Diabetes mellitus increases the risk of early gastric cancer development

BackgroundThe significance of diabetes mellitus (DM) in gastric carcinogenesis still remains unclear. We investigated whether DM would be a risk factor for the development of early gastric cancer.MethodsFactors related to the presence of gastric cancer were examined in patients undergoing medical health checkups. We then investigated whether DM was related to the development of early gastric cancer during an endoscopic follow-up study.ResultsGastric cancer was detected in 14 (1.0%) of 1463 patients at the first endoscopic examination and was significantly associated with the severity of gastric atrophy and the presence of DM. During the follow-up period (range 36–108 months; mean 70.0 months), early gastric cancer was newly detected in 26 (1.8%) of the 1449 patients in whom gastric cancer had not been detected at the first examination. Gastric cancer was detected in 17 (1.3%) of 1301 patients without DM, and in 9 (6.1%) of 148 patients with DM (P < 0.0001). Multivariate analyses demonstrated that open-type gastric atrophy and DM were independently related to the development of early gastric cancer (P < 0.0001 and P = 0.020, respectively). Gastric cancer was identified in 14 (5.1%) of 274 patients who had open-type atrophic gastritis without DM, whereas it was identified in 8 (16.0%) of 50 patients who had both open-type atrophic gastritis and DM (P = 0.0042).ConclusionDM increases the risk of early gastric cancer development.     

Increased stomach cancer risk following radiotherapy for testicular cancer

Background:

Abdominal radiotherapy for testicular cancer (TC) increases risk for second stomach cancer, although data on the radiation dose–response relationship are sparse.

Methods:

In a cohort of 22 269 5-year TC survivors diagnosed during 1959–1987, doses to stomach subsites were estimated for 92 patients who developed stomach cancer and 180 matched controls. Chemotherapy details were recorded. Odds ratios (ORs) were estimated using logistic regression.

Results:

Cumulative incidence of second primary stomach cancer was 1.45% at 30 years after TC diagnosis. The TC survivors who received radiotherapy (87 (95%) cases, 151 (84%) controls) had a 5.9-fold (95% confidence interval (CI) 1.7–20.7) increased risk of stomach cancer. Risk increased with increasing stomach dose (P-trend<0.001), with an OR of 20.5 (3.7–114.3) for ⩾50.0 Gy compared with <10 Gy. Radiation-related risks remained elevated ⩾20 years after exposure (P<0.001). Risk after any chemotherapy was not elevated (OR=1.1; 95% CI 0.5–2.5; 14 cases and 23 controls).

Conclusions:

Radiotherapy for TC involving parts of the stomach increased gastric cancer risk for several decades, with the highest risks after stomach doses of ⩾30 Gy. Clinicians should be aware of these excesses when previously irradiated TC survivors present with gastrointestinal symptoms and when any radiotherapy is considered in newly diagnosed TC patients.     

Radiotherapy combined with tegafur for inoperable advanced gastric cancer

A total of 58 cases with inoperable advanced gastric carcinomas were treated by radiotherapy combined with tegafur, and the result was analyzed mainly from the aspects of life expectancies and some prognostic factors. Median survival time of all cases was 8.9 months. Actuarial survival rates at one, two, three, four and five years were 45%, 22%, 14%, 14% and 11% respectively. Cancer type, histologic type, tumor size and radiation effect on the primary lesion were chosen as the prognostic factors, and examined using median survival time as a parameter. Borrmann IV type cancer showed an unequivocally poor prognosis, whereas no significant prognostic differences were seen among other types. Poorly differentiated adenocarcinoma gave a poor prognosis. Radiation effect on the primary lesion seemed to have a positive correlation with prognosis, while life expectancies became shorter with the increase of tumor size. It seems, from the present study, that this combination therapy contributes a great deal to life prolongation of patients with inoperable advanced gastric carcinomas.     

Radiotherapy for stage II testicular seminoma

PURPOSE: To compare the outcome of patients with Stage II seminoma treated with prophylactic mediastinal irradiation, without any supradiaphragmatic irradiation, and with prophylactic left supraclavicular irradiation (PLSCI). METHODS AND MATERIALS: Between 1960 and 1999, 73 men with Stage II seminoma received postorchiectomy radiotherapy. Before 1984, 36 received prophylactic mediastinal irradiation (Series I); between 1984 and 1992, 17 received no supradiaphragmatic irradiation (Series II); and after 1992, 20 received PLSCI (Series III). The outcomes in these series were compared. RESULTS: The abdominal tumor sizes were as follows: Series I, 2 and 5 and 2 and 5 and 2 and 5 and 相似文献   

Radiotherapy treatment planning for testicular seminoma

Virtually all patients with Stage I testicular seminoma are cured regardless of postorchiectomy management. For patients treated with adjuvant radiotherapy, late toxicity is a major concern. However, toxicity may be limited by radiotherapy techniques that minimize radiation exposure of healthy normal tissues. This article is an evidence-based review that provides radiotherapy treatment planning recommendations for testicular seminoma. The minority of Stage I patients who choose adjuvant treatment over surveillance may be considered for (1) para-aortic irradiation to 20 Gy in 10 fractions, or (2) carboplatin chemotherapy consisting of area under the curve, AUC = 7 × 1-2 cycles. Two-dimensional radiotherapy based on bony anatomy is a simple and effective treatment for Stage IIA or IIB testicular seminoma. Centers with expertise in vascular and nodal anatomy may consider use of anteroposterior-posteroanterior fields based on three-dimensional conformal radiotherapy instead. For modified dog-leg fields delivering 20 Gy in 10 fractions, clinical studies support placement of the inferior border at the top of the acetabulum. Clinical and nodal mapping studies support placement of the superior border of all radiotherapy fields at the top of the T12 vertebral body. For Stage IIA and IIB patients, an anteroposterior-posteroanterior boost is then delivered to the adenopathy with a 2-cm margin to the block edge. The boost dose consists of 10 Gy in 5 fractions for Stage IIA and 16 Gy in 8 fractions for Stage IIB. Alternatively, bleomycin, etoposide, and cisplatin chemotherapy for 3 cycles or etoposide and cisplatin chemotherapy for 4 cycles may be delivered to Stage IIA or IIB patients (e.g., if they have a horseshoe kidney, inflammatory bowel disease, or a history of radiotherapy).     

Prenatal and perinatal risk factors for testicular cancer

In an attempt to determine the risk factors responsible for the dramatic increases in testicular cancer incidence in young adults, mothers of testicular cancer cases and controls were questioned about in utero exposures, pregnancy-related conditions, and perinatal factors during their pregnancies with the 202 cases and the 206 controls. The strongest risk factor was low birth weight with a greater than 12-fold risk (confidence interval = 2.8 to 78.1) for subjects weighing 5 lb or less at birth compared to those who weighed over 5 lb. A statistically significant 2-fold increase in risk was associated with unusual bleeding or spotting during pregnancy, regardless of whether medication was taken for this condition. Other exposures during pregnancy associated with a statistically significant increase in risk were: use of "sedatives"; alcohol consumption; and exposure to X-rays. No excess risk was associated with the use of hormones during pregnancy. The findings for birth weight and abnormal uterine bleeding suggest that significant compromise of the normal maternal-fetal environment may be associated with subsequent increase in risk of testicular cancer. However, this increase in risk is not great enough to explain the dramatic increases in testicular cancer that have occurred in young adults.     

放疗在胃癌综合治疗中的应用

放疗是治疗胃癌的一种有效手段,放疗与化疗联合应用于胃癌的术前、术后及姑息性治疗,能够改善胃癌患者的局部控制率和生存率。近几年来随着三维适形和调强放疗技术的发展,放疗在胃癌的综合治疗中有了更广泛的应用。     

Radiotherapy for gastric cancer: a systematic review and meta-analysis

There have been many trials trying to prove the benefit of radiotherapy for gastric cancer; however, the results were either inclusive or controversial. The purpose of the study was to elucidate the effect of radiotherapy on gastric cancer delivered as perioperative or palliative treatment. We conducted systematic searches for trials exploring the effect of radiotherapy on gastric cancer. In the subgroup of patients receiving preoperative radiotherapy for gastric cancer, a significant benefit was found on 10-year overall survival with a hazard ratio (HR) of 0.75 (95 % confidence interval (CI), 0.61 to 0.91); however, the benefit on 5-year overall survival was not proven (HR, 0.68; 95 %CI, 0.45 to 1.01). There are also no significant differences in resection rate and radical resection rate between group of patients receiving radiotherapy and control group with a relative risk (RR) of 1.06 (95 %CI, 0.99 to 1.13) and 1.12 (95 %CI 0.93 to 1.36), respectively. In the subgroup of patients receiving postoperative radiotherapy for gastric cancer, survival benefits were found on 3- and 5-year progression-free survival with HR of 0.69 (95 %CI, 0.53 to 0.90) and HR of 0.70 (95 %CI, 0.61 to 0.80), respectively. Survival benefits of adjuvant radiotherapy on 3- and 5-year progression-free survival were also found; nonetheless, there was no evidence of significant difference in 3-year overall survival (HR, 0.70; 95 %CI, 0.61 to 1.01). The effect of radiotherapy on 5-year overall survival was also quite controversial. In short, gastric cancer patients could benefit from radiotherapy both in the form of preoperative radiotherapy and postoperative radiotherapy.     

放疗联合手术治疗胃癌的Meta-分析

Objective:We carried out a meta-analysis to assess the effectiveness and safety of radiotherapy combined with surgery for gastric cancer.Methods:Randomized Clinical Trials (RCTs) in which radiotherapy (preoperative,intraoperative and postoperative),was compared with surgery alone in resectable gastric cancer were identified by searching Cochrane Library (Issue 2,2009),PubMed (Jan 1966-Jun 2009),EMBASE (Jan 1974-Jun 2009),Chinese Biomedical Literature Database (Jan 1978-Jun 2009),Chinese Science and Technolo...     

中国胃癌放疗指南(2020版)

胃癌是我国高发的恶性肿瘤之一,且多数患者诊断时已处于进展期,放疗是多学科诊疗的重要组成部分。《中国胃癌放疗指南》由来自代表国内胃癌治疗领先水平的22家医院的放疗科、外科、内科、影像科的35位专家共同编写完成。作为中国首部胃癌放疗指南,将为我国胃癌放射治疗及综合治疗提供重要依据和参考,其在临床实践中的不断完善和更新,将会造福广大胃癌患者并促进学科的发展。     

Sports activities and risk of testicular cancer

The relationship of testicular seminoma with several factors was explored using a case-control study. Previously recognized associations with cryptorchidism and infantile inguinal hernia were confirmed and relationships were also found with cycling and horse-riding. These findings represent the first relationships of testicular cancer with well-defined postnatal risk factors.     

Lifetime growth and risk of testicular cancer

Adult height is associated with testicular cancer risk. We studied to what extent this association is explained by parental height, childhood height and age at puberty. We conducted a case–control study on germ‐cell testicular cancer patients diagnosed in 1997–2008 and resident in the Province of Turin. Information was collected using mailed questionnaires in 2008–2011. Specifically, we asked for adult height (in cm), height at age 9 and 13 (compared to peers) and age at puberty (compared to peers). We also asked for paternal and maternal height (in cm) as indicators of genetic components of adult height. The analysis included 255 cases and 459 controls. Odds ratios (ORs) of testicular cancer were estimated for the different anthropometric variables. Adult height was associated with testicular cancer risk [OR: 1.16, 95% confidence interval (CI): 1.03–1.31 per 5‐cm increase]. The risk of testicular cancer was only slightly increased for being taller vs. shorter than peers at age 9 (OR: 1.55, 95% CI: 0.91–2.64) or age 13 (OR: 1.26, 95% CI: 0.78–2.01), and parental height was not associated with testicular cancer risk. The OR for adult height was 1.32 (95% CI: 1.12–1.56) after adjustment for parental height. Among participants with small average parental height (<167 cm or less), the OR of testicular cancer for tall (>180 cm) vs. short (<174 cm) subjects was 3.47 (95% CI: 1.60–7.51). These results suggest that the association between height and testicular cancer is likely to be explained by environmental factors affecting growth in early life, childhood and adolescence.     

Birth order and risk of testicular cancer

To explore the etiology of testicular cancer, cases of testicular cancer were identified among members of a cobort of Danish boys born between 1941 and 1957 (inclusive), who had attended schools in Copenhagen and Gentofte and whose school health records were contained in an archive under the supervision of the Danish Cancer Registry. One hundred and eighty-three cases of testicular cancer diagnosed before 31 December 1984 were identified; 366 controls, matched to cases by sex and age, were selected from the same cohort. Information on potential risk factors and confounders was obtained from two sources: school health records and midwife protocols, both of which were recorded prior to the diagnosis of testicular cancer in cases. Relative risks (RR) approximated by the odds ratios were calculated and, in logistic regression analyses, adjustments were done for known or suspected confounders. A decreasing risk of testicular cancer with increasing birth order was observed (P=0.020). Compared with being firstborn, being number four or more in birth order was associated with a significantly decreased RR for all testicular cancers (RR=0.3,95 percent confidence interval [CI]=0.3–0.8) and testicular seminoma (RR=0.1, CI=0.02–0.9). No association was observed between high social class and the risk of testicular cancer (RR=1.4, CI=0.8–2.3); neither was age at which the study subjects had mumps or measles related to risk of testicular cancer. No cases of mumps orchitis were observed before or during school years. A slightly increased RR for testicular cancer among boys from small families could be explained by the association between family size and birth order. The observed association between rank in birth order and the risk of testicular cancer was attributed to the reported differences in maternal estrogen levels in first cf second pregnancy, and supports the hypothesis of a tumor-initializing effect of high levels of estrogen early in a pregnancy on the developing testicular tissues.Dr Jensen, formerly Director of the Danish Cancer Registry and member of the CCC Editorial Board, died last year.     

放疗联合手术治疗胃癌的Meta分析

目的:评价放疗联合手术治疗与单纯手术治疗相比,在治疗胃癌方面的有效性及安全性.方法:检索Cochrane图书馆(2009年第2期)、PubMed(1966年1月-2009年6月)、EMBASE(1974年1月-2009年6月)、中国生物医学文献数据库(1978年1月-2009年6月)、中文科技期刊数据库(1989年1月-2009年6月)、中国期刊全文数据库(1994年1月-2009年6月)和万方数据库(1997年1月-2009年6月),纳入有关放疗联合手术治疗胃癌的随机对照试验(randomized controlled trial, RCT),评价文献的方法学质量,并进行Meta分析.结果:最终纳入9个RCT,共包括1 548例患者,其中5个RCT为术前放疗联合手术与单纯手术的对照,2个RCT为手术联合术中放疗与单纯手术的对照,2个RCT为手术联合术后放疗与单纯手术的对照.Meta分析的结果显示:(1)相比于单纯手术治疗,术前放疗联合手术治疗可提高胃癌患者的3年生存率[比值比为1.78(95%的可信区间:1.14～2.78)]、5年生存率[比值比为1.67(95%的可信区间:1.22～2.29)]和10年生存率[比值比为1.64(95%的可信区间:1.03～2.60)],降低肿瘤复发率[比值比为0.59(95%的可信区间:0.37～0.92)]和肿瘤转移率[比值比为0.44(95%的可信区间:0.27～0.73)];(2)手术联合术中放疗与单纯手术治疗相比,在肿瘤复发率[比值比为0.19(95%的可信区间:0.03～1.14)]和肿瘤转移率[比值比为0.09(95%的可信区间:0.00～1.77)]方面无差异;(3)与单纯手术相比,手术联合术后放疗在改善胃癌患者的1年生存率[比值比为0.83(95%的可信区间:0.60～1.15)]及3年生存率[比值比为0.75(95%的可信区间:0.51～1.11)]、肿瘤复发率[比值比为0.59(95%的可信区间:0.33～1.05)]和肿瘤转移率[比值比为0.90(95%的可信区间:0.51～1.59)]方面无差异,但在改善胃癌患者的5年生存率[比值比为0.57(95%的可信区间:0.34～0.95)]方面,单纯手术组要优于手术联合术后放疗组. 结论:术前放疗联合手术是一种较为合理的胃癌综合治疗方式.然而,就手术联合术中和术后放疗而言,由于纳入的RCT数量较少,因此今后尚需要开展高质量的RCT以作进一步的论证.     

Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer

We conducted a longitudinal cohort study to determine the association of Helicobacter pylori infection and the progression of chronic atrophic gastritis (CAG) with gastric cancer. A cohort of 4655 healthy asymptomatic subjects was followed for a mean period of 7.7 years. H. pylori infection was established by serum specific antibodies and the presence of CAG was confirmed by serum pepsinogen. During the follow-up period, 45 gastric cancer cases were detected (incidence rate, 126/100000 person-years). A univariate analysis after adjustment for age showed that both H. pylori and CAG were significantly associated with gastric cancer. To clarify the interaction between H. pylori and CAG, an analysis stratified by H. pylori- and CAG-status was performed. No cancer developed in the H. pylori(-)/CAG(-) group during the study period. This supports the theory that it is quite rare for any type of gastric cancer to develop in an H. pylori-free healthy stomach. With the progression of H. pylori-induced gastritis, the risk of gastric cancer increased in a stepwise fashion from CAG-free gastritis [H. pylori(+)/CAG(-) group] (HR=7.13, 95%CI=0.95-53.33) to CAG [H. pylori(+)/CAG(+) group] (HR=14.85, 95%CI=1.96-107.7) and finally to severe CAG with extensive intestinal metaplasia [H. pylori(-)/CAG(+) group] (HR=61.85, 95%CI=5.6-682.64) in which loss of H. pylori from the stomach is observed. Therefore, it is probable that H. pylori alone is not directly associated with stomach carcinogenesis. Instead, H. pylori appears to influence stomach carcinogenesis through the development of CAG. The observed positive correlation between the extent of H. pylori-induced gastritis and the development of cancer was strong, especially for the intestinal type. These results are compelling evidence that severe gastritis with extensive intestinal metaplasia is a major risk factor for gastric cancer, and they confirm the previously described model of stomach carcinogenesis: the gastritis-metaplasia-carcinoma sequence.     

Acute primary testicular failure due to radiotherapy increases risk of severe postoperative adverse events in rectal cancer patients

AimThe aim of this study is to analyze postoperative adverse events (AE) in relation to acute primary testicular failure after radiotherapy (RT) for rectal cancer.MethodThis relation was assessed in 104 men, included in a previous prospective cohort study of men treated with surgical resection of the rectum for rectal cancer stage I-III. Postoperative AE were graded according to Clavien-Dindo (2004). Grade 3 or more was set as cut-off for severe postoperative AE. The impact of primary testicular failure on postoperative AE was related to the cumulative mean testicular dose (TD) and the change in Testosterone (T) and Luteinizing hormone (LH) sampled at baseline and after RT.ResultsTwenty-six study participants (25%) had severe postoperative AE. Baseline characteristics and endocrine testicular function did not differ significantly between groups with (AE+) and without severe postoperative AE (AE-). After RT, the LH/T-ratio was higher in AE+, 0.603 (0.2–2.5) vs 0.452 (0.127–5.926) (p = 0.035). The longitudinal regression analysis showed that preoperative change in T (OR 0.844, 95% CI 0.720–0.990, p = 0.034), LH/T-ratio (OR 2.020, 95% CI 1.010–4.039, p = 0.047) and low T (<8 nmol/L, OR 2.605, 95 CI 0.951–7.139, p = 0.063) were related to severe postoperative AE.ConclusionPreoperative decline in T due to primary testicular failure induced by preoperative RT could be a risk factor regarding short-term outcome of surgery in men with rectal cancer.     

Radiotherapy for oral cancer as a risk factor for second primary cancers

Radiation exposure, known to cause DNA damage, may be a potential source of field cancerization of the upper aerodigestive tract. Radiotherapy for head and neck cancers has been examined as a possible risk factor for second primary cancers, but the results have been equivocal. We evaluated the impact of therapeutic radiation for oral cancer on the risk of second primary cancers with data from the Surveillance, Epidemiology, and End Results (SEER) program for 1973–1999. Among 30,221 first primary oral squamous cell carcinoma patients, 6163 (20.4%) patients developed a second primary cancer, 5042 of which were metachronous. Patients treated with radiation only (RR=1.64, 95%CI=1.18–2.29) or radiation with surgery (RR=1.49, 95%CI=1.07, 2.06) had elevated risks of developing a second primary tumor, whereas patients treated with surgery only did not appear to be at increased risk (RR=1.28, 95%CI=0.93, 1.76). Consistent with an expected latent period between radiation exposure and tumor occurrence, radiation became a risk factor after 10 years of follow-up for solid cancers of the oral cavity (RR=2.8, 95%CI=1.5, 5.2), pharynx (RR=5.9, 95%CI=1.7, 20.7), esophagus (RR=3.9, 95%CI=1.1, 13.4) and lung (RR=1.5, 95%CI=1.0, 2.4), and after 1–5 years of follow-up for second primary leukemia (RR=2.5, 95%CI=1.0, 6.7). Radiotherapy for oral cancer appears to be a risk factor for second primary tumors. Further studies that account for chemotherapy and examine frequency and duration of radiotherapy would be of interest in confirming the observed association.