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1.
  相似文献   

2.

Background:

The potential of an increased risk of breast cancer in women with diabetes has been the subject of a great deal of recent research.

Methods:

A meta-analysis was undertaken using a random effects model to investigate the association between diabetes and breast cancer risk.

Results:

Thirty-nine independent risk estimates were available from observational epidemiological studies. The summary relative risk (SRR) for breast cancer in women with diabetes was 1.27 (95% confidence interval (CI), 1.16–1.39) with no evidence of publication bias. Prospective studies showed a lower risk (SRR 1.23 (95% CI, 1.12–1.35)) than retrospective studies (SRR 1.36 (95% CI, 1.13–1.63)). Type 1 diabetes, or diabetes in pre-menopausal women, were not associated with risk of breast cancer (SRR 1.00 (95% CI, 0.74–1.35) and SRR 0.86 (95% CI, 0.66–1.12), respectively). Studies adjusting for body mass index (BMI) showed lower estimates (SRR 1.16 (95% CI, 1.08–1.24)) as compared with those studies that were not adjusted for BMI (SRR 1.33 (95% CI, 1.18–1.51)).

Conclusion:

The risk of breast cancer in women with type 2 diabetes is increased by 27%, a figure that decreased to 16% after adjustment for BMI. No increased risk was seen for women at pre-menopausal ages or with type 1 diabetes.  相似文献   

3.
  总被引：2，自引：0，他引：2  
Associations between childhood BMI and adult cancer risk were investigated in a historical cohort study based on the Carnegie (\"Boyd Orr\") Survey of Diet and Health in Pre-War Britain (1937-9). In 14 centres in England and Scotland, children had their height and weight measured. We included 2,347 individuals aged between 2 and 14 years 9 months at the time of measurement, who were traced through the National Health Service Central Register. Relative cancer risk (registration or death) was estimated in relation to age- and sex-specific BMI SD scores. We studied associations with (i) all cancers, (ii) cancer groups stratified according to their relationship to smoking and (iii) certain site-specific cancers. In the 50 years of follow-up, 188 men and 192 women developed cancer. There was a 9% increase (95% CI -3 to 22%) in risk of cancer in adulthood per SD increase in BMI measured in childhood. There was no evidence of confounding by childhood or adulthood socioeconomic position, other anthropometric variables, childhood energy intake or birth order. There was a 30% increase (95% CI 10-54%) in risk of smoking-related cancers per SD increase in childhood BMI. There was no relationship between BMI and cancers not related to smoking. Associations for all cancers and non-smoking-related cancers tended to be stronger in children who were measured at an older (>8 years) rather than a younger (< or =8 years) age. We conclude that childhood BMI is related to increased risk of cancer in later life, particularly smoking-related cancers.  相似文献   

4.
摘 要：［目的］ 探讨营养风险及身体质量指数（BMI）与老年早期食管癌放疗患者预后的关系。［方法］ 收集2011年7月至2014年12月于连云港市第二人民医院接受根治性放疗的41例≥70岁、Ⅰ/Ⅱ,N0期食管鳞癌患者临床资料。应用营养风险筛查工具2002（NRS-2002）行营养风险评估,营养风险定义为NRS-2002评分≥3分。分析NRS-2002评分与食管癌患者临床资料的关系,Kaplan-Meier法计算生存率并Log-rank检验差异,Cox比例风险模型进行多因素分析。［结果］ 27例患者（65.85%）放疗前存在营养风险。营养风险患者营养支持治疗前后血清白蛋白水平有统计学差异（P=0.0127）。NRS-2002评分与血清白蛋白水平及BMI有关（P＜0.05）。单因素分析显示肿瘤长度≥6cm 、BMI<18.5kg/m2、NRS-2002评分≥3分是食管癌放疗患者预后不良因素（P＜0.05）。多因素生存分析显示NRS-2002评分及BMI是食管癌放疗患者总生存时间的独立预后因素（P＜0.05）。［结论］ 营养风险及消瘦可作为预测老年早期食管癌放疗患者的预后不良指标。  相似文献   

5.

BACKGROUND:

Convincing epidemiologic evidence links excess body mass to increased risks of endometrial and postmenopausal breast cancers, but the relation between body mass index (BMI) and ovarian cancer risk remains inconclusive. Potential similarities regarding a hormonal mechanism in the etiology of female cancers highlight the importance of investigating associations according to menopausal hormone therapy (MHT) use. However, to the authors' knowledge, data addressing whether the relation between BMI and ovarian cancer differs by MHT use are very sparse.

METHODS:

The authors prospectively investigated the association between BMI and ovarian cancer among 94,525 US women who were followed between 1996 through 1997 to December 31, 2003. During 7 years of follow‐up, 303 epithelial ovarian cancer cases were documented.

RESULTS:

Compared with normal weight women (BMI of 18.5‐24.9 kg/m2), the multivariate relative risk (MVRR) of ovarian cancer for obese women (BMI of ≥30 kg/m2) in the cohort as a whole was 1.26 (95% confidence interval [95% CI], 0.94‐1.68). Among women who never used MHT, the MVRR for obese versus normal weight women was 1.83 (95% CI, 1.18‐2.84). In contrast, no relation between BMI and ovarian cancer was apparent among women who ever used MHT (MVRR = 0.96; 95% CI, 0.65‐1.43; P interaction = 0.02). Exploratory analyses also suggested a positive association between BMI and ovarian cancer among women without a family history of ovarian cancer (MVRR comparing obese vs normal weight women = 1.36; 95% CI, 1.00‐1.86), but no relation with BMI was apparent among women with a positive family history of ovarian cancer (MVRR = 0.74; 95% CI, 0.34‐1.62 [P interaction = .02]).

CONCLUSIONS:

Based on the results of the current study, the authors suspect that obesity is associated with enhanced ovarian cancer risk through a hormonal mechanism. Cancer 2009. Published 2009 by the American Cancer Society.  相似文献   

6.
    
The relationship between two measures of excess body weight, body mass index (BMI) and body size score, and risk of pancreatic cancer was examined among 574 pancreatic cancer cases and 596 frequency-matched controls from the Czech Republic and Slovakia enrolled between 2004 and 2009. Analyses using multivariable logistic regression showed an increased risk of pancreatic cancer associated with elevated quartiles of BMI at ages 20 [fourth quartile: odds ratio (OR) = 1.79, 95% confidence interval (CI): 1.23, 2.61] and 40 (fourth quartile: OR = 1.57, 95% CI: 1.09, 2.27) compared to the lowest quartile. Consistent results were observed for body size score at ages 20 (high versus low: OR = 1.66, 95% CI: 1.08, 2.57) and 40 (medium versus low: OR = 1.36, 95% CI: 1.00, 1.86), but no association was found for BMI and body size score at 2 years before the interview. Stronger risk estimates for BMI were observed in males than females, particularly at age 20, but the analysis of body size yielded similar estimates by sex. When considering excess body weight at both ages 20 and 40 jointly, the highest risk estimates were observed among subjects with elevated levels at both time periods in the analysis of BMI (OR = 1.86, 95% CI: 1.32, 2.62) and body size (OR = 1.53, 95% CI: 1.09, 2.13). These findings, based on two different measures, provide strong support for an increased risk of pancreatic cancer associated with excess body weight, possibly strongest during early adulthood.  相似文献   

7.
OBJECTIVE: Estrogen plays a central role in breast cancer. It has been suggested that many known breast cancer risk factors may exert their effect via levels of endogenous sex hormones. The objective of this analysis is to evaluate the association between measures of body size, dietary macronutrient intake, and reproductive factors with levels of endogenous sex hormones among women living in Shanghai, China. METHODS: Included in this study were 420 post-menopausal healthy women randomly selected from the general population as controls who participated in the Shanghai Breast Cancer Study, a population-based case-control study conducted in Shanghai, China between 1996 and 1998. Comprehensive dietary and reproductive information was collected using a structured questionnaire during an in-person interview and anthropometrics were measured by trained interviewers according to a standard protocol. Hormone levels were log-transformed and Pearson correlation coefficients were calculated to determine the correlation between hormone levels and selected breast cancer risk factors. RESULTS: Measures of body size were strongly correlated with hormone levels. In particular, weight, waist circumference, and hip circumference were significantly positively correlated (p < 0.05) with levels of testosterone, estradiol, estrone, and significantly negatively correlated with sex hormone binding globulin. Macronutrient intake and reproductive factors were not correlated with endogenous sex hormone levels. CONCLUSIONS: These data suggest that breast cancer risk associated with measures of body size may be mediated, at least partially, by levels of endogenous sex hormones.  相似文献   

8.
摘 要： ［目的］ 应用欧洲营养筛查方法(NRS 2002) 分析胃癌患者营养风险。［方法］ 收集胃癌患者82例,患者入院48h进行营养风险筛查,采用NRS2002评估表进行评分。NRS2002总分≥3分为存在营养风险。［结果］ 在82例住院胃癌患者中,NRS 2002 营养风险筛查评分为(2.51±1.08)分,NRS2002≥3分24例,营养风险发生率为29.3%。随着患者临床分期的升高,营养风险发生率随之升高,Ⅰ期患者营养风险发生率为5.9%,而Ⅳ期患者的营养风险发生率为57.1%。营养风险发生率与患者的年龄、居住地和医疗费用相关。营养不良者（BMI＜18.5kg/m2）发生营养风险发生率为100%,但25.9%（14/54）患者的BMI 虽处于正常范围仍存在营养风险。NRS 2002≥3分存在营养风险的患者平均住院天数为(14.4±9.2)d,明显长于NRS 2002＜3分无营养风险的患者的(9.0±4.8)d (P＝0.041)。［结论］ NRS2002 对住院患者营养风险和营养支持率的调查可有效鉴别住院患者的营养风险,并为营养支持提供依据。  相似文献   

9.
    
Excess weight has been associated with increased risk of cancer. The effect of body mass index (BMI, kg/m(2)) on overall cancer risk and on risk of developing several common cancer types was examined in a population-based cohort study. Height and weight measurements were available for 35,362 women and 33,424 men recruited in the Northern Sweden Health and Disease Cohort between 1985 and 2003. Among cohort members, 2,691 incident cancer cases were identified. The association of BMI with cancer risk was examined using Poisson regression. Women with BMI > 27.1 (top quartile) had a 29% higher risk of developing any malignancy compared to women with BMI of 18.5-22.2 (lowest quartile), which increased to 47% in analysis limited to nonsmokers. Analyses according to WHO cut-off points showed that obese women (BMI > or = 30) had a 36% higher risk of cancer than women with BMI in the normal range (18.5-25). Individual cancer sites most strongly related to obesity were endometrium (risk for top quartile = 3.53, 95% confidence interval 1.86-7.43), ovary (2.09, 1.13-4.13) and colon (2.05, 1.04-4.41). BMI was inversely related to breast cancer occurring before age 49 (0.58, 0.29-1.11, p(trend) < 0.04). In men, there was no association of BMI with overall cancer risk. Obese men (BMI > or = 30), however, were at increased risk of developing kidney cancer (3.63, 1.23-10.7) and, after exclusion of cases diagnosed within 1 year of recruitment, colon cancer (1.77, 1.04-2.95). Our study provides further evidence that BMI is positively associated with cancer risk. In women from northern Sweden, up to 7% of all cancers were attributable to overweight and obesity and could be avoided by keeping BMI within the recommended range.  相似文献   

10.
    
The influence of body size on postmenopausal breast cancer risk was investigated among five racial/ethnic groups in the Multiethnic Cohort. Participants were 45-75 years old at recruitment (1993-1996), living in Hawaii and California. Of the 82,971 White, African American, Native Hawaiian, Japanese and Latina women included in this analysis, 3,030 were diagnosed with invasive breast cancer. Body mass index (BMI), height, weight and adulthood weight gain were associated with a significantly higher risk and, with the exception of height, were found to vary across ethnic groups. Native Hawaiians and Japanese with a BMI≥30.0 compared to 20.0-24.9 kg/m2 had the highest risk (hazard ratio=1.82, 95% confidence interval: 1.31, 2.54, p-trend=0.001, and hazard ratio=1.59, 95% confidence interval: 1.24, 2.05, p-trend<0.0001, respectively). Current hormone replacement therapy use modified the impact of a high BMI, as non- and former users had a significantly higher risk compared to current users. BMI also had a more pronounced risk for advanced tumors compared to localized tumors. When both BMI and adult weight gain were analyzed simultaneously, adult weight gain, rather than BMI, was a significant risk factor overall. These findings emphasize the significance of maintaining a healthy weight throughout adulthood for the prevention of postmenopausal breast cancer.  相似文献   

11.
    
The cyclooxygenase 2 (COX‐2) pathway is upregulated in many pancreatic cancer cells, and it is believed that carcinogenetic effects of COX‐2 upregulation are largely through prostaglandin E2 (PGE2) overproduction. We tested this hypothesis by evaluating the association between urinary PGE2 metabolites (PGE‐M), a biomarker of in vivo PGE2 overproduction, and pancreatic cancer risk. We conducted a case–control study with 722 subjects (239 cases and 483 controls) nested within two prospective cohort studies, the Shanghai Women's Health Study (SWHS) and Shanghai Men's Health Study (SMHS). Pre‐diagnosis urine samples were measured for PGE‐M using a liquid chromatography/tandem mass spectrometric method. Conditional logistic regression was used to estimate odds ratio (OR) and 95% confidence intervals (95%CI), with adjustment for potential confounders. Compared to those with the lowest urine level of PGE‐M (the first quartile), individuals with higher urine levels of PGE‐M had an increased risk of developing pancreatic cancer, with adjusted ORs (95%CI) of 1.63 (0.98–2.73), 1.55 (0.90–2.69) and 1.94 (1.07–3.51), for the second to the fourth quartile groups, respectively (p for trend = 0.054). This dose–response positive association was more evident among those who had BMI <25 kg/m2 than overweight individuals (p for interaction = 0.058). After excluding cases diagnosed in the first year of follow‐up and their matched controls, this positive association persisted (p for trend = 0.037) and the interaction became statistically significant (p for interaction = 0.017). Our study adds additional evidence that the COX‐2 pathway is involved in pancreatic carcinogenesis and suggests that urinary PGE‐M may serve as a biomarker for predicting pancreatic cancer risk.  相似文献   

12.
    
Epidemiological evidence indicates that the association between body weight and breast cancer risk may differ across menopausal status as well as the estrogen receptor (ER) and progesterone receptor (PR) tumor status. To date, no meta-analysis has been conducted to assess the association between body weight and ER/PR defined breast cancer risk, taking into account menopausal status and study design. We searched MEDLINE for relevant studies published from January 1, 1970 through December 31, 2007. Summarized risk estimates with 95% confidence intervals (CIs) were calculated using a random-effects model. The summarized results of 9 cohorts and 22 case-control studies comparing the highest versus the reference categories of relative body weight showed that the risk for ER+PR+ tumors was 20% lower (95% CI=-30% to -8%) among premenopausal (2,643 cases) and 82% higher (95% CI=55-114%) among postmenopausal (5,469 cases) women. The dose-response meta-analysis of ER+PR+ tumors showed that each 5-unit increase in body mass index (BMI, kg/m2) was associated with a 33% increased risk among postmenopausal women (95% CI=20-48%) and 10% decreased risk among premenopausal women (95% CI=-18% to -1%). No associations were observed for ER-PR- or ER+PR- tumors. For discordant tumors ER+PR- (pre) and ER-PR+ (pre/post) the number of cases were too small (<200) to interpret results. The relation between body weight and breast cancer risk is critically dependent on the tumor's ER/PR status and the woman's menopausal status. Body weight control is the effective strategy for preventing ER+PR+ tumors after menopause.  相似文献   

13.
    
Although adult obesity is known to increase endometrial cancer risk, evidence for childhood obesity is limited. We prospectively examined the association between body fatness throughout life and endometrial cancer risk. 47,289 participants in the Nurses' Health Study (NHS) and 105,386 of the Nurses' Health Study II (NHS II) recalled their body fatness at ages 5, 10 and 20 using a pictogram. Childhood and adolescent body fatness were derived as the average at ages 5 and 10 and ages 10 and 20, respectively. We obtained adult weight from concurrent questionnaires. We calculated hazard ratios (HR) of endometrial cancer using Cox proportional hazards models. During follow‐up, 757 incident cases of endometrial cancer were diagnosed. Body fatness in childhood, at age 10, in adolescence and at age 20 were positively associated with endometrial cancer risk (HR for ≥ Level 5 versus ≤ Level 2 in adolescence: 1.83 (95% CI 1.41–2.37). After adjusting for most recent BMI, none of the associations persisted. Weight change since age 18 was positively associated with endometrial cancer risk [HR for ≥ 25 kg gain versus stable: 2.54 (95% CI 1.80–3.59). Adult BMI was strongly associated with endometrial cancer risk [HR BMI ≥ 35 kg/m2 versus BMI ≤ 25 kg/m2: 4.13 (95% CI 3.29–5.16)]. In postmenopausal women, the association with BMI was significantly stronger among non‐users of hormone therapy. In conclusion, obesity throughout life is positively associated with endometrial cancer risk, with adult obesity one of the strongest risk factors. Maintaining a healthy weight throughout life remains important.  相似文献   

14.
    
Obesity later in adulthood is associated with increased risks of many cancers. However, the effect of body fatness in early adulthood, and change in weight from early to later adulthood on cancer risk later in life is less clear. We used data from 13,901 people aged 45–64 in the Atherosclerosis Risk in Communities cohort who at baseline (1987–1989) self‐reported their weight at the age of 25 and had weight and height measured. Incident cancers were identified through 2006 and cancer deaths were ascertained through 2009. Multivariable Cox proportional hazard models were used to relate body mass index (BMI) at age 25 and percent weight change from age 25 to baseline to cancer incidence and mortality. After adjusting for weight change from age 25 until baseline, a 5 kg/m2 increment in BMI at age 25 was associated with a greater risk of incidence of all cancers in women [hazard ratio (95% confidence interval): 1.10 (1.02–1.20)], but not in men. Associations with incident endometrial cancer were strong [1.83 (1.47–2.26)]. After adjusting for BMI at age 25, a 5% increment in weight from age 25 to baseline was associated with a greater risk of incident postmenopausal breast cancer [1.05 (1.02–1.07)] and endometrial cancer [1.09 (1.04–1.14)] in women and incident colorectal cancer [1.05 (1.00–1.10)] in men. Excess weight during young adulthood and weight gain from young to older adulthood may be independently associated with subsequent cancer risk. Excess weight and weight gain in early adulthood should be avoided.  相似文献   

15.
    
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16.
    
Different subtypes of ovarian cancer appear to have different causes; however, the association between body mass index (BMI) and the different subtypes is unclear. We examined the associations between body-mass index (BMI) and weight gain and risk of the different histological subtypes of epithelial ovarian cancer in a case-control study in Australia. Cases aged 18-79 with a new diagnosis of invasive epithelial ovarian cancer (n = 1,269) or borderline tumor (n = 311) were identified through a network of clinics and cancer registries throughout Australia. Controls (n = 1,509) were selected from the Electoral Roll. Height and weight (1 year previously, at age 20 and maximum weight) and other risk factor information were ascertained via a self-administered questionnaire. Obesity was positively associated with clear cell tumors (Odds Ratio 2.3; 95% confidence interval 1.2-4.2) but not invasive endometrioid or mucinous tumors. Although there was no association with invasive serous tumors overall (0.9; 0.7-1.2), we did see an increased risk of serous peritoneal tumors (2.9; 1.7-4.9), but not of serous tumors of the ovary and fallopian tube. Of the borderline subtypes, obesity was positively associated with serous (1.8; 1.1-2.8) but not mucinous tumors (1.1; 0.7-1.7). Overweight was not associated with any subtype overall. There was no association with BMI at age 20, or weight gain for any of the histological subtypes. These results add to the current evidence that obesity increases a woman's risk of developing distinct histological subtypes of ovarian cancer.  相似文献   

17.
    
The causal relationship between body mass index (BMI) and type 2 diabetes (T2D) and breast cancer prognosis is still ambiguous. The aim of this study was to investigate the prognostic effect of BMI and T2D on breast cancer disease-free survival (DFS) among Asian individuals. In this two-sample Mendelian randomization (MR) study, the instrumental variables (IVs) were identified using a genome-wide association study (GWAS) among 24,000 participants in the Taiwan Biobank. Importantly, the validity of these IVs was confirmed with a previous large-scale GWAS (Biobank Japan Project, BBJ). In this study, we found that a genetic predisposition toward higher BMI (as indicated by BMI IVs, F = 86.88) was associated with poor breast cancer DFS (hazard ratio [HR] = 6.11; P < 0.001). Furthermore, higher level of genetically predicted T2D (as indicated by T2D IVs) was associated with an increased risk of recurrence of and mortality from breast cancer (HR = 1.43; P < 0.001). Sensitivity analyses, including the weighted-median approach, MR-Egger regression, Radial regression and Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) supported the consistency of our findings. Finally, the causal relationship between BMI and poor breast cancer prognosis was confirmed in a prospective cohort study. Our MR analyses demonstrated the causal relationship between the genetic prediction of elevated BMI and a greater risk of T2D with poor breast cancer prognosis. BMI and T2D have important clinical implications and may be used as prognostic indicators of breast cancer.  相似文献   

18.
目的 探讨绝经后女性乳腺癌的发病与血清性激素水平和体重指数的关系。方法 选择2013年3月—12月在哈尔滨医科大学附属肿瘤医院乳腺外科接受手术治疗的初诊绝经后乳腺癌118例作为病例组以及60例绝经后乳腺良性病变者作为对照组,并收集所有受试对象的身高、体重等基本资料。应用酶联免疫吸附实验(ELISA)方法检测受试对象的血清雌二醇(Estradiol,E2)、雌酮(Estrone,E1)、睾酮(Testesterone,TSTO)以及雄烯二酮(Androstenedione,AED)水平,并对结果进行分析。结果 病例组血清E2、E1、AED水平显著高于对照组(P＜0.05),病例组的血清TSTO平均水平稍高于对照组,但差异无统计学意义(P＞0.05);病例组体重指数(BMI)与对照组无明显差异(P＞0.05);病例组血清E1以及总研究对象的血清E1、TSTO、AED在超重组内的水平明显高于非超重组(P＜0.05),未发现其余各组的激素水平与BMI指数具有相关性(P＞0.05)。结论 绝经后女性乳腺癌患者的血清性激素水平升高,血清E2、E1、AED水平升高可能是与绝经后女性乳腺癌的发病相关,BMI高的绝经后女性的血清性激素水平较高。  相似文献   

19.
    
Excess adiposity is associated with increased risks of developing adult malignancies. To inform public health policy and guide further research, the incident cancer burden attributable to excess body mass index (BMI ≥ 25 kg/m2) across 30 European countries were estimated. Population attributable risks (PARs) were calculated using European‐ and gender‐specific risk estimates from a published meta‐analysis and gender‐specific mean BMI estimates from a World Health Organization Global Infobase. Country‐specific numbers of new cancers were derived from Globocan2002. A ten‐year lag‐period between risk exposure and cancer incidence was assumed and 95% confidence intervals (CI) were estimated in Monte Carlo simulations. In 2002, there were 2,171,351 new all cancer diagnoses in the 30 countries of Europe. Estimated PARs were 2.5% (95% CI 1.5–3.6%) in men and 4.1% (2.3–5.9%) in women. These collectively corresponded to 70,288 (95% CI 40,069–100,668) new cases. Sensitivity analyses revealed estimates were most influenced by the assumed shape of the BMI distribution in the population and cancer‐specific risk estimates. In a scenario analysis of a plausible contemporary (2008) population, the estimated PARs increased to 3.2% (2.1–4.3%) and 8.6% (5.6–11.5%), respectively, in men and women. Endometrial, post‐menopausal breast and colorectal cancers accounted for 65% of these cancers. This analysis quantifies the burden of incident cancers attributable to excess BMI in Europe. The estimates reported here provide a baseline for future modelling, and underline the need for research into interventions to control weight in the context of endometrial, breast and colorectal cancer.  相似文献   

20.
目的：探讨体质量指数与甲状腺癌组织瘦素（Leptin）表达水平的相关性,为临床诊断及治疗分化型甲状腺癌提供依据。方法：选择分化型甲状腺癌患者167例,根据体质量指数分为体重正常组（n ＝64）、超重组（n ＝47）和肥胖组（n ＝56）,观察各组的甲状腺组织 Leptin 及其受体（OB －R）表达水平。结果：正常组的肿瘤大小以＜1cm 为主,而肥胖组则以≥1cm 居多（P ＜0．05）;正常组肿瘤分期 I、Ⅱ期比例居多,肥胖组以Ⅲ、Ⅳ期为主（P ＜0．05）;三组患者的 Leptin、OB －R 表达水平随着患者体质量指数的增加而逐渐升高（P ＜0．05）;甲状腺癌患者体质量指数与 Leptin 表达水平呈正相关。结论：Leptin 与甲状腺癌的发生、进展密切相关,同时 Leptin 与患者体质量指数密切相关。  相似文献   

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