Protective effects of Yerba mate (IIex paraguariensis) on prostate cancer development.

OBJECTIVES: Prostate cancer (PCa) is the most common adenocarcinoma in men >50 y of age. It has a long latency period, which provides time for preventive strategies like incorporating healthy eating habits. Yerba mate (YM) intake has been associated with numerous health benefits. Since YM is one of the most popular infusions in Argentina, the of this study was to examine the influence of YM on PCa development. METHODS: We carried out an in vivo model of PCa through subcutaneous inoculation of transgenic adenocarcinoma of the mouse prostate-C1 cells in C57BL/6 mice. Subsequently, the animals were divided into two groups: mate (25 mg/mL of YM in drinking water, n = 15), and control (only drinking water, n = 15). We also developed an in vitro model to study the direct effects of YM on three human PCa cell lines: lymph node carcinoma of the prostate (LNCaP), PC-3, and DU-145. RESULTS: Our in vivo model showed that YM intake slightly reduced body weight, increased the latency of tumor appearance (P <0.01), and diminished the tumor volume (P <0.05) compared with the control group. In agreement, the expression of proliferating cell nuclear antigen, and nuclear estrogen receptor α were lower in the tumors of the mate animals (P <0.05). In vitro, YM decreased the viability, proliferation, and adhesion of the three tumor cell lines (P < 0.001) and retarded the migration of LNCaP (P <0.05) and DU-145 (P <0.005), without modifying the migration of PC-3 cells. CONCLUSIONS: YM showed anticancer effects in vitro and in vivo and were more effective on the androgen-sensitive cell line (LNCaP).

The epigenetic role of breastfeeding in mammary differentiation.

Maternal milk consumption can cause changes in the mammary epithelium of the offspring that result in the expression of molecules involved in the induction of differentiation, reducing the risk of developing mammary cancer later in life. We previously showed that animals that maintained a higher intake of maternal milk had a lower incidence of mammary cancer. In the present study, we evaluated one of the possible mechanisms by which the consumption of maternal milk could modify the susceptibility to mammary carcinogenesis. We used Sprague Dawley rats reared in litters of 3 (L3), 8 (L8), or 12 (L12) pups per mother in order to generate a differential consumption of milk. Whole mounts of mammary glands were performed to analyze the changes in morphology. Using real-time polymerase chain reaction (PCR), we analyzed the expression of mammary Pinc, Tbx3, Stat6, and Gata3 genes. We use the real-time methylation-specific polymerase chain reaction method to assess the methylation status of Stat6 and Gata3 CpG sites. Our findings show an increase in the size of the epithelial tree and a smaller number of ducts called terminal end buds in L3 vs. L12. We observed an increased expression of mRNA of Stat6, Gata3, Tbx3, and a lower expression of Pinc in L3 with respect to L12. Stat6 and Gata3 are more methylated in the CpG islands of the promoter analyzed in L12 vs. L3. In conclusion, the increased consumption of maternal milk during the postnatal stage generates epigenetic and morphological changes associated with the differentiation of the mammary gland.

[Expression of Hemeoxygenase-1 and clear cell renal cell carcinoma aggressiveness.] / Expresión de Hemo Oxigenasa-1 y agresividad del carcinoma renal de células claras.

OBJECTIVE: Hemoxigenase 1 (HO-1) is an enzyme that has anti-apoptotic and proliferative effects on tumor cells. However, there is little epidemiological and clinical evidence on the role of HO-1 in urologic tumors. OBJECTIVE: To determine if there is correlation between the expression of HO-1 and the histological characteristics, evolution, Disease Free Survival (DFS) and cancer mortality in Clear Cell Renal Cell Carcinoma (cRCC). MATERIALS AND METHODS: A retrospective study including 34 patients (9 women and 25 men) with cRCC from the "Servicio de Urología del Policlínico Neuquén" (Argentina) throughout 2003-2008. The expression of HO-1 by Immunohistochemistry (IHC) was determined. The statistical analysis was performed using the Student'sT test and Pearson correlation coefficient (p≤0.05). RESULTS: HO-1 was expressed in the epithelial cells of the tubules from normal kidney tissue and in the cytoplasmof cRCC tumor cells. There were no differences in the HO-1 expression related to the gender, age, tumorsize, stage of disease and 5 years DFS. High FuhrmancRCC had a greater expression of HO-1 compared with low Fuhrman cRCC (p≤0.05). The score of immunostaining for HO-1 was greater in those tumors located in the mesorrenal area, which coincidentally presented a more advanced stage of the disease. CONCLUSIONS: Over expression of HO-1 in tumors located in the interpolar zone and with high Furhman grade suggest that HO-1 could be a good adjunctive marker for the aggressiveness of the cRCC.

OBJETIVO: Hemoxigenasa 1 (HO-1) es una enzima que tiene efectos antiapoptóticos y proliferativos en células tumorales. Sin embargo, existe poca evidencia epidemiológica y clínica sobre el rol de la HO-1 en los tumores urológicos. Objetivo: determinar si existe correlación entre la expresión de HO-1 y las características histológicas, evolución, Sobrevida Libre de Enfermedad (SLE) y mortalidad por cáncer en Carcinomas Renales de Células Claras (cRCC). MATERIALES Y MÉTODOS: Se realizó un estudio retrospectivo en 34 pacientes (9 mujeres y 25 hombres) con cRCC del Servicio de Urología del Policlínico Neuquén, reclutados entre los años 2003 y 2008. Se determinó la expresión de HO-1 por Inmunohistoquímica (IHQ). El análisis estadístico se realizó mediante la prueba T de Student y Coeficiente de correlación de Pearson (p<0,05). RESULTADOS: HO-1 se expresó en el epitelio de los túbulos del tejido renal normal y en el citoplasma de las células tumorales de cRCC. No se observaron diferencias en la expresión de HO-1 según género, edad, tamaño tumoral, estadio de la enfermedad y SLE a los 5 años. Los tumores con Fuhrman alto presentaron una mayor expresión de HO-1 que los Furhman bajo (p≤0,05). El score de inmunotinción de HO-1 fue mayor en los tumores localizados en la zona interpolar, que coincidentemente presentaban un estadio más avanzado de la enfermedad. CONCLUSIONES: La sobreexpresión de HO-1 en tumores localizados en la zona interpolar y con grado de Furhman alto sugieren que HO-1 podría ser un buen marcador complementario de la agresividad del cRCC.

Expresión de Hemo Oxigenasa-1 y agresividad del carcinoma renal de células claras / Expression of Hemeoxygenase-1 and clear cell renal cell carcinoma aggressiveness

OBJETIVO: Hemoxigenasa 1 (HO-1) es una enzima que tiene efectos antiapoptóticos y proliferativos en células tumorales. Sin embargo, existe poca evidencia epidemiológica y clínica sobre el rol de la HO-1 en los tumores urológicos. OBJETIVO: determinar si existe correlación entre la expresión de HO-1 y las características histológicas, evolución, Sobrevida Libre de Enfermedad (SLE) y mortalidad por cáncer en Carcinomas Renales de Células Claras (cRCC). MATERIALES Y MÉTODOS: Se realizó un estudio retrospectivo en 34 pacientes (9 mujeres y 25 hombres) con cRCC del Servicio de Urología del Policlínico Neuquén, reclutados entre los años 2003 y 2008. Se determinó la expresión de HO-1 por Inmunohistoquímica (IHQ). El análisis estadístico se realizó mediante la prueba T de Student y Coeficiente de correlación de Pearson (p < 0,05). RESULTADOS: HO-1 se expresó en el epitelio de los túbulos del tejido renal normal y en el citoplasma de las células tumorales de cRCC. No se observaron diferencias en la expresión de HO-1 según género, edad, tamaño tumoral, estadio de la enfermedad y SLE a los 5 años. Los tumores con Fuhrman alto presentaron una mayor expresión de HO-1 que los Furhman bajo (p≤0,05). El score de inmunotinción de HO-1 fue mayor en los tumores localizados en la zona interpolar, que coincidentemente presentaban un estadio más avanzado de la enfermedad. CONCLUSIONES: La sobreexpresión de HO-1 en tumores localizados en la zona interpolar y con grado de Furhman alto sugieren que HO-1 podría ser un buen marcador complementario de la agresividad del cRCC

OBJECTIVE: Hemoxigenase 1 (HO-1) is an enzyme that has anti-apoptotic and proliferative effects on tumor cells. However, there is little epidemiological and clinical evidence on the role of HO-1 in urologic tumors. OBJECTIVE: To determine if there is correlation between the expression of HO-1 and the histological characteristics, evolution, Disease Free Survival (DFS) and cancer mortality in Clear Cell Renal Cell Carcinoma (cRCC). MATERIALS AND METHODS: A retrospective study including 34 patients (9 women and 25 men) with cRCC from the "Servicio de Urología del Policlínico Neuquén" (Argentina) throughout 2003-2008. The expression of HO-1 by immunohistochemistry (IHC) was determined. The statistical analysis was performed using the Student's T test and Pearson correlation coefficient (p≤0.05). RESULTS: HO-1 was expressed in the epithelial cells of the tubules from normal kidney tissue and in the cytoplasm of cRCC tumor cells. There were no differences in the HO-1 expression related to the gender, age, tumor size, stage of disease and 5 years DFS. High Fuhrman cRCC had a greater expression of HO-1 compared with low Fuhrman cRCC (p≤0.05). The score of immunostaining for HO-1 was greater in those tumors located in the mesorrenal area, which coincidentally presented a more advanced stage of the disease. CONCLUSIONS: Overexpression of HO-1 in tumors located in the interpolar zone and with high Furhman grade suggest that HO-1 could be a good adjunctive marker for the aggressiveness of the cRCC

Human renal adipose tissue induces the invasion and progression of renal cell carcinoma.

We evaluated the effects of conditioned media (CMs) of human adipose tissue from renal cell carcinoma located near the tumor (hRATnT) or farther away from the tumor (hRATfT), on proliferation, adhesion and migration of tumor (786-O and ACHN) and non-tumor (HK-2) human renal epithelial cell lines. Human adipose tissues were obtained from patients with renal cell carcinoma (RCC) and CMs from hRATnT and hRATfT incubation. Proliferation, adhesion and migration were quantified in 786-O, ACHN and HK-2 cell lines incubated with hRATnT-, hRATfT- or control-CMs. We evaluated versican, adiponectin and leptin expression in CMs from hRATnT and hRATfT. We evaluated AdipoR1/2, ObR, pERK, pAkt y pPI3K expression on cell lines incubated with CMs. No differences in proliferation of cell lines was found after 24 h of treatment with CMs. All cell lines showed a significant decrease in cell adhesion and increase in cell migration after incubation with hRATnT-CMs vs. hRATfT- or control-CMs. hRATnT-CMs showed increased levels of versican and leptin, compared to hRATfT-CMs. AdipoR2 in 786-O and ACHN cells decreased significantly after incubation with hRATfT- and hRATnT-CMs vs. control-CMs. We observed a decrease in the expression of pAkt in HK-2, 786-O and ACHN incubated with hRATnT-CMs. This result could partially explain the observed changes in migration and cell adhesion. We conclude that hRATnT released factors, such as leptin and versican, could enhance the invasive potential of renal epithelial cell lines and could modulate the progression of the disease.

Effects of parity and serum prolactin levels on the incidence and regression of DMBA-induced tumors in OFA hr/hr rats.

Prolactin (PRL) is a key player in the development of mammary cancer. We studied the effects of parity or hyperprolactinemia on mammary carcinogenesis in OFA hr/hr treated with 7,12-dimethylbenzanthracene. They were divided into three groups: nulliparous (Null), primiparous (PL, after pregnancy and lactation), and hyperprolactinemic rats (I, implanted in the arcuate nucleus with 17ß-estradiol). The tumor incidence was similar in the three groups. However, a higher percentage of regressing tumors was evident in the PL group. Serum PRL, mammary development, and mammary ß-casein content were higher in I rats compared to Null. The expression of hormone receptors was similar in the different groups. However, mammary tissue from PL rats bearing tumors had increased expression of PRL and estrogen alpha receptors compared to rats free of tumors. Our results suggest that serum PRL levels do not have relevance on the incidence of tumors, probably because the low levels of PRL in OFA rats are not further decreased by PL like in other strains. However, supraphysiological levels of PRL affect carcinogenesis. PL induces regression of the tumors due to the differentiation produced on the mammary cells. Alterations in the expression of hormonal receptors may be involved in progression and regression of tumors.

The inhibitory effect of progesterone on lactogenesis during pregnancy is already evident by mid- to late gestation in rodents.

Lactogenesis is a very complex process highly dependent on hormonal regulation. In the present study the time-course of the inhibitory actions of progesterone on prolactin secretion, mammary gland morphology and lactogenesis from mid- to late gestation in rodents was investigated. Groups of pregnant rats were luteectomised or administered with mifepristone on Day 10, 13, 15 or 17 of gestation and decapitated 28 or 48h later. Whole-blood samples and the inguinal mammary glands were taken for determinations of hormone levels and for measurement of mammary content of casein and lactose and for tissue morphology analyses, respectively. Luteectomy or mifepristone evoked prolactin increases only after Day 17 of gestation. Mammary content of casein was increased by both treatments regardless of timing or duration. Mifepristone was less effective than luteectomy in inducing lactose production and the effect was only observed after Day 15 of gestation. Analysis of mammary gland morphology confirmed the observed effect of progesterone on lactogenesis. Both treatments triggered remarkable secretory activity in the mammary gland, even without a parallel epithelial proliferation, demonstrating that the mammary epithelium is able to synthesise milk compounds long before its full lobulo-alveolar development is achieved, provided that progesterone action is abolished. Thus, the present study demonstrates that progesterone is a potent hormonal switch for the prolactin and prolactin-like effects on mammary gland development and its milk-synthesising capacity during pregnancy, and that its inhibitory action is already evident by mid-pregnancy in rodents.

Leptin increases prostate cancer aggressiveness

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Recent studies indicate that adipose tissue and adipocytokines might affect the development of prostate cancer (PCa). Leptin would have a stimulating effect on prostate cancer cells by inducing promotion and progression, whereas adiponectin would have a protective effect. The aim of this study was to determine the relation between body composition, leptin, and adiponectin levels with the prevalence and aggressiveness of PCa in men of Mendoza, Argentina. Seventy volunteers between 50 and 80 years (35 healthy men as control group and 35 with PCa) were selected. The PCa group was subclassified according to the Gleason Score (GS). Digital rectal examination, transrectal ultrasound, and prostatic biopsy were performed; PSA, testosterone, leptin, and adiponectin levels were determined; and a nutritional interview including anthropometric measurements and a food frequency questionnaire was carried out. Statistical analysis was performed by Student t test, ANOVA I, and Bonferroni (p < 0.05). Body mass index and percentage of body fat mass were not statistically different between PCa and control groups. However, body fat mass was higher in subjects with more aggressive tumors (p = 0.032). No differences were observed regarding leptin levels between the groups. Nevertheless, leptin levels were higher in subjects with high GS (p < 0.001). Adiponectin levels showed no statistical differences regarding the presence and aggressiveness of the tumor (p = 0.131). Finally, consumption and nutrient intake did not differ in the studied groups. In conclusion, body composition and leptin are related to the PCa aggressiveness but not with its prevalence (AU)

Regulation of prolactin secretion during the estrus in rats: possible role of glucocorticoids.

Mifepristone (MIF) administration to cycling rats at proestrus induces hypersecretion of prolactin (PRL) at the following estrus. We aimed to assess whether this effect is due to the antiprogesterone or antiglucocorticoid action of MIF and to help underscore the nature of the circulating hormone(s) regulating PRL secretion at estrus. Female cycling rats in proestrus were treated with vehicle; the progesterone (Pg) and glucocorticoid receptor antagonists, MIF (5 mg/kg) or ORG-33628 (5 mg/kg); the glucocorticoid agonist dexamethasone (DEX; 27 mg/kg)±MIF; or the inhibitor of steroid synthesis aminoglutethimide (AG; 150 mg/kg)±MIF. The animals' blood was sampled the same day at 1800 h and at 1800 h of the following day to assess for circulating PRL and Pg levels. To distinguish antiglucocorticoid from antiprogesterone effects of MIF, we administered a highly specific neutralizing antibody against Pg. None of the antagonists modified serum PRL values at proestrus but increased PRL levels at estrus. DEX decreased the secretion of PRL at proestrus, yet the effect was entirely blocked by MIF. Furthermore, DEX decreased PRL at estrus in a MIF-reversible manner, suggesting that adrenal corticoids during proestrous may regulate PRL secretion at estrus. AG increased PRL secretion at estrus, whereas its association with MIF produced an even higher response. PRL concentration at estrus was not modified by the antiprogesterone antibody, suggesting that the effect of MIF is a consequence of its antiglucocorticoid effect and not due to its antiprogesterone properties. In conclusion, PRL secretion in the afternoon of the estrus is most likely regulated by glucocorticoids through an inhibitory action.

Leptin increases prostate cancer aggressiveness.

Recent studies indicate that adipose tissue and adipocytokines might affect the development of prostate cancer (PCa). Leptin would have a stimulating effect on prostate cancer cells by inducing promotion and progression, whereas adiponectin would have a protective effect. The aim of this study was to determine the relation between body composition, leptin, and adiponectin levels with the prevalence and aggressiveness of PCa in men of Mendoza, Argentina. Seventy volunteers between 50 and 80 years (35 healthy men as control group and 35 with PCa) were selected. The PCa group was subclassified according to the Gleason Score (GS). Digital rectal examination, transrectal ultrasound, and prostatic biopsy were performed; PSA, testosterone, leptin, and adiponectin levels were determined; and a nutritional interview including anthropometric measurements and a food frequency questionnaire was carried out. Statistical analysis was performed by Student t test, ANOVA I, and Bonferroni (p < 0.05). Body mass index and percentage of body fat mass were not statistically different between PCa and control groups. However, body fat mass was higher in subjects with more aggressive tumors (p = 0.032). No differences were observed regarding leptin levels between the groups. Nevertheless, leptin levels were higher in subjects with high GS (p < 0.001). Adiponectin levels showed no statistical differences regarding the presence and aggressiveness of the tumor (p = 0.131). Finally, consumption and nutrient intake did not differ in the studied groups. In conclusion, body composition and leptin are related to the PCa aggressiveness but not with its prevalence.

[Body mass index and diet affect prostate cancer development]. / El indice de masa corporal y la dieta afectan el desarrollo del cancer de próstata.

INTRODUCTION: Prostate cancer (CaP) is one of the most important causes of morbidity and mortality in the world. There is evidence that obesity and inadequate eating habits may promote CaP development. OBJECTIVE: To analyze and compare the body mass index (BMI) and the food intake, especially fats and antioxidants, among subjects with CaP and those free of disease as a control group. MATERIAL AND METHODS: A sample of 40 men between 50 and 80 years old were selected for the study: 20 with CaP and 20 healthy men as control group. All volunteers underwent a digital rectal examination, prostate specific antigen level, ultrasound and transrectal prostate biopsy, and a nutritional interview where a dietary history and different anthropometric measurements were made. Statistical analysis was performed using the Student T test for independent samples (p < 0.05). RESULTS: BMI in the subjects with CaP was higher than in controls (29.8 kg/m2 vs. 27.96 kg/m2, p = 0.13) but not statistically significant. However, there was a direct correlation between BMI and tumor aggressiveness (r = 0.79, P < 0.001). Total, saturated, monounsaturated and polyunsaturated fat intake was significantly higher in subjects with CaP; while omega3 fatty acids, vitamin C and lycopene intake was significantly lower than in controls (p < 0.05). CONCLUSIONS: A healthy weight and a diet low in total fat, saturated, monounsaturated and polyunsaturated fat and rich in n3 fatty acids, vitamin C and lycopene is associated with a lower risk of CaP.

El índice de masa corporal y la dieta afectan el desarrollo del cáncer de próstata / Body mass index and diet affect prostate cancer development

Introducción: El adenocarcinoma de próstata (CaP) es una de las causas más importantes de morbimortalidad en el mundo. La obesidad y los hábitos alimentarios inadecuados favorecerían el desarrollo del CaP. Objetivo: Analizar y comparar el índice de masa corporal (IMC) y la historia alimentaria, especialmente el consumo de grasas y antioxidantes, entre sujetos con CaP diagnosticado y sujetos libres de enfermedad. Material y Métodos: fueron seleccionados 40 hombres entre 50 y 80 años: 20 con cáncer de próstata diagnosticado y 20 libres de enfermedad como grupo control, a los cuales se les realizó tacto rectal, medición de antígeno prostático específico, ecografía transrectal y biopsia ecodirigida de próstata; y una entrevista nutricional que incluyó una historia dietética detallada y mediciones antropométricas. El análisis estadístico se realizó mediante Test de Student para muestras independientes (p<0,05).Resultados: El IMC en los sujetos con CaP fue superior que en los controles (29,8kg/m2 vs. 27,96kg/m2; p=0,13) aunque estadísticamente no significativo. Sin embargo, se observó una correlación directa entre el IMC y la agresividad del tumor (r=0,79; p<0.001). El consumo de grasas totales, saturadas, monoinsaturadas y poliinsaturadas fue significativamente mayor en los sujetos con CaP (p=0,001); mientras que la ingesta de ácidos grasos ω3, vitamina C y licopeno fue significativamente menor independientemente del Score de Gleason que presentasen (p<0,05).Conclusiones: Un peso saludable y una alimentación baja en grasas totales, saturadas, monoinsaturadas y poliinsaturadas y rica en ácidos grasos ω3, vitamina C y licopeno se asocia a un menor riesgo de CaP (AU)

Introduction: Prostate cancer (CaP) is one of the most important causes of morbidity and mortality in the world. There is evidence that obesity and inadequate eating habits may promote CaP development. Objective: To analyze and compare the body mass index (BMI) and the food intake, especially fats and antioxidants, among subjects with CaP and those free of disease as a control group. Material and Methods: A sample of 40 men between 50 and 80 years old were selected for the study: 20 with CaP and 20 healthy men as control group. All volunteers underwent a digital rectal examination, prostate specific antigen level, ultrasound and transrectal prostate biopsy, and a nutritional interview where a dietary history and different anthropometric measurements were made. Statistical analysis was performed using the Student T test for independent samples (p <0.05). Results: BMI in the subjects with CaP was higher than in controls (29.8 kg/m2 vs. 27.96 kg/m2, p = 0.13) but not statistically significant. However, there was a direct correlation between BMI and tumor aggressiveness (r = 0.79, P <0.001). Total, saturated, monounsaturated and polyunsaturated fat intake was significantly higher in subjects with CaP; while ω3 fatty acids, vitamin C and lycopene intake was significantly lower than in controls (p <0.05).Conclusions: A healthy weight and a diet low in total fat, saturated, monounsaturated and polyunsaturated fat and rich in ω3 fatty acids, vitamin C and lycopene is associated with a lower risk of CaP (AU)

[Influence of leptin and adiponectin on prostate cancer]. / Influencia de la leptina y adiponectina en el cáncer de próstata.

BACKGROUND: Many studies have investigated the association between obesity, adipose tissue-derived factors (leptin and adiponectin) and prostate cancer (CaP) but the results are still inconsistent. METHODS: The aim of this study was to carry out a comprehensive review of the existing evidence about the role of leptin and adiponectin in prostate carcinogenesis and to provide an overview of it. RESULTS: Recent evidence suggests that leptin may play a rol in prostate cancer progression, while adiponectin may act as an "antiprostatic cancer" adipokine. CONCLUSIONS: Obesity may promote the progression of established prostate cancer and and adipokines may provide a molecular mechanism whereby obesity exerts its effects on prostate tumour biology.

Influencia de la Leptina y adiponectina en el cáncer de próstata / Influence of leptin and adiponectin on prostate cancer

OBJETIVO: Numerosos estudios han investigado la asociación entre la obesidad, las sustancias secretadas por el tejido adiposo (leptina y adiponectina) y el cáncer de próstata (CaP), aunque los resultados no han sido concluyentes. El objetivo del presente trabajo es realizar una revisión bibliográfica sobre el rol de la leptina y la adiponectina en el desarrollo del CaP.MÉTODOS: Se realizó una búsqueda bibliográfica y lectura compresiva de artículos relacionados con “leptina”, “adiponectina”, “obesidad” y “cáncer de próstata” en Pubmed y revistas científicas; y se efectuó una breve descripción sobre el tema.RESULTADOS: Estudios recientes indican que el tejido adiposo y las diferentes sustancias que éste secreta, denominadas adipoquinas, podrían promover o prevenir el desarrollo del CaP. La leptina tendría un efecto promotor del tumor; mientras que la adiponectina tendría un efecto protector.CONCLUSIÓN: La obesidad podría influenciar la carcinogénesis prostática mediante un mecanismo molecular en el que participarían las adipoquinas(AU)

OBJECTIVES: Many studies have investi-gated the association between obesity, adipose tissue-derived factors (leptin and adiponectin) and prostate cancer (CaP) but the results are still inconsistent.METHODS: The aim of this study was to carry out a comprehensive review of the existing evidence about the role of leptin and adiponectin in prostate carcinoge-nesis and to provide an overview of it.RESULTS: Recent evidence suggests that leptin may play a rol in prostate cancer progression, while adiponectin may act as an “anti- prostatic cancer” adipokine.CONCLUSIONS: Obesity may promote the progression of established prostate cancer and and adipokines may provide a molecular mechanism whereby obesity exerts its effects on prostate tumour biology(AU)