381 research outputs found
How to Manage the Obese Patient With Cancer
Full text linkPurposeObesity (body mass index [BMI] ≥ 30 kg/m2) is common among patients with cancer. We reviewed management issues in the obese patient with cancer, focusing on how obesity influences treatment selection (including chemotherapy dosing), affects chemotherapy toxicity and surgical complications, and might be a treatment effect modifier.MethodsThe majority of evidence is drawn from observational studies and secondary analyses of trial data, typically analyzed in N × 3 BMI categories (normal weight, overweight, and obese) matrix structures. We propose a methodological framework for interpretation focusing on sample size and composition, nonlinearity, and unmeasured confounding.ResultsThere is a common perception that obesity is associated with increased treatment-related toxicity. Accordingly, cytotoxic chemotherapy dose reduction is common in patients with elevated BMI. Contrary to this, there is some evidence that full dosing in obese patients does not result in increased toxicity. However, these data are from a limited number of regimens, and fail to fully capture cytotoxic drug pharmacodynamics and pharmacokinetic variability in obese patients. Among patients undergoing surgery, there is evidence that elevated BMI is associated with increased perioperative mortality and increased rates of infectious complications. A novel finding is that these relationships hold after surgery for malignancy, but not for benign indications. There are biologic plausibilities that obesity might be an effect modifier of treatment, but supporting evidence from clinical studies is inconsistent.ConclusionIn line with the ASCO 2012 guidelines, chemotherapy dosing is probably best performed using actual body weight in obese patients. However, specific regimens known to be associated with increased toxicity in this group should be used with caution. There is no guidance on dose for obese patients treated with biologic agents. Currently, there are no specific recommendations for the surgical management of the obese patient with cancer
sj-docx-1-mpp-10.1177_23814683231171363 – Supplemental material for Estimating the Cost of 3 Risk Prediction Strategies for Potential Use in the United Kingdom National Breast Screening Program
No full textSupplemental material, sj-docx-1-mpp-10.1177_23814683231171363 for Estimating the Cost of 3 Risk Prediction Strategies for Potential Use in the United Kingdom National Breast Screening Program by Stuart J. Wright, Martin Eden, Helen Ruane, Helen Byers, D. Gareth Evans, Michelle Harvie, Sacha J. Howell, Anthony Howell, David French and Katherine Payne in MDM Policy & Practice</p
sj-zip-1-whe-10.1177_17455057231160348 – Supplemental material for Optimising the delivery of breast cancer risk assessment for women aged 30–39 years: A qualitative study of women’s views
No full textSupplemental material, sj-zip-1-whe-10.1177_17455057231160348 for Optimising the delivery of breast cancer risk assessment for women aged 30–39 years: A qualitative study of women’s views by Sarah Hindmarch, Louise Gorman, Rhiannon E Hawkes, Sacha J Howell and David P French in Women’s Health</p
Predictors of weight gain in a cohort of premenopausal early breast cancer patients receiving chemotherapy
Full text linkAim In breast cancer patients, post chemotherapy weight gain is linked with increased risk of cancer recurrence. We prospectively studied a cohort of premenopausal women receiving contemporary chemotherapy following a diagnosis of breast cancer to examine factors predicting weight increase. Methods Between May 2005 and January 2008, 523 patients from the Prospective Outcomes in Sporadic versus Hereditary(POSH) cohortcohort entered this sub-study comparing weight prior to chemotherapy and weight and waist/hip measurements 12-months following chemotherapy. Results Data from 380 patients were available. Mean (standard deviation [SD]) pre-treatment body mass index (BMI) was 26.3 [5.6] kg/m2; 30% women gained > 5% body weight during the study period. Lower BMI at diagnosis predicted greater subsequent post treatment weight gain (4.3% relative weight gain for those in the 1st quartile of BMI compared to 0.8% for those in the 4th quartile; r=-0.22; p<0.001). No link to chemotherapy regimens, cigarette smoking, previous parity or chemotherapy induced amenorrhoea was noted. A total of 44% of women had central obesity (post-treatment waist measurement of >88cm). Conclusions Almost a third of premenopausal patients receiving adjuvant chemotherapy for breast cancer will gain clinically significant weight and over 40% will have central obesity 12-months following diagnosis. A greater weight gain is predicted by lower pretreatment BMI
Author Correction: Pathogen-derived HLA-E bound epitopes reveal broad primary anchor pocket tolerability and conformationally malleable peptide binding.
Full text linkThe original version of this Article contained an error in the spelling of the author Jonah B Sacha, which was incorrectly given as Jonah Sacha. These errors have now been corrected in both the PDF and HTML versions of the Article
Endocrine therapy
No full textThe link between ovarian hormones and breast cancer began to be formed as early as 1882 when TW Nunn observed the spontaneous regression of breast cancer in a woman 6 months after her menstruation ceased [1]. Oophorectomy was first proposed by the German clinician, Schinzinger, on the basis of his observation that younger women had more aggressive breast cancer [2]. However, it was not until 1896 that Beatson reported the first results of therapeutic oophorectomy in women with recurrent and locally advanced breast cancer, demonstrating regressions in three cases [3]. This paved the way for several other surgeons to replicate his work and demonstrate response rates in the order of 20-30% in terms of pain control and objective regression [4-6]. Oestrogen itself wasn't isolated and identified until 1923, and the first man-made oestrogen was synthesised in 1933 [7, 8]. In the mid 1940s, such synthetic oestrogens became some of the first addivive systemic therapies for breast cancer and it wasn't until the early 1970s that the first systemic anti-oestrogen, tamoxifen, came into clinical practice (Table 18.1). Tamoxifen, largely overtook additive oestrogen therapy, not due to increased efficacy, but rather its better tolerability. The majority of subsequent developments in breast cancer endocrine pharmacotherapy have centred around the generation of alternative strategies to abrogate the effects of oestrogen on breast cancer cells, including inhibition of the aromatase enzyme, oestrogen receptor (ER) downregulation and pharmacological suppression of ovarian oestrogen production (Table 18.1). In the following chapter, we review the available data on such endocrine agents. As with the drug development paradigm in all fields of oncology, we start with advanced breast cancer and then describe how such therapies have been translated to the adjuvant and neoadjuvant settings. Table 18.1 Timeline of the introduction of endocrine therapies in use today a Therapy Authorb (reference) Date Ovarian ablation (OA) Beatson [3] 1896 Ovarian irradiation DeCourmelles [9] 1922 Androgens Ulrich [97] 1938 Oestrogens Haddow [84] 1944 Progestins Escher [106] 1951 Hypophysectomy Perrault [61] 1952 Adrenalectomy Huggins [69] 1953 Tamoxifen Cole [32] 1971 Aminoglutethamide Griffiths [71] 1973 LHRHHanalogues Klijn [19] 1982 Raloxifine Buzdar [42] 1988 Letrozole Iveson [162] 1993 Exemestane Zilembo [163] 1995 Pureanti-oestrogens Howell [55] 1995 Anastrazole Jonat [164] 1996 aIncludes the important conceptual advances of hypophysectomy and adrenalectomy bfirst author of first paper</p
Resistance to Endocrine Therapy in Breast Cancer: Are Breast Cancer Stem Cells Implicated?:Ciara S. O’Brien, Sacha J. Howell, Gillian Farnie and Robert B. Clarke
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