From obesity to cancer: a review on proposed mechanisms

Tahergorabi, Zoya; Khazaei, Majid; Moodi, Mitra; Chamani, Elham

doi:10.1002/cbf.3229

Cited by 93 publications

(59 citation statements)

References 176 publications

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“…Furthermore, tumor-derived factors such as islet amyloid polypeptide (IAPP) contribute to both cachexia and the loss of appetite [16,17]. A silent, subclinical (smoldering) inflammation with increased C-reactive protein (CRP), present in many solid tumors and well described in pancreatic cancer [18], also contributes, to a certain degree, to both energy expenditure and loss of appetite; indeed, elevated CRP levels can be used as a marker for cachexia in pancreatic cancer [19] and can even predict a poor prognosis [20]. Finally, as most of the tumors occur in the head of the pancreas, tumor growth results in the obstruction of the main pancreatic duct and the subsequent (complete) reduction of the secretion of pancreatic enzymes during meals.…”

Section: Pathophysiological Considerationsmentioning

confidence: 99%

Pancreatic Exocrine Insufficiency in Pancreatic Cancer

et al. 2017

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Cancer patients experience weight loss for a variety of reasons, commencing with the tumor’s metabolism (Warburg effect) and proceeding via cachexia to loss of appetite. In pancreatic cancer, several other factors are involved, including a loss of appetite with a particular aversion to meat and the incapacity of the pancreatic gland to function normally when a tumor is present in the pancreatic head. Pancreatic exocrine insufficiency is characterized by a deficiency of the enzymes secreted from the pancreas due to the obstructive tumor, resulting in maldigestion. This, in turn, contributes to malnutrition, specifically a lack of fat-soluble vitamins, antioxidants, and other micronutrients. Patients with pancreatic cancer and pancreatic exocrine insufficiency have, overall, an extremely poor prognosis with regard to surgical outcome and overall survival. Therefore, it is crucial to be aware of the mechanisms involved in the disease, to be able to diagnose pancreatic exocrine insufficiency early on, and to treat malnutrition appropriately, for example, with pancreatic enzymes.

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Section: Pathophysiological Considerationsmentioning

confidence: 99%

Pancreatic Exocrine Insufficiency in Pancreatic Cancer

et al. 2017

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“…1 Recently, both clinical and basic science studies have made considerable progress in the therapeutic strategies used in CRC; these currently include surgery, radiotherapy, and, most notably, chemotherapy. [3][4][5][6] Despite its therapeutic benefits, 5-FU has also shown limited efficacy, high resistance, and a low response rate in advanced CRC patients. 2 5-fluorouracil (5-FU) treatment, alone or in combination with other chemical cytotoxic drugs, is among the routinely used standard therapies in CRC.…”

Section: Introductionmentioning

confidence: 99%

Crocin synergistically enhances the antiproliferative activity of 5‐flurouracil through Wnt/PI3K pathway in a mouse model of colitis‐associated colorectal cancer

Amerizadeh

Rezaei

Rahmani

et al. 2018

J of Cellular Biochemistry

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Colorectal cancer (CRC) is the third most common cause of cancer-related death, and hence there is a need for the identification of novel-agents to improve the efficacy of existing therapies. There is growing evidence for the antitumor activity of crocin, although its activity and molecular mechanisms in CRC remains to be elucidated. Here we explored the therapeutic application of crocin or its combination with 5-flurouracil in a mouse model of colitis-associated colon cancer. The antiproliferative activity of crocin was assessed in two-dimensional and three-dimensional cell-culture models. The migratory behaviors were determined, while the expression levels of several genes were assessed by quantitative reverse transcriptase polymerase chain reaction/Western blot analysis. We examined the anti-inflammatory properties of crocin by pathological evaluation and disease-activity index as well as oxidative or antioxidant markers: malondialdehyde (MDA) and total-thiols (T-SH) levels and superoxide dismutase (SOD) and catalase (CAT) activity. Crocin suppressed cell-growth and the invasive behavior of CRC cells through modulation of the Wnt-pathway and E-cadherin. Moreover, administration of crocin alone, or in combination with 5-FU dramatically reduced the tumor number and tumor size in both distal/mid-colon followed by reduction in disease-activity index. Crocin also suppressed the colonic inflammation induced by dextran-sulfate-sodium and notably recovered the increased levels of MDA, decreased thiol levels and activity of CAT levels. Crocin was able to ameliorate the severe inflammation with mucosal ulcers and high-grade dysplastic crypts as detected by inflammation score, crypt loss, pathological changes and histology scores. We demonstrated an antitumor activity of crocin in CRC and its potential role in improvement of inflammation with mucosal ulcers and high-grade dysplastic crypts, supporting the desireability of further investigations on the therapeutic potential of this approach in CRC.

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“…The mechanisms behind the association between adiposity and increased cancer risk are however not fully understood. Current theories include oncogenic effects of chronic inflammation, influence of hormones such as leptin and adiponectin, as well as increased levels of oestrogen and overstimulation of insulin‐ and IGF‐I receptors …”

Section: Discussionmentioning

confidence: 99%

Overweight and obesity during adolescence increases the risk of renal cell carcinoma

Landberg

Fält

Montgomery

et al. 2019

Intl Journal of Cancer

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While overweight among adults has been linked with renal cell carcinoma (RCC) risk, little is known about the potential influence of overweight and obesity during adolescence. To ascertain if adolescent body mass index is associated with subsequent risk of RCC, we identified a cohort of 238,788 Swedish men who underwent mandatory military conscription assessment between 1969 and 1976 at a mean age of 18.5 years. At the time of conscription assessment, physical and psychological tests were performed including measurements of height and weight. Participants were followed through linkage to the Swedish Cancer Registry to identify incident diagnoses of RCC. The association between body mass index (BMI, kg/m2) at conscription assessment and subsequent RCC was evaluated using multivariable Cox regression. During a follow‐up of up to 37 years, 266 men were diagnosed with RCC. We observed a trend for higher RCC risk with increasing BMI during adolescence, where one‐unit increase in BMI conferred a 6% increased risk of RCC (95% CI 1.01–1.10). compared to normal weight men (BMI 18.5‐ < 25), men with overweight (BMI 25‐ < 30) or obesity (BMI ≥30) had hazard ratios for RCC of 1.76 (95% CI 1.16–2.67) and 2.87 (95% CI 1.26–6.25), respectively. The link between overweight/obesity and RCC appear to be already established during late adolescence. Prevention of unhealthy weight gain during childhood and adolescence may thus be a target in efforts to decrease the burden of RCC in the adult population.

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From obesity to cancer: a review on proposed mechanisms

Cited by 93 publications

References 176 publications

Pancreatic Exocrine Insufficiency in Pancreatic Cancer

Pancreatic Exocrine Insufficiency in Pancreatic Cancer

Crocin synergistically enhances the antiproliferative activity of 5‐flurouracil through Wnt/PI3K pathway in a mouse model of colitis‐associated colorectal cancer

Overweight and obesity during adolescence increases the risk of renal cell carcinoma

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