understand. The "Talking Touchscreen" is a practical, user-friendly method that provides greater opportunities to assess QOL in Spanish-speaking patients with a range of literacy skills.

Computer Literacy↗

Telomere Length Dynamics as a Biomarker of Individual Radiation Sensitivity and Pneumonitis in Lung Cancer Patients Receiving Thoracic Radiation Therapy.

PURPOSE: Telomere shortening is a biomarker for genome instability and aging, and the vulnerability of telomeric DNA to oxidative damage suggests its potential role in mediating radiation therapy (RT) side effects. This study evaluates telomere length (TL) as a biomarker for clinical radiosensitivity and adverse outcomes in thoracic RT-treated patients. METHODS AND MATERIALS: Patients with cancer receiving thoracic RT (2019-2022) were prospectively enrolled at Brigham and Women's Hospital, Boston, Massachusetts. Peripheral blood mononuclear cells (PBMCs) were collected pre-RT and ≤12 months post-RT. TL was measured using quantitative PCR, and multipathway DNA repair capacity (DRC) was simultaneously assessed by fluorescence multiplex host cell reactivation assays. RT outcomes included patient-reported quality of life and radiation pneumonitis. Linear mixed-effects models were used to analyze TL dynamics; risk prediction models for RT outcomes were evaluated using area under the curve. RESULTS: Pre-RT TL decreased with age (0.44% lower per year; 95% CI, 0.12%-0.77%) and advanced cancer stage (6.87% lower per step increase of stage; 95% CI, 3.45%-10.16%). Radical RT was associated with telomere shortening (3.7% lower; 95% CI, 0.27%-7.07%) in PBMCs, detectable ≤6 months post-RT. Pre-RT TL strongly predicted post-RT changes, and TL dynamics outperformed static measures in predicting symptom burden and radiation pneumonitis. Positive associations were observed between TL and DRC against oxidative lesions, with A:8-oxoG repair capacity mediating 12.8% of RT-induced TL shortening. CONCLUSIONS: Lymphocyte TL can reflect individual radiosensitivity and interact with oxidative damage repair. Longitudinal assessment of TL dynamics provides additional predictive value for adverse RT outcomes compared with static measures. Further studies are needed to fully determine the clinical utility of TL.

Humans↗

Genetics and oncology nursing.

OBJECTIVES: To review oncology nursing practice in the genetic era, how genetic information is used across the cancer care continuum, practice guidelines, and opportunities for genetic nursing education. DATA SOURCES: Published articles. CONCLUSION: Genetic information in oncology health care is used not only to predict risk but to elucidate disease biology, explain individual variation in vulnerability to environmental carcinogens, diagnose and characterize malignancies, design treatment regimens specific to a cancer's genetic fingerprint, develop new, therapeutic modalities, and clarify modulators of drug metabolism, efficacy, and interactions. IMPLICATIONS FOR NURSING PRACTICE: With current and emerging genetic discoveries, all oncology nurses will use genetic information in their practice.

Clinical Competence↗