Background Body image is a critical psychosocial issue for cancer patients as they often undergo significant changes to appearance and functioning. In this review article, our primary purpose was to identify empirically-supported approaches to treat body image difficulties of adult cancer patients that can be incorporated into high-quality comprehensive cancer care. Methods We provided an overview of theoretical models of body image relevant to cancer patients, and presented findings from published literature on body image and cancer from 2003–2013. We integrated these data with information from the patient-doctor communication literature to delineate a practical approach for assessing and treating body image concerns of adult cancer patients. Results Body image difficulties were found across patients with diverse cancer sites, and were most prevalent in the immediate postoperative and treatment period. Age, body mass index, and specific cancer treatments have been identified as potential risk factors for body image disturbance in cancer patients. Current evidence supports the use of time-limited cognitive-behavioral therapy interventions for addressing these difficulties. Other intervention strategies also show promise but require further study. We identified potential indicators of body image difficulties to alert healthcare professionals when to refer patients for psychosocial care, and proposed a framework for approaching conversations about body image that can be used by the oncologic treatment team. Conclusions Body image issues affect a wide array of cancer patients. Providers can use available evidence combined with information from the healthcare communication literature to develop practical strategies for treating body image concerns of cancer patients.

Anorexia and weight loss are negative prognostic factors in patients with cancer. Although total ghrelin levels are increased in energy-negative states, levels of the biologically active octanoylated ghrelin and the anorexigenic peptide YY (PYY) have not been reported in patients with cancer-induced cachexia. We hypothesized that abnormal ghrelin and/or PYY levels contribute to cancer-induced cachexia. We evaluated 21 patients with cancer-induced cachexia; 24 cancer patients without cachexia; and 23 age-, sex-, race-, and BMI-matched subjects without cancer. Active ghrelin levels and the active to total ghrelin ratio were significantly increased in subjects with cancer-induced cachexia, compared with cancer and noncancer controls. PYY levels were similar among groups. Appetite measured by a visual analog scale was not increased in subjects with cachexia. The increase in active ghrelin levels is likely to be a compensatory response to weight loss. Cachexia may be a state of ghrelin resistance because appetite does not correlate with ghrelin levels. Changes in the active to total ghrelin ratio suggest that a mechanism other than increased secretion must be responsible for the increase in active ghrelin levels. PYY is unlikely to play an important role in cancer-induced cachexia.

IMPORTANCEThe use of benzodiazepines to control agitation in delirium in the last days of life is controversial.OBJECTIVE To compare the effect of lorazepam vs placebo as an adjuvant to haloperidol for persistent agitation in patients with delirium in the setting of advanced cancer. DESIGN, SETTING, AND PARTICIPANTS Single-center, double-blind, parallel-group, randomized clinical trial conducted at an acute palliative care unit at MD Anderson Cancer Center, Texas, enrolling 93 patients with advanced cancer and agitated delirium despite scheduled haloperidol from February 11, 2014, to June 30, 2016, with data collection completed in October 2016.INTERVENTIONS Lorazepam (3 mg) intravenously (n = 47) or placebo (n = 43) in addition to haloperidol (2 mg) intravenously upon the onset of an agitation episode. MAIN OUTCOMES AND MEASURES The primary outcome was change in Richmond Agitation-Sedation Scale (RASS) score (range, −5 [unarousable] to 4 [very agitated or combative]) from baseline to 8 hours after treatment administration. Secondary end points were rescue neuroleptic use, delirium recall, comfort (perceived by caregivers and nurses), communication capacity, delirium severity, adverse effects, discharge outcomes, and overall survival.RESULTS Among 90 randomized patients (mean age, 62 years; women, 42 [47%]), 58 (64%) received the study medication and 52 (90%) completed the trial. Lorazepam + haloperidol resulted in a significantly greater reduction of RASS score at 8 hours (−4.1 points) than placebo + haloperidol (−2.3 points) (mean difference, −1.9 points [95% CI, −2.8 to −0.9]; P < .001). The lorazepam + haloperidol group required less median rescue neuroleptics (2.0 mg) than the placebo + haloperidol group (4.0 mg) (median difference, −1.0 mg [95% CI, −2.0 to 0]; P = .009) and was perceived to be more comfortable by both blinded caregivers and nurses (caregivers: 84% for the lorazepam + haloperidol group vs 37% for the placebo + haloperidol group; mean difference, 47% [95% CI, 14% to 73%], P = .007; nurses: 77% for the lorazepam + haloperidol group vs 30% for the placebo + haloperidol group; mean difference, 47% [95% CI, 17% to 71%], P = .005). No significant between-group differences were found in delirium-related distress and survival. The most common adverse effect was hypokinesia (3 patients in the lorazepam + haloperidol group [19%] and 4 patients in the placebo + haloperidol group [27%]). CONCLUSIONS AND RELEVANCEIn this preliminary trial of hospitalized patients with agitated delirium in the setting of advanced cancer, the addition of lorazepam to haloperidol compared with haloperidol alone resulted in a significantly greater reduction in agitation at 8 hours. Further research is needed to assess generalizability and adverse effects.

Much of the early literature on 'cultural competence' focuses on the 'categorical' or 'multicultural' approach, in which providers learn relevant attitudes, values, beliefs, and behaviors of certain cultural groups. In essence, this involves learning key 'dos and don'ts' for each group. Literature and educational materials of this kind focus on broad ethnic, racial, religious, or national groups, such as 'African American', 'Hispanic', or 'Asian'. The problem with this categorical or 'list of traits' approach to clinical cultural competence is that culture is multidimensional and dynamic. Culture comprises multiple variables, affecting all aspects of experience. Cultural processes frequently differ within the same ethnic or social group because of differences in age cohort, gender, political association, class, religion, ethnicity, and even personality. Culture is therefore a very elusive and nebulous concept, like art. The multicultural approach to cultural competence results in stereotypical thinking rather than clinical competence. A newer, cross cultural approach to culturally competent clinical practice focuses on foundational communication skills, awareness of cross-cutting cultural and social issues, and health beliefs that are present in all cultures. We can think of these as universal human beliefs, needs, and traits. This patient centered approach relies on identifying and negotiating different styles of communication, decision-making preferences, roles of family, sexual and gender issues, and issues of mistrust, prejudice, and racism, among other factors. In the current paper, we describe 'cultural' challenges that arise in the care of four patients from disparate cultures, each of whom has advanced colon cancer that is no longer responding to chemotherapy. We then illustrate how to apply principles of patient centered care to these challenges.

BACKGROUNDPatients with cancer often develop anorexia, fatigue, and decreased muscle mass. These signs and symptoms are nonspecific, and they frequently occur in other conditions, including hypogonadism.METHODSThe objectives of this study were 1) to measure testosterone levels in patients with cancer and 2) to examine the correlations between testosterone, tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), insulin‐like growth factor‐1 (IGF‐1), ghrelin levels, and appetite in patients with cancer patients and in a noncancer control group. This was designed as a cross‐sectional study in the setting of a university‐affiliated Veterans Affairs Medical Center. The study population included 31 male patients with cancer and 25 gender‐matched noncancer controls of similar age. The variables total testosterone (TT), calculated free testosterone (cFT), calculated bioavailable testosterone (cBT), sex hormone‐binding globulin (SHBG), luteinizing hormone (LH), TNF‐α, IL‐6, IGF‐1, and active ghrelin were measured in fasting morning plasma samples. Appetite was measured according to a visual analog scale. The main outcome measures were cFT and cBT.RESULTSCancer patients had mean TT levels similar to levels in the noncancer control group but significantly lower levels of cFT, cBT, IGF‐1, and appetite. SHBG, LH, TNF‐α, IL‐6, and ghrelin levels were increased in patients with cancer compared with the control group. cFT and cBT levels were correlated inversely with IL‐6 and ghrelin levels and were correlated directly with IGF‐1 levels and appetite.CONCLUSIONSPatients with cancer had lower levels of biologically active testosterone. TT was not adequate for the evaluation of hypogonadism, because SHBG levels were increased. A reliable measurement of FT and/or BT should be used. LH was elevated in the patients with cancer, indicating that low FT levels were caused by primary testicular dysfunction. The authors postulated that high IL‐6 or ghrelin levels inhibit testosterone synthesis, although a secondary effect at the hypothalamic‐pituitary levels cannot be excluded. Cancer 2006. © 2006 American Cancer Society.

Animal studies have shown that dietary methionine restriction selectively inhibits growth of a variety of human tumor xenografts but has relatively few deleterious effects on normal tissues. The objectives of the present study were to determine whether enteral methionine restriction is safe and tolerable in adults with metastatic cancer and whether it reduces plasma methionine levels. Eight patients with a variety of metastatic solid tumors were enrolled in a phase I clinical trial. A commercially available methionine-free medical food served as the primary dietary protein source for all patients. Patients were prescribed diets containing 0.6-0.8 g of protein, 25-35 kcal, and 2 mg of methionine per kilogram per day. Participants remained on the experimental diet for an average of 17.3 wk (range 8-39 wk). Plasma methionine levels fell from 21.6 +/- 7.3 to 9 +/- 4 microM within 2 wk, representing a 58% decline. Serum albumin and prealbumin levels remained stable or increased. Mean energy intake increased during participation compared with baseline, and protein intake was maintained at target levels. The only side effect was weight loss of approximately 0.5% of body mass index (0.5 kg) per week. We conclude that enteral dietary methionine restriction is safe and tolerable in adults with metastatic solid tumors and results in significant reduction in plasma methionine levels.

Androgen is essential for the physiological maintenance of the integrity of prostatic epithelial cells, and castration causes the cells to undergo apoptosis. To study the molecular mechanism of androgen-dependent cell growth, we showed that androgen up-regulates the expression of the cyclin-dependent kinase inhibitor p21 (WAF1, CIP1, SDI1, CAP20) gene at both the mRNA and protein levels. Nuclear run-on assays demonstrated that androgen stimulates endogenous p21 gene expression at the transcriptional level. Transient transfection experiments showed that androgen can enhance the activity of a 2.4-kb promoter of the p21 gene linked to a luciferase reporter. These results suggested that a putative androgen response element (ARE), which mediates androgen response to enhance the p21 transcription, is included in the 2.4-kb promoter fragment. Deletion analysis of the promoter revealed a functional ARE (AGCACGCGAGGTTCC) located at -200 bp of the p21 gene proximal to the promoter region. Electrophoretic mobility shift assay further demonstrated that the androgen receptor specifically binds to this element. Wild-type ARE, but not mutant ARE, confers androgen responsiveness to a heterologous promoter. The up-regulation of p21 gene expression by androgen suggests that p21 may have an antiapoptotic function in prostatic epithelial cells. However, this hypothesis will need to be tested in future experiments.

Previous studies have shown that androgen up-regulates expression of the p21 (WAF1, CIP1, SDI1, CAP20) gene, which contains a canonical androgen response element (ARE) in its proximal promoter region. We undertook the current studies to determine whether elements in the p21 promoter other than the ARE mediate androgen action. We found that deletion of the ARE did not completely abolish the promoter responsiveness to androgen, suggesting that additional cis-regulatory elements within the p21 core promoter may also be involved in androgen responsiveness. The p21 core promoter is GC-rich and contains six binding sites for transcription factor Sp1. We determined whether one or more of these Sp1 sites mediate androgen responsiveness of the p21 promoter. To do so, we used a transient transfection assay with p21 promoter-luciferase reporter constructs. The reporter activity of a construct lacking the ARE but containing all six Sp1 sites was induced approximately 3-fold by androgen. Mutation of Sp1-3 nearly eliminated basal promoter activity as well as androgen responsiveness, whereas deletion of Sp1-1 and Sp1-2 sites and mutation of Sp1-4, Sp1-5, and Sp1-6 sites had relatively little effect. We also used the mammalian one-hybrid assay and coimmunoprecipitation assay to show that androgen receptor (AR) and transcription factor Sp1 interact with one another. The current studies suggest a model in which AR and transcription factor Sp1 not only bind to their respective consensus sites within the p21 promoter, but also complex with one another, thereby recruiting coactivators and general transcription factors and inducing p21 transcription.