Underweight women and those with obesity, defined as having a body mass index (BMI) ≥ 30 kg/m2, diagnosed with breast cancer (BC) are known to have worse prognosis. Whether BMI impacts BC stage at diagnosis and BC specific survival (BCSS) is not understood. We aim to better understand the relationship between BMI with stage at BC diagnosis and BCSS.

Women age ≥ 15 years old diagnosed with BC between 2014 and 2019 were identified from the California Cancer Registry. BMI at diagnosis was classified as underweight (< 18.5 kg/m2), normal weight (18.5-24.9 kg/m2), overweight (25-29.9 kg/m2), obesity class 1-2 (30-39.9 kg/m2), and obesity class 3 (≥ 40 kg/m2). BC late stage of diagnosis was defined as American Joint Committee on Cancer stage 3 and 4. Multivariate logistic regression was performed to compare sociodemographic and clinical factors associated with late stage. Multivariable cox proportional hazards regression models assessed association of BMI and BCSS.

Of 159,248 patients: 2.2% were underweight, 34.6% normal weight, 30.5% overweight, 26.7% obesity class 1-2, and 6.0% obesity class 3. Compared to normal weight, patients who were underweight [Hazard Ratio (HR) 1.54, 95% Confidence Interval (CI) 1.51-1.57], obesity class 1-2 [HR 1.06, 1.05-1.07], and obesity class 3 [HR 1.14, 1.12-1.16] were more likely to be diagnosed with late-stage BC. In models stratified by age, patients ≥ 40 years who were underweight had worse BCSS, while patients ≥ 51 years with obesity class 1-2 had better BCSS.

Patients with obesity class 1-2 were more likely to be diagnosed with a later stage, but had improved BCSS, supporting an "obesity paradox" in BC and suggesting that other measures are needed to better assess body composition, adipose distribution, and metabolic health of patients. Patients who were underweight had worse survival, suggesting this high-risk group may benefit from being assessed and treated for possible sarcopenia and malnourishment.

To explore whether there is a relationship between perirenal fat area (PFA) and the pathological types of renal cell carcinoma (RCC).

Two hundred ninety-seven cases of RCC patients were included in our study, which is a retrospective analysis. Based on pathological type, we divided the 297 RCC patients into two groups: the clear cell renal cell carcinoma (ccRCC) group (236 cases) and the non-clear cell renal cell carcinoma (non-ccRCC) group (61 cases). Computed tomography (CT) images at the renal vein level were used to measure PFA. A multivariate logistic regression model was employed to examine the connection between various pathological types of RCC and PFA.

Significant differences were observed between ccRCC and non-ccRCC patients in PFA (P = 0.007), contralateral PFA (P = 0.011), weight (P = 0.002), BMI (P < 0.001), pathological stage 1 (P = 0.010), and pathological stage 2 (P = 0.002). To study the link between pathological subtypes and PFA, a multivariate logistic regression model was employed. Stratifying patients by tumor location in the kidney, the multivariate logistic regression analysis showed that when the tumor is located outside the polar lines of the kidney (OPLK), for every 1 cm2 increase in PFA, the probability of developing ccRCC increases by 5% [1.05 (1.01, 1.10) P = 0.0153]. Furthermore, after stratifying patients by tumor location and pathological stage, it was found that in T1 stage patients with tumors located OPLK, for every 1 cm2 increase in PFA, the probability of developing ccRCC increases by 6% [1.06 (1.01, 1.11) P = 0.0300].

When the tumor is located OPLK in T1 stage patients, PFA is positively correlated with ccRCC. Perirenal adipose tissue may be a risk factor for ccRCC.

Background: The primary endpoint was to assess the nutritional status in patients diagnosed with prostate cancer (PCa) in Romania. The secondary endpoint was to analyze the impact of obesity on mortality and disease recurrence. Methods: In this retrospective cohort study, we analyzed the files of 354 patients diagnosed with PCa between August 2001 and May 2022 and referred to the Medical Oncology Department of Neolife Medical Center. A total of 257 patients fulfilled the inclusion criteria and were the subject of this study. Results: Excess weight was seen in 190 (73.9%) patients, with 119 (46.3%) being overweight and 71 (27.6%) having obesity. Subgroup analysis showed that at diagnosis, patients with obesity (PwO) were younger (p = 0.022), had lower PSA (p = 0.016), and had lower 10-year all-cause mortality rates (p = 0.04) than patients without obesity. Patients with metastases had lower weight (p = 0.001) and BMI (p = 0.033), higher PSA (p < 0.001), Gleason scores (p = 0.002), ISUP grade group (p < 0.001), and 10-year all-cause mortality rate (p < 0.001) than patients without metastases. Weight (AUROC = 0.637, 95% CI: 0.557-0.717, p = 0.001; cut-off = 77.5 kg, Se = 52.5%, Sp = 71.2%) and BMI (AUROC = 0.591, 95% CI: 0.507-0.676, p = 0.033; cut-off = 23.5 kg/m2, Se = 25.4%, Sp = 91.9%) were independent predictors of the presence of metastases at diagnosis. In the androgen deprivation therapy (ADT) group, PwO had a shorter time to castration resistance than patients without obesity (Log Rank test: χ2 = 4.395, p = 0.036). Conclusions: Weight and BMI are accessible tools that could be useful in determining the presence of metastatic disease. PwO on ADT may develop castration resistant PCa faster than patients without obesity.

Obesity in mid-life is a well-established risk factor for developing renal cell carcinoma (RCC); however, patients with RCC who are obese at the time of diagnosis have more favorable survival outcomes. To get better insight into the obesity paradox and determine the extent to which weight around diagnosis is stable, we examined pre- and post-diagnosis weight changes in patients with localized RCC.

We included 334 patients with localized RCC from the prospective cohort ReLife who self-reported body weight at multiple time points ranging from 2 years before to 2 years after diagnosis. Multivariable linear mixed-effects regression models were used to compare weight at each timepoint to weight at diagnosis for the overall study population, as well as stratified by BMI at diagnosis, tumor stage, and tumor grade.

Most patients were classified as overweight (38.3%) or obese (29.6%) at diagnosis. Overall, patients experienced on average 1.45 kg (95% confidence interval (CI) 0.84, 2.06) weight loss in the 2 years before diagnosis. Pre-diagnosis weight loss was higher in patients who were non-obese at diagnosis, and who presented with higher tumor stage and grade. On average, pre-diagnosis weight loss was at least partially regained within two years after diagnosis.

Patients who were non-obese and patients with higher stage and grade tumors had higher pre-diagnosis weight loss, which was at least partially regained after treatment. These patterns suggest there are subgroups of patients with localized RCC who experience disease-related weight loss, which could contribute to the obesity paradox.

Neuroendocrine neoplasms (NENs) originating in the gastroenteropancreatic (GEP) tract are rare tumors often associated with significant metabolic disturbances and nutritional challenges. This review explores the intricate relationship between nutritional status and the development, progression, and prognosis of GEP-NENs. Through an extensive literature search encompassing studies up to April 2024, we examined various factors, including obesity, malnutrition, metabolic syndrome and type 2 diabetes mellitus, and their roles in the development and progression of GEP-NENs. The review highlights the dual role of obesity, both as a risk factor and a potential prognostic indicator, drawing attention to the 'obesity paradox' observed in cancer research. Additionally, we discuss the impact of malnutrition on patient outcomes and emphasize the need for comprehensive nutritional assessments beyond BMI. This analysis highlights the importance of incorporating nutritional interventions into preventive and therapeutic strategies for GEP-NEN patients. Future research should further clarify these associations and develop personalized nutritional management protocols to improve patient prognosis and quality of life. Acronyms adopted in the text and tables: AOR: adjusted odd ratio, BIA: Bioelectrical Impedance Analysis, BMI: Body Mass Index, CI: confidence interval, CLARINET: Controlled Study of Lanreotide Antiproliferative Response in Neuroendocrine Tumor, FLI: fatty liver index, GEP: gastroenteropancreatic, GLIM: global leadership into malnutrition, HR: hazard ratio, MS: metabolic syndrome, MUST: malabsorption universal screening tool, NEC: neuroendocrine carcinoma, NENs: Neuroendocrine neoplasms, NETs: Neuroendocrine tumors, NRS: Nutritional Risk Screening, OR: odd ratio, OS: overall survival, PFS: progression-free survival, RR: risk ratio, SGA: Subjective Global Assessment, T2DM: type 2 diabetes mellitus, VAI: visceral adiposity index, WD: well-differentiated.

As healthy living becomes crucial for cancer survivors, discussing the health risk behaviors of male cancer survivors, who are more prone to such behaviors, is essential. This study compared health-related behaviors and obesity among male cancer survivors and the general male population in Korea.

This cross-sectional, matched case-control study used data from the Korea National Health and Nutrition Examination Survey (KNHANES). Of 11,760 participants, 349 cancer survivors and 1,047 controls were matched by propensity scores. Logistic regression evaluated differences in BMI, smoking, alcohol consumption, physical activity, and diet.

Cancer survivors had lower odds of being overweight and higher odds of being former smokers and drinkers than controls. No significant differences were found in physical activity or diet. However, the middle-aged and older cancer survivors were more likely to be overweight and obese, respectively. The middle-aged survivors were also more likely to be former smokers, while the older survivors were more likely to be former drinkers.

Cancer survivors were more likely to have a normal weight, be past smokers, or be former drinkers compared with controls. Education on cancer prevention is required to improve health-related behaviors and prevent secondary cancer.

This study aimed to investigate the impact of a Western diet and resistance training on cardiac remodeling in a rat model of chemically induced mammary cancer. Fifty-six female Wistar rats were randomly assigned to one of eight experimental groups, evaluating the impact of Western and standard diets, exercise and sedentarism, and the induction of mammary cancer. Mammary cancer was induced via the intraperitoneal administration of N-methyl-N-nitrosourea (MNU) (50 mg/kg) at seven weeks of age. The resistance training protocol consisted of ladder climbing three times per week for an 18-week period, with a gradual increase in load over time. At the end of the 20-week experimental period, the animals were anesthetized and underwent echocardiography. Subsequently, the animals were euthanized, and organs and visceral adipose tissue (VAT) were collected and analyzed. A histopathological examination was performed on the mammary tumors. The Western diet increased relative VAT and contributed to cardiovascular and tumor-related changes, including an increase in interventricular septum thickness (IVS) and left ventricle posterior wall thickness (LVPW) at end-systole. Exercise reduced fat accumulation, improved cardiac performance, and helped regulate cardiovascular function, as indicated by a higher eccentricity index (EI) in the WD+EX group compared to the WD group. The WD was associated with increased VAT accumulation and initially delayed tumor initiation; however, over time, it contributed to bigger tumor aggressiveness. This diet also delayed tumor initiation but increased LVPW. Exercise, when combined with a WD, accelerated tumorigenesis, malignant transformation and invasiveness, resulted in the higher prevalence of invasive tumors. These findings underscore the complex and potentially compounding effects of diet and exercise on cancer progression.

Pb (lead) is a heavy metal, its carcinogenicity for bladder cancer is still debated, the link between blood lead levels (BLLs) and bladder cancer was investigated in this study.

This cross-sectional study, using the NHANES (1999-2018) database, explored the relationship between BLLs and bladder cancer among Americans aged 20-85. It employed weighted multivariable logistic regression for analysis. Additionally, subgroup analyses and smoothed curve fitting were also performed.

This study included a total of 40,486 participants, the body mass index (BMI) of the participants is 28.71 ± 6.68 kg/m2. The average BLL is 0.0858 μmol/L (range: 0-2.96 μmol/L). A fully adjusted model showed that the BLL was associated with bladder cancer (odds ratio [OR] = 2.946, 95% confidence interval [CI] = 1.025 to 8.465, P = 0.047) in people with BMI < 28 kg/m2. However, no difference was found in the BMI ≥ 28 kg/m2 subgroup or in the general population. According to the subgroup analysis of participants with a BMI < 28 kg/m2, blood lead was associated with bladder cancer in the male, nonhypertensive, and < 70-year-old subgroups (p < 0.05) but no significantly different is observed in other subgroups. In addition, we discovered a nonlinear association between the BLLs and bladder cancer risk using a linear regression model.

In this cross-sectional study, we found that the degree of correlation between BLLs and the risk of bladder cancer may vary among people with different BMIs. In people with BMI < 28 kg/m2, a higher BLL was independently associated with bladder cancer. However, more experiments are needed to confirm this finding.

Obesity, a global health concern, is associated with severe health issues like type 2 diabetes, heart disease, and respiratory complications. It also increases the risk of various cancers, including melanoma, endometrial, prostate, pancreatic, esophageal adenocarcinoma, colorectal carcinoma, renal adenocarcinoma, and pre-and post-menopausal breast cancer. Obesity-induced cellular changes, such as impaired CD8+ T cell function, dyslipidemia, hypercholesterolemia, insulin resistance, mild hyperglycemia, and fluctuating levels of leptin, resistin, adiponectin, and IL-6, contribute to cancer development by promoting inflammation and creating a tumor-promoting microenvironment rich in adipocytes. Adipocytes release leptin, a pro-inflammatory substance that stimulates cancer cell proliferation, inflammation, and invasion, altering the tumor cell metabolic pathway. Adiponectin, an insulin-sensitizing adipokine, is typically downregulated in obese individuals. It has antiproliferative, proapoptotic, and antiangiogenic properties, making it a potential cancer treatment. This narrative review offers a comprehensive examination of the molecular interconnections between obesity and cancer, drawing on an extensive, though non-systematic, survey of the recent literature. This approach allows us to integrate and synthesize findings from various studies, offering a cohesive perspective on emerging themes and potential therapeutic targets. The review explores the metabolic disturbances, cellular alterations, inflammatory responses, and shifts in the tumor microenvironment that contribute to the obesity-cancer link. Finally, it discusses potential therapeutic strategies aimed at disrupting these connections, offering valuable insights into future research directions and the development of targeted interventions.

Obesity increases the risk for developing several cancers, including colorectal cancer (CRC), and is associated with liver perturbations, which likely impacts treatment tolerance. 5 fluorouracil (5FU) remains a first line treatment for CRC, but efficacy is hampered by interpatient variable responsiveness and off-target toxicities. The current study examined the impact of diet-induced obesity (DIO) on 5FU cytopenia and efficacy using two established CRC models: MC38 (C57BL/6) and C26 (CD2F1). DIO increased tumor size in both MC38 and C26. DIO reduced liver dihydropyrimidine dehydrogenase (dpyd) expression, the enzyme that catalyzes 5FU's catabolism to become inactive, in MC38 mice, but not in C26. 5FU remained efficacious against early MC38 and C26 tumor growth; however, 5FU-induced tumor and liver immune cell death was exacerbated following three cycles of 5FU with MC38. DIO caused dramatic changes to liver Kupffer cells (KCs), wherein there were increased prometastatic, immunosuppressive KCs in Obese Control and MC38. 5FU, however, depleted these KCs and increased inflammatory KCs in both Lean and Obese MC38. DIO yielded a milder obesity phenotype in CD2F1 mice, and 5FU-induced cytopenia was not different between Lean and Obese. DIO increased total liver KCs; however, C26 tumors increased liver KCs, which were normalized with 5FU treatment, irrespective of DIO. Although 5FU remained efficacious in both models of CRC and did not reduce survival, multiple cycles of 5FU monotherapy increased liver and tumor immune cell death in DIO mice. Altogether, obesity was not protective but rather exacerbated chemotherapy-induced cytotoxicity and promoted a prometastatic liver environment.NEW & NOTEWORTHY The current study aimed to examine the impact of obesity on tumorigenesis and 5FU safety and efficacy with two established murine models of colorectal cancer. Diet-induced obesity increased tumor burden in both models, and 5FU's antitumor efficacy remained and extended survival with both tumor models. Obese mice demonstrated increased 5FU-induced immune cell cytotoxicity following multiple cycles of 5FU with distinct changes to liver macrophages, suggesting an increased propensity for liver metastasis.

Central obesity and breast cancer (BC) have been identified as relevant by empirical research. The weight-adjusted-waist index (WWI) is a novel methodology for quantifying central obesity. Inspection of the association between WWI and BC in American adult women was the primary goal of the current investigation.

Cross-sectional assessments were conducted on information gathered from 10,193 National Health and Nutrition Examination Survey (NHANES) participants from 2011 to 2018. The waist circumference was divided by the square root of the body's mass to compute WWI. Data were assessed via descriptive statistics to present data distributions according to BC grouping and WWI grouping, receiver operating characteristic curves (ROCs) to evaluate the obesity indicators' applied value, logistic regression to reflect associations between WWI and BC prevalence, and restricted cubic splines (RCSs) and subgroup analysis forest plots to visualise and complement the relationships.

This study enrolled 10,193 participants whose WWI ranged from 8.38 to 14.41, 259 of whom were diagnosed with BC, and the results revealed significant differences in baseline characteristics between the groups. With an area under the curve (AUC) value (95% confidence interval) (CI)of 0.611 (0.577-0.644), WWI was a promising indicator of BC with good application value rather than waist circumference (WC), body mass index (BMI), or waist-height ratio (WHtR). WWI and BC laid out a substantial relationship, yielding an odds ratio (OR) of 1.54 and a 95% CI of (1.34, 1.79), which remained at 1.19 (1.00, 1.42) after considerable adjustments were made, according to the logistic regression analysis. Compared with the lowest quartile of WWI, the highest quartile had a 62% greater in the probability of suffering from BC. With the RCS's inverted U-shape highlighting the importance of considering the nonlinear nature of the relationship and subgroup analyses reflecting variations among populations, all the results demonstrated that WWI was a well-suggestive indicator of BC hazard.

The current investigation revealed a meaningful association between the prevalence of BC and WWI, which was superior to other obesity indicators, albeit one that was more complex than the positive relationship initially derived. There existed a turning point for BC prevalence at WWI of approximately 12 cm/√kg. Nevertheless, maintaining WWI in the lower range is critical for preventing and administering BC and minimizing disease risk.

Preclinical evidence suggests that host obesity is associated with tumor progression due to immuno-metabolic dysfunction, but the impact of obesity on immunity and clinical outcomes in patients is poorly understood, with some studies suggesting an obesity paradox. We recently reported that high-adiposity and low-muscle body composition phenotypes are associated with striking increases in epithelial ovarian cancer (EOC) mortality and we observed no evidence of an obesity paradox. However, whether at-risk versus optimal body composition phenotypes are associated with distinct immuno-metabolic milieus remains a fundamental gap in knowledge. Herein, we defined differentially abundant circulating immuno-metabolic biomarkers according to body composition phenotypes in EOC.

Muscle and adiposity cross-sectional area (cm2) was assessed using CT images from 200 EOC patients in The Body Composition and Epithelial Ovarian Cancer Survival Study at Roswell Park. Adiposity was dichotomized as low versus high; patients with skeletal muscle index (SMI) <38.5 (muscle cm2/height m2) were classified as low SMI (sarcopenia). Joint-exposure phenotypes were categorized as: Fit (normal SMI/low-adiposity), Overweight/Obese (normal SMI/high-adiposity), Sarcopenia/Obese (low SMI/high adiposity), and Sarcopenia/Cachexia (low SMI/low-adiposity). Treatment-naïve serum samples were assessed using Biocrates MxP Quant 500 for targeted metabolomics and commercially available Luminex kits for adipokines and Th1/Th2 cytokines. Limma moderated T-tests were used to identify differentially abundant metabolites and cytokines according to body composition phenotypes.

Patients with 'risk' phenotypes had significantly increased abundance of metabolites and cytokines that were unique according to body composition phenotype. Specifically, the metabolites and cytokines in increased abundance in the at-risk phenotypes are implicated in immune suppression and tumor progression. Conversely, increased abundance of lauric acid, IL-1β, and IL-2 in the Fit phenotype was observed, which have been previously implicated in tumor suppression and anti-tumor immunity.

In this pilot study, we identified several significantly differentially abundant metabolites according to body composition phenotypes, confirming that clinically significant joint-exposure body composition phenotypes are also biologically distinct. Although we observed evidence that at-risk phenotypes were associated with increased abundance of immuno-metabolic biomarkers indicated in immune suppression, additional confirmatory studies focused on defining the link between body composition and immune cell composition and spatial relationships in the EOC tumor microenvironment are warranted.

Previous studies have shown that general and central obesity are each linked to adverse outcomes in gastrointestinal cancers. However, their combined effect on gastrointestinal cancers surgery outcomes were less understood. This study aims to integrate both general and central obesity to examine the outcomes of gastric cancer surgery in different obesity patterns. We retrospectively analyzed 248 patients who underwent gastric cancer surgery between 2021 and 2023 in a single institute. The Inbody720 body composition analyzer measured body composition. We evaluated the relationship between obesity patterns - combining BMI with central obesity measures (waist circumference, waist-to-hip ratio, visceral fat area) - and postoperative complications and 30-day readmission. Central-only obesity were more likely to induce fistula (P = 0.025), while non-obesity was more likely to develop postoperative abdominal effusion (P = 0.049) and bleeding (P = 0.042). Central-only obesity was significantly associated with severe postoperative complications after adjustment for hypertension, diabetes, abdominal surgery history, preoperative albumin levels, age, sex, and surgical types. This remains significant even after adjusting for muscle mass. However, we did not find the same results for significant complications. Regarding 30-day readmission, there are no differences between different patterns of obesity. Central-only obesity is an independent risk factor for severe postoperative complications in gastric cancer, while a high BMI appears to be associated with a lower risk compared to non-obese patients, but not significant postoperative complications. The likelihood of readmission within 30 days post-surgery may not be related to the patient's pattern of obesity.

Body composition may be related to survival in patients with clear-cell renal cell carcinoma (ccRCC), but studies have not simultaneously considered adipose and muscle tissue quantity and radiodensity.

We analyzed data from 1,022 patients with ccRCC who underwent nephrectomy between 2000 and 2020 at Memorial Sloan Kettering Cancer Center. Skeletal muscle, visceral adipose tissue, and subcutaneous adipose tissue indexes (cm2/m2) and radiodensities [Hounsfield units (HU)] were assessed from noncontrast presurgical CT scans; clinical and demographic characteristics were available from the time of surgery. HRs and confidence intervals were estimated for overall (OS) and disease-free survival (DFS) through March 2023 in multivariable models that simultaneously accounted for all body composition measures.

The median age of the patients was 58 years, 69% were male, and 90% were White. There were 169 OS events over 8,392 person-years and 253 DFS events over 7,753 person-years of follow-up. In adjusted analyses, poor OS was associated with lower skeletal muscle radiodensity [-10 HU, HR (95% confidence interval), 1.37 (1.05-1.77)] and greater visceral adipose tissue radiodensity [+10 HU, 1.66 (1.06-2.59)], with similar findings for DFS. Poor survival was also associated with greater visceral adipose tissue index [+40 cm2/m2, OS: 1.32 (0.97, 1.79); DFS: 1.33 (1.04, 1.71)]. Associations with skeletal muscle radiodensity were limited to patients with stage 1/2 disease.

Radiodensities of skeletal muscle and visceral adipose tissues may be novel presurgical prognostic factors for patients with ccRCC.

The findings underscore the importance of evaluating the full range of body composition features simultaneously in multivariable models.

Delirium is a common neurocognitive disorder in patients with advanced cancer and is associated with poor clinical outcomes. As a potentially reversible phenomenon, early recognition of delirium by identifying the risk factors demands attention. We aimed to develop a model to predict the occurrence of delirium in hospitalized patients with advanced cancer.

This retrospective study included patients with advanced cancer admitted to the oncology ward of four tertiary cancer centers in Korea for supportive cares and excluded those discharged due to death. The primary endpoint was occurrence of delirium. Sociodemographic characteristics, clinical characteristics, laboratory findings, and concomitant medication were investigated for associating variables. The predictive model developed using multivariate logistic regression was internally validated by bootstrapping.

From January 2019 to December 2020, 2,152 patients were enrolled. The median age of patients was 64 years, and 58.4% were male. A total of 127 patients (5.9%) developed delirium during hospitalization. In multivariate logistic regression, age, body mass index, hearing impairment, previous delirium history, length of hospitalization, chemotherapy during hospitalization, blood urea nitrogen and calcium levels, and concomitant antidepressant use were significantly associated with the occurrence of delirium. The predictive model combining all four categorized variables showed the best performance among the developed models (area under the curve 0.831, sensitivity 80.3%, and specificity 72.0%). The calibration plot showed optimal agreement between predicted and actual probabilities through internal validation of the final model.

We proposed a successful predictive model for the risk of delirium in hospitalized patients with advanced cancer.

Background/Objectives: Increasing evidence indicates that body composition can significantly influence prognosis in women with breast cancer. However, alterations in body composition, particularly among young women (<40 years), remain largely unknown and underexplored. This study aimed to investigate the relationship of computed tomography (CT)-derived body composition with mortality rates among young women recently diagnosed with breast cancer, identifying the best-correlated cutoff value. Methods: This is a bi-set cohort study with retrospective data collection. Women newly diagnosed with ductal invasive breast cancer, aged 20 to 40 years, treated in reference oncology units were included. Body composition was assessed using CT scans at the third lumbar vertebra (L3) level, including muscle and adipose compartments. The outcome of interest was the incidence of overall mortality. A maximally selected log-rank Cox-derived analysis was employed to assess the cutoffs associated with mortality. Results: A total of 192 women were included before any form of treatment (median age of 35 years, IQ range: 31-37). Overall mortality occurred in 12% of the females. Stages III-IV were the most frequent (69.5%). Patients who died had a significantly lower muscle area index. CT-derived muscle area was inversely associated with mortality. Each 1 cm2/m2 decrease in skeletal muscle index increased the mortality hazard by 9%. Higher values of adiposity compartments were independently associated with higher mortality. Conclusions: Our study highlights the predictive significance of skeletal muscle area and adipose tissue in predicting survival among young women recently diagnosed with breast cancer.

The association of body composition with epithelial ovarian carcinoma (EOC) mortality is poorly understood. To date, evidence suggests that high adiposity is associated with decreased mortality (an obesity paradox), but the impact of muscle on this association has not been investigated. Herein, we define associations of muscle and adiposity joint-exposure body composition phenotypes with EOC mortality.

Body composition from 500 women in the Body Composition and Epithelial Ovarian Cancer Survival Study was dichotomized as normal or low skeletal muscle index (SMI), a proxy for sarcopenia, and high or low adiposity. Four phenotypes were classified as fit (normal SMI and low adiposity; reference; 16.2%), overweight or obese (normal SMI and high adiposity; 51.2%), sarcopenia and overweight or obese (low SMI and high adiposity; 15.6%), and sarcopenia or cachexia (low SMI and low adiposity; 17%). We used multivariable Cox models to estimate associations of each phenotype with mortality for EOC overall and high-grade serous ovarian carcinoma (HGSOC).

Overweight or obesity was associated with up to 51% and 104% increased mortality in EOC and HGSOC [Hazard Ratio (HR)] = 1.51, 95% CI = 1.05 to 2.19 and HR = 2.04, 95% CI = 1.29 to 3.21). Sarcopenia and overweight or obesity was associated with up to 66% and 67% increased mortality in EOC and HGSOC (HR = 1.66, 95% CI = 1.13 to 2.45 and HR = 1.67, 95% CI = 1.05 to 2.68). Sarcopenia or cachexia was associated with up to 73% and 109% increased mortality in EOC and HGSOC (HR = 1.73, 95% CI = 1.14 to 2.63 and HR = 2.09, 95% CI = 1.25 to 3.50).

Overweight or obesity, sarcopenia and overweight or obesity, and sarcopenia or cachexia phenotypes were each associated with increased mortality in EOC and HGSOC. Exercise and dietary interventions could be leveraged as ancillary treatment strategies for improving outcomes in the most fatal gynecological malignancy with no previously established modifiable prognostic factors.

Lifestyle factors after cancer diagnosis could influence cancer survival. This study aimed to investigate the joint effects of smoking, physical activity, alcohol consumption, diet and sleep duration on all-cause, cancer and non-cancer mortality of cancer survivors in UK biobank.

The follow-up period concluded in December 2021, with post-diagnostic lifestyle factors assessed at baseline. A lifestyle score ranging from 0 to 5 was assigned based on adherence to the selected lifestyle factors. The study employed Cox regression models for hazard ratios (HRs) and Kaplan-Meier for survival rates, with stratified and sensitivity analyses to assess the robustness of our findings under various assumptions.

During a median follow-up of 12.7 years, 5652 deaths were documented from 34,184 cancer survivors. Compared to scoring 0-1, the HRs (95% CIs) for all-cause mortality with lifestyle scores of 2, 3, 4, and 5 were 0.70 (95% CI: 0.64, 0.76), 0.57 (0.52, 0.62), 0.50 (0.45, 0.54) and 0.43 (0.38, 0.48), respectively. Specific cancer types, particularly digestive, breast, female reproductive, non-solid, and skin cancers, showed notable benefits from adherence to healthy lifestyle, with the HRs of 0.55 (0.39, 0.79), 0.54 (0.42, 0.70), 0.32 (0.19, 0.53), 0.58 (0.39, 0.86), and 0.36 (0.28, 0.46) for lifestyle score of 5, respectively. Stratified analyses indicated the association was particularly significant among those with normal/lower BMI and higher Townsend Deprivation Index (Pinteraction = 0.001 and < 0.001, respectively).

Healthier lifestyles were significantly linked with reduced mortality among cancer survivors. These findings highlight the need for adherence to healthy lifestyle habits to improve survival.

The obesity paradigm has been a health concern globally for many years, its meaning is controversial. In this study, we assess the characteristics and causes of obesity paradigm and detail the mediation of obesity and inflammation on survival.

The original cohort included participants from the US National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018, a prospective cohort of a nationally representative sample of adult participants; the oncology validation cohort included patients from the Investigation on Nutrition Status and Clinical Outcome of Common Cancers (INSCOC) from 2013 to 2021, a prospective cohort of Chinese patients with cancer. Survival analysis was performed using weighted (NHANES) or unweighted (INSCOC) Cox survival analyses. The normal BMI group was used as a reference for all comparisons. Systemic inflammation was defined as neutrophil-to-lymphocyte ratio (NLR) > 3. Model-based causal mediation analysis was used to identify the mediators.

A total of 52 270 (weighted population: 528506229) participants of the NHANES [mean follow-up times: 10.2 years; mean age (SD): 47 (19.16) years] were included in the original cohort; and a total of 17 418 patients with cancer of INSCOC [mean follow-up times: 2.9 years; mean age (SD): 57.37 (11.66) years] were included in the validation cohort. In the subgroups of all the participants, the obesity paradigm was more apparent in older participants and participants with disease [HR (95% CI): age ≥ 65 years, 0.84 (0.76, 0.93); with cancer, 0.84 (0.71, 0.99); with CVD, 0.74 (0.65, 0.85)]. As aged, the protective effect of a high BMI on survival gradually increased and a high BMI showed the effect of a protective factor on older participants [for obese II, HR (95% CI): young adults, 1.91 (1.40, 2.62); middle age, 1.56 (1.28, 1.91); old adults, 0.85 (0.76, 0.96]). The aged-related obesity paradigm in patients with cancer from the NHANES was verified in the INSCOC cohorts [for obese, HR (95%CI): 0.65 (0.52, 0.81)]. The NLR is an important mediator of the effect of BMI on survival (proportion of mediation = 15.4%).

The obesity paradigm has a strong correlation with age. Relative to normal weight, obese in young people was association with higher all-cause mortality, and obese in elderly people was not association with higher mortality. The protection of obesity is association with systemic inflammation.

Lung cancer is a leading cause of cancer mortality globally, highlighting the importance of understanding its mortality risks to design effective patient-centered therapies. The National Lung Screening Trial (NLST) employed computed tomography texture analysis, which provides objective measurements of texture patterns on CT scans, to quantify the mortality risks of lung cancer patients. Partially linear Cox models have gained popularity for survival analysis by dissecting the hazard function into parametric and nonparametric components, allowing for the effective incorporation of both well-established risk factors (such as age and clinical variables) and emerging risk factors (eg, image features) within a unified framework. However, when the dimension of parametric components exceeds the sample size, the task of model fitting becomes formidable, while nonparametric modeling grapples with the curse of dimensionality. We propose a novel Penalized Deep Partially Linear Cox Model (Penalized DPLC), which incorporates the smoothly clipped absolute deviation (SCAD) penalty to select important texture features and employs a deep neural network to estimate the nonparametric component of the model. We prove the convergence and asymptotic properties of the estimator and compare it to other methods through extensive simulation studies, evaluating its performance in risk prediction and feature selection. The proposed method is applied to the NLST study dataset to uncover the effects of key clinical and imaging risk factors on patients' survival. Our findings provide valuable insights into the relationship between these factors and survival outcomes.

The obesity paradox in patients with advanced non-small cell lung cancer receiving immune checkpoint inhibitor therapy has been observed, but its underlying mechanism is not fully understood. We aimed to investigate whether body composition affects the prognostic impact of obesity, as determined by body mass index (BMI), on survival.

This retrospective study evaluated the data collected from Asian patients who were treated with immune checkpoint inhibitors for advanced non-small cell lung cancer between October 2015 and October 2021. We used abdominal cross-sectional imaging to calculate the skeletal muscle and visceral fat indices (cm2 /m2 ) by dividing the cross-sectional areas of the skeletal muscle and visceral fat by the height squared. Cox proportional-hazards regression was performed to determine the correlation between BMI according to the Asia-Pacific classification, body composition metrics and overall survival.

We analysed the data of 820 patients (630 men and 190 women, with a mean age of 64.3 years [standard deviation: 10.4 years]) and observed 572 (69.8%) deaths with the 1-year mortality rate of 0.58 (95% confidence interval, 0.55-0.62). Obese BMI was associated with longer overall survival, independent of clinical covariates (hazard ratio, 0.64; 95% confidence interval: 0.52-0.80). The prognostic value of obese BMI remained after additional adjustments for skeletal muscle index (hazard ratio, 0.68; 95% confidence interval, 0.53-0.87) or visceral fat index (hazard ratio, 0.54; 95% confidence interval: 0.41-0.70). No association was observed between sex and the impact of BMI on overall survival (P-value for interaction >0.05).

In Asian patients with advanced non-small cell lung cancer who received immune checkpoint inhibitors, obese BMI was associated with favourable overall survival independent of skeletal muscle or visceral fat mass.

Biomarkers are needed to identify patients with metastatic renal cell carcinoma (mRCC) most likely to benefit from immune checkpoint inhibitors. We examined associations between radiographically assessed body composition (BC) variables and body mass index (BMI) with clinical outcomes for patients with mRCC receiving first-line ipilimumab + nivolumab (ipi/nivo).

We retrospectively reviewed all patients with mRCC treated with first-line ipi/nivo at one institution before June 1, 2021 with an analyzable baseline computed tomography (CT) scan. BC variables (skeletal muscle index [SMI], subcutaneous adipose tissue index [SATI], and visceral adipose tissue index [VATI]) were measured using baseline CT scans. Relationships between BC variables and clinical outcomes were examined using Cox proportional hazard regression models.

Ninety-nine patients were analyzed (74% male, 64% overweight/obese, 75% low SMI). Controlling for age, IMDC risk, and sex (for BMI analyses), high vs. low SMI (HR=2.433, CI: 1.397-4.238, P=.0017), high vs. low SATI (HR=1.641, CI: 1.023-2.632, P=.0398), and obese BMI (≥ 30 kg/m2) vs. normal/overweight BMI (<30 kg/m2) (HR=1.859, CI: 1.156-2.989, P=.0105) were significantly associated with progression-free survival (PFS). Median overall survival (OS) for low SMI patients was higher (42.74 months, CI: 26.84, NR) than median OS for high SMI patients (27.01 months, CI: 15.28, NR) (adjusted HR=1.728, CI: 0.909-3.285, P=.0952). No BC variables were significantly associated with OS or objective response rate.

Low SMI and low SATI were associated with significantly better PFS for patients with mRCC receiving first-line ipi/nivo. Radiographic BC variables may be useful prognostic biomarkers in this setting.

An obesity paradox has been described in relation to adverse clinical outcomes (e.g., mortality) with lower body mass index (BMI).

We sought to evaluate the association between BMI and weight loss with long-term all-cause mortality in adult populations under the care of family physicians.

LIPIDOGRAM studies were conducted in primary care in Poland in 2004, 2006, and 2015 and enrolled a total of 45,615 patients. The LIPIDOGRAM Plus study included 1627 patients recruited in the LIPIDOGRAM 2004 and repeated measurements in 2006 edition. Patients were classified by BMI categories as underweight, normal weight, overweight and class I, II, or III (obesity). Follow-up data up to December 2021 were obtained from the Central Statistical Office. Differences in all-cause mortality were analyzed using Kaplan‒Meier and Cox regression analyses.

Of 45,615 patients, 10,987 (24.1%) were normal weight, 320 (0.7%) were underweight, 19,134 (41.9%) were overweight, and 15,174 (33.2%) lived with obesity. Follow-up was available for 44,620 patients (97.8%, median duration 15.3 years, 61.7% females). In the crude analysis, long-term all-cause mortality was lowest for the normal-weight group (14%) compared with other categories. After adjusting for comorbidities, the highest risk of death was observed for the class III obesity and underweight categories (hazard ratio, HR 1.79, 95% CI [1.55-2.05] and HR 1.57, 95% CI [1.22-2.04]), respectively. The LIPIDOGRAM Plus analysis revealed that a decrease in body weight (by 5 and 10%) over 2 years was associated with a significantly increased risk of death during long-term follow-up-HR 1.45 (95% CI 1.05-2.02, p = 0.03) and HR 1.67 (95% CI 1.02-2.74, p < 0.001). Patients who experienced weight loss were older and more burdened with comorbidities.

Being underweight, overweight or obese is associated with a higher mortality risk in a population of patients in primary care. Patients who lost weight were older and more burdened with cardiometabolic diseases, which may suggest unintentional weight loss, and were at higher risk of death in the long-term follow-up. In nonsmoking patients without comorbidities, the lowest mortality was observed in those with a BMI < 25 kg/m2, and no U-curve relationship was observed.

An inverse relationship coined the "obesity paradox" has been propositioned, in which body mass index (BMI) may be contradictorily protective in patients undergoing surgery or treatment of chronic disease. This study sought to investigate the BMI associated with the lowest rate of medical complications after total shoulder arthroplasty (TSA).

The American College of Surgeons National Surgical Quality Improvement Project database was queried to identify adults who underwent elective primary TSA between January 2012 and December 2020. Thirty-day postoperative medical complications were extracted, which included death, readmission, pneumonia, pulmonary embolism, renal failure, and cardiac arrest, among others. BMI was classified into five categories (underweight [BMI <18.5 kg/m 2 ], normal weight [BMI ≥18.5 and <25 kg/m 2 ], overweight [BMI ≥25 and <30 kg/m 2 ], obese [BMI ≥30 and <40 kg/m 2 ], and morbidly obese [BMI ≥40 kg/m 2 ]). We examined the risk of any 30-day postoperative complications and BMI categorically and on a continuous basis using multivariable logistic regression controlling for age, sex, procedure year, and comorbidities.

Of the 31,755 TSAs, 84% were White, 56% were female, and the average age of patients was 69.2 ± 9.3 years. Thirty-day postoperative medical complications occurred in 4.53% (n = 1,440). When assessed on a continuous basis, the lowest risk was in patients with a BMI between 30 and 35 kg/m 2 . Underweight individuals (BMI <18.5 kg/m 2 ) had the highest postoperative complication rates overall. The probability of medical complications increased with age and was greater for female patients.

The relationship between BMI and complication risk in TSA is nonlinear. A BMI between 30 and 35 kg/m 2 was associated with the lowest risk of medical complications after TSA, and BMI<18.5 kg/m 2 had the highest risk overall, indicating some protective aspects of BMI against 30-day medical complications. Thus, obesity alone should not preclude patients from TSA eligibility, rather surgical candidacy should be evaluated in the context of patients' overall health and likelihood of benefit from TSA.

III, Retrospective Comparative Study.

Obesity and smoking have been associated with poor prostate cancer (PC) outcomes. We investigated associations between obesity and biochemical recurrence (BCR), metastasis, castrate resistant-PC (CRPC), PC-specific mortality (PCSM), and all-cause mortality (ACM) and examined if smoking modified these associations.

We analyzed SEARCH Cohort data from men undergoing RP between 1990 and 2020. Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between body mass index (BMI) as a continuous variable and weight status classifications (normal: 18.5 ≤ 25 kg/m2; overweight: 25-29.9 kg/m2; obese: ≥ 30 kg/m2) and PC outcomes.

Among 6,241 men, 1,326 (21%) were normal weight, 2,756 (44%) overweight and 2159 (35%) obese; 1,841 (30%) were never-smokers, 2,768 (44%) former and 1,632 (26%) current-smokers. Among all men, obesity was associated with non-significant increased risk of PCSM, adj-HR = 1.71; 0.98-2.98, P = 0.057, while overweight and obesity were inversely associated with ACM, adj-HR = 0.75; 0.66-0.84, P < 0.001 and adj-HR = 0.86; 0.75-0.99, P = 0.033, respectively. Other associations were null. BCR and ACM were stratified for smoking status given evidence for interactions (P = 0.048 and P = 0.054, respectively). Among current-smokers, overweight was associated with an increase in BCR (adj-HR = 1.30; 1.07-1.60, P = 0.011) and a decrease in ACM (adj-HR = 0.70; 0.58-0.84, P < 0.001). Among never-smokers, BMI (continuous) was associated with an increase in ACM (adj-HR = 1.03; 1.00-1.06, P = 0.033).

While our results are consistent with obesity as a risk factor for PCSM, we present evidence of effect modification by smoking for BCR and ACM highlighting the importance of stratifying by smoking status to better understand associations with body weight.

Patients with digestive system cancers (DSCs) are at a high risk for hospitalizations; however, the risk factors for readmission remain unknown. Here, we established a retrospective cohort study to assess the association between metabolic obesity phenotypes and readmission risks of DSC.

A total of 142,753 and 74,566 patients at index hospitalization were ultimately selected from the Nationwide Readmissions Database (NRD) 2018 to establish the 30-day and 180-day readmission cohorts, respectively. The study population was classified into four groups: metabolically healthy non-obese (MHNO), metabolically healthy obese (MHO), metabolically unhealthy non-obese (MUNO), and metabolically unhealthy obese (MUO). Multivariate Cox regression analysis was used to estimate the effect of metabolic obesity phenotypes on DSC readmission.

The MUNO phenotype had 1.147-fold (95% CI: 1.066, 1.235; p < 0.001) increased 180-day readmission risks in patients with neoplasm of the upper digestive tract. The MUNO phenotype had 1.073-fold (95% CI: 1.027, 1.121; p = 0.002) increased 30-day readmission risks and 1.067-fold (95% CI: 1.021, 1.115; p = 0.004) increased 180-day readmission risks in patients with neoplasm of the lower digestive tract. The MUNO and MUO phenotypes were independent risk factors of readmission in patients with liver or pancreatic neoplasm. Metabolic obesity status was independently associated with a high risk of severe and unplanned hospitalization within 30 days or 180 days.

Both obesity and metabolic abnormalities are associated with a high risk for the poor prognosis of DSC patients. The effect of metabolic categories on the short- or long-term readmission of liver or pancreas cancers may be stronger than that of obesity.

The purpose of this study was to evaluate the prognostic impact of body composition parameters based on computed tomography (CT) in patients with non-small cell lung cancer (NSCLC) who received ICI treatment.

This retrospective study analyzed the data from advanced NSCLC patients treated with ICI therapy between 2013 and 2019. We included patients with NSCLC who underwent baseline CT scans. The exclusion criteria included patients who received three or more lines of chemotherapy, those with insufficient clinical information, or those without treatment response evaluation.

A total of 136 patients were enrolled. Among the volumetric body composition parameters, patients in the highest quartiles (Q2-4) of the visceral fat index (VFI) exhibited a higher response rate to ICI therapy than those in the lowest quartile (Q1) of VFI (Q1 vs. Q2-4: 18.2% vs. 43.1%, p = 0.012). Patients with a VFI in Q2-4 had significantly prolonged progression-free survival (PFS) and overall survival (OS) (PFS, Q1 vs. Q2-4: 3.0 months vs. 6.4 months, p = 0.043; OS, Q1 vs. Q2-4: 5.6 months vs. 16.3 months, p = 0.004). Kaplan-Meier analysis based on the VFI and visceral fat Hounsfield unit (HU) revealed that patients with VFI in Q1 and HU in Q2-4 had the worst prognosis.

Visceral fat volume is significantly associated with treatment outcomes in ICI-treated patients with NSCLC. Moreover, fat quality may impact the treatment outcomes. This finding underscores the potential significance of both fat compartments and fat quality as prognostic indicators.

Visceral fat volume is significantly associated with treatment outcomes in ICI-treated patients with non-small cell lung cancer. Moreover, fat quality may impact the treatment outcomes. This finding underscores the potential significance of both fat compartments and fat quality as prognostic indicators.

• We found that visceral fat volume positively correlated with treatment response and survival in patients with non-small cell lung cancer receiving immune checkpoint inhibitors. • Additionally, a trend toward a negative correlation between visceral fat attenuation and survival was observed. • The findings highlight the prognostic utility of fat compartments and fat quality.

Since the application of Immune checkpoint inhibitors (ICI), the clinical outcome for metastatic cancer has been greatly improved. Nevertheless, treatment response varies in patients, making it urgent to identify patients who will receive clinical benefits after ICI therapy. Adipose body composition has proved to be associated with tumor response. In this systematic review, we aimed to summarize the current evidence on imaging adipose biomarkers that predict clinical outcomes in patients treated with ICI in various cancer types.

Embase and PubMed were searched from database inception to 1st February 2023. Articles included investigated the association between imaging-based adipose biomarkers and the clinical outcomes of patients treated with ICI. The methodological quality of included studies was evaluated through Newcastle- Ottawa Quality Assessment Scale and Radiomics Quality Score tools.

Totally, 22 studies including 2256 patients were selected. Non-small cell lung cancer (NSCLC) had the most articles (6 studies), followed by melanoma (5 studies), renal cell carcinoma (RCC) (3 studies), urothelial carcinoma (UC) (2 studies), head and neck squamous cell carcinoma (HNSCC) (1 study), gastric cancer (1 study) and liver cancer (1 study). The remaining 3 studies investigated metastatic solid tumors including various types of cancers. Adipose biomarkers can be summarized into 5 categories, including total fat, visceral fat, subcutaneous fat, intramuscular fat and others, which exerted diverse correlations with patients' prognosis after being treated with ICI in different cancers. Most biomarkers of body fat were positively associated with survival benefits. Nevertheless, more total fat was predictable of worse outcomes in NSCLC, while inter-muscular fat was associated with poor clinical benefits in UC.

There is relatively well-supported evidence for imaging-based adipose biomarkers to predict the clinical outcome of ICI. In general, most of the studies show that adipose tissue is positively correlated with clinical outcomes. This review summarizes the significant biomarkers proven by researches for each cancer type. Further validation and large independent prospective cohorts are needed in the future. The protocol of this systematic review has been registered at the International Prospective Register of Systematic Reviews (http://www.crd.york.ac.uk/PROSPERO, registration no: CRD42023401986).

Many clinical trials have looked at the relationship between obesity and lung cancer (LC), however, there is scarcity of literature specifically addressing the association between metabolically healthy obesity and metastasis in LC patients. To address this gap in the body of evidence, the study was conducted to observe the association between metabolically healthy obesity and metastasis in LC patients.

We conducted a pre-registered systematic review by searching six major online databases to identify studies relevant related to our investigation, in adherence with the PRISMA guidelines. A proper data extraction protocol was further established to synthesize the findings from the selected papers through a meta-analysis.

Eleven (11) studies met the requisite selection criterion and were included in the study. A random-effect model was used. Obesity was found to have a significant impact on readmission in LC patients. The combined analysis showed a significant effect size of 0.08 (95% CI 0.07 to 0.08), indicating a noticeable impact of obesity. It was also assessed that obese individuals had a 34% reduced risk of LC compared to normal weight individuals. Obesity was associated with a lower risk of surgical complications with a pooled risk ratio of 0.13 (95% CI 0.12 to 0.14). A statistically significant decreased risk of LC (pooled RR = 0.72, 95% CI: 0.68 to 0.77) was also observed in the obese individuals.

The analysis reveals that obesity is associated with a noticeable increase in readmissions, although the impact on LC risk itself is negligible. Moreover, obesity appears to have a beneficial effect by reducing the risk of surgical complications. These results highlight the complex relationship between the two aforementioned factors, emphasizing the importance of considering obesity as a significant factor in patient management and healthcare decision-making.

https://www.crd.york.ac.uk/prospero/, identifier CRD42023427612.

Nutrition therapy aims to prevent weight loss and its health consequences in patients with cancer. The aim of this study was to assess Greek patients' adherence to the ESPEN guidelines for oncology patients and its prospective effect on their body weight (BW) and nutritional status. In total, 152 patients with cancer were recruited from the Attikon University Hospital, Greece, and provided data in 2019 (baseline) and 2020 (follow-up) (drop-out rate = 28.3%). Nutritional status was assessed with the PG-SGA questionnaire. Patients were categorized based on whether they adhered at least to the minimum ESPEN-recommended intakes of energy (≥25 kcal/kg/day) or protein (≥1.0 g/kg/day) or not. On average, patients did not adhere to ESPEN guidelines for energy and protein intake. Most patients meeting the minimum recommendations had an improvement of their nutritional status at follow-up and increased their BW compared to those not meeting them. All patients with head, neck, and spinal cancer who met the minimum recommendations for energy intake improved their nutritional status at follow-up. This study showed that consuming at least the minimum amounts of protein and energy recommended by ESPEN may prevent from weight loss and improve nutritional status; however, the exact amounts need to be personalized.

Obesity, defined by body mass index (BMI), is an established risk factor for specific renal cell carcinoma (RCC) subtypes such as clear cell RCC, the most common RCC histology. Many studies have identified an association between obesity and improved survival after diagnosis of RCC, a potential "obesity paradox." Clinically, there is uncertainty whether improved outcomes observed after diagnosis are driven by stage, type of treatment received, or artifacts of longitudinal changes in weight and body composition. The biological mechanisms underlying obesity's influence on RCC are not fully established, but multiomic and mechanistic studies suggest an impact on tumor metabolism, particularly fatty acid metabolism, angiogenesis, and peritumoral inflammation, which are known to be key biological hallmarks of clear cell RCC. Conversely, high-intensity exercise associated with increased muscle mass may be a risk factor for renal medullary carcinoma, a rare RCC subtype that predominantly occurs in individuals with sickle hemoglobinopathies. Herein, we highlight methodologic challenges associated with studying the influence of obesity on RCC and review the clinical evidence and potential underlying mechanisms associating RCC with BMI and body composition.

Patients with mantle cell lymphoma (MCL), an incurable B-cell malignancy, benefit from accurate pretreatment disease stratification. We curated an extensive database of 862 patients diagnosed between 2014 and 2022. A machine learning (ML) gradient-boosted model incorporated baseline features from clinicopathologic, cytogenetic, and genomic data with high predictive power discriminating between patients with indolent or responsive MCL and those with aggressive disease (AUC ROC = 0.83). In addition, we utilized the gradient-boosted framework as a robust feature selection method for multivariate logistic and survival modeling. The best ML models incorporated features from clinical and genomic data types highlighting the need for correlative molecular studies in precision oncology. As proof of concept, we launched our most accurate and practical models using an application interface, which has potential for clinical implementation. We designated the 20-feature ML model-based index the "integrative MIPI" or iMIPI and a similar 10-feature ML index the "integrative simplified MIPI" or iMIPI-s. The top 10 baseline prognostic features represented in the iMIPI-s are: lactase dehydrogenase (LDH), Ki-67%, platelet count, bone marrow involvement percentage, hemoglobin levels, the total number of observed somatic mutations, TP53 mutational status, Eastern Cooperative Oncology Group performance level, beta-2 microglobulin, and morphology. Our findings emphasize that prognostic applications and indices should include molecular features, especially TP53 mutational status. This work demonstrates the clinical utility of complex ML models and provides further evidence for existing prognostic markers in MCL.

Our model is the first to integrate a dynamic algorithm with multiple clinical and molecular features, allowing for accurate predictions of MCL disease outcomes in a large patient cohort.

Although chimeric antigen receptor (CAR) T cell therapy (CAR-T) has altered the treatment landscape for relapsed/refractory B cell malignancies and multiple myeloma, only a minority of patients attain long-term disease remission. The underlying reasons for CAR-T resistance are multifaceted and can be broadly divided into host-related, tumor-intrinsic, microenvironmental and macroenvironmental, and CAR-T-related factors. Emerging host-related determinants of response to CAR-T relate to gut microbiome composition, intact hematopoietic function, body composition, and physical reserve. Emerging tumor-intrinsic resistance mechanisms include complex genomic alterations and mutations to immunomodulatory genes. Furthermore, the extent of systemic inflammation prior to CAR-T is a potent biomarker of response and reflects a proinflammatory tumor micromilieu characterized by infiltration of myeloid-derived suppressor cells and regulatory T cell populations. The tumor and its surrounding micromilieu also can shape the response of the host to CAR-T infusion and the subsequent expansion and persistence of CAR T cells, a prerequisite for efficient eradication of tumor cells. Here, focusing on both large B cell lymphoma and multiple myeloma, we review resistance mechanisms, explore therapeutic avenues to overcome resistance to CAR-T, and discuss the management of patients who relapse after CAR-T.