The cancer registry in cancer control

The sole justification for a cancer registry is that use is made of its data. The information stored and produced by a cancer registry forms the scientific basis for planning and organization of the treatment and prevention of cancer in the community. Its data can also be used in the testing of various hypotheses concerning the aetiology and biology of malignant neoplasms and it may also give rise to various new hypotheses.     

Pancreatic cancer: progress in cancer therapy

Pancreatic cancer continues to be a highly lethal disease. In fact the overall 5-year survival rate is less than 4% and has hardly improved over the past two decades. Surgery is the only potential curative treatment, but the majority of patients have an unresectable disease at the diagnosis. After the demonstration in 1997 that gemcitabine could lead to an improvement in clinical benefit and overall survival this chemotherapy agent became the standard of care for advanced pancreatic cancer patients. Several authors tried to improve results obtained with single agent gemcitabine by exploring the activity of novel chemotherapy on biologically targeted agents in combination with gemcitabine. Unfortunately, global findings were often disappointing with only a marginally significant survival benefit. New treatment strategies and a more careful evaluation of innovative therapies are clearly needed for this disease. In this review we will focus on treatment strategies both in resectable and advanced pancreatic cancer.     

The cancer registry in cancer control--a review

The author reviews key elements in the contribution of the cancer registry to cancer control. A cancer registry always requires the direct or indirect cooperation of the medical profession in the reporting of new cancer cases and it must in return provide services which the physician can use in the care of cancer patients. Survival of patients can be assessed and treatment evaluated for the entire reporting area and not just for selected groups. Projections of the needs for future material and manpower resources can be made on the basis of data collected by the registry. The cancer registry is also in an ideal position to monitor the efficacy of screening programs. Data collected by the registry are the basis for epidemiologic investigations. The magnitude of the cancer problem can be measured and variation by time and place identified. The origin of cancer can be studied by a variety of epidemiologic approaches using data from the cancer registry. Should a suspected etiologic factor be altered in the environment the impact of the intervention may be followed using trend data from the registry. The linkage if individual records is essential if the registry is to function accurately and efficiently. Appropriate safeguards for the confidentiality of medical data must be insured. Adequate staffing with persons interested in and able to undertake the analysis and interpretation of the data collected is a must if the cancer registry is to live up to its potential.     

Colorectal cancer in hereditary breast cancer kindreds

PURPOSE: This study compared characteristics of colorectal cancer between families with dominant breast cancer inheritance and the general population. The cumulative incidence of colorectal cancer was also studied in genetically determined breast cancer syndrome subjects with BRCA1 and BRCA2 mutations and compared with the general population. METHODS: Subjects included 42 patients with colorectal cancer from 32 clinically determined hereditary breast cancer kindreds based on the autosomal dominant inheritance of breast cancers and early age of onset. The general population colorectal cancer cohort was composed of 755 patients from a tumor registry. Lifetime risk of colorectal cancer was determined in 164 BRCA1 and 88 BRCA2 gene mutation carriers and compared with the general population. Mean age of colorectal cancer onset, anatomic site distribution, histologic stage at presentation, and five year stage-stratified survival rates were compared between clinically determined hereditary breast cancer family members and the general population. RESULTS: The lifetime risk of colorectal cancer in male BRCA1 and BRCA2 mutation carriers was 5.6 percent, which was not different from 6 percent in males from the general population. Likewise, the lifetime colorectal cancer risk in female BRCA1 and BRCA2 mutation carriers was 3.2 percent, which was not different from 5.9 percent in females from the general population. Mean age of onset ± standard error for patients with colorectal cancer was 60±2 years for hereditary breast cancer kindreds compared with 67±0.4 years for the general population (P=0.0004). Colorectal cancer site distribution did not vary between hereditary breast cancer and the general population. Overall colorectal cancer stage distribution was significantly different, with more Stage I and fewer Stage IV cancers in subjects with hereditary breast cancer compared with the general population (P=0.01). Overall five year stage-stratified colorectal cancer survival rate ± standard error was 66±8 percent for hereditary breast cancer kindreds and 46±2 percent for the general population (P=0.023). CONCLUSION: Lifetime cumulative colorectal cancer incidence in subjects with BRCA1 and BRCA2 gene mutations was not different from the general population. However, significant differences in colorectal cancer were noted between hereditary breast cancer family members and the general population. Hereditary breast cancer-associated colorectal cancer had an earlier age of onset, lower tumor stage, and better survival rate than the general population. Except for age of onset, colorectal cancer in hereditary breast cancer kindreds exhibited more favorable characteristics than colorectal cancer in the general population.Read at the meeting of The American Society of Colon and Rectal Surgeons, San Antonio, Texas, May 2 to 7, 1998.     

Angiogenesis in human cancer: implications in cancer therapy

Angiogenesis represents an essential step in tumor proliferation, expansion, and metastasis. Tumor cells may express both proangiogenic and/or antiangiogenic factors. Under normal circumstances, angiogenesis is controlled through the equilibrium of these factors. This balance is disrupted in malignancy, resulting in promotion of angiogenesis. Among angiogenic molecules, VEGF appears to have a central role in the angiogenic process: it is the target of many proangiogenic factors, but it also regulates molecules that are implicated in endothelial proliferation. It has been suggested that VEGF may be a proximate angiogenic factor through which others act. The degree of angiogenesis and the expression of angiogenic factors have been associated with prognosis in several human neoplasms. In addition, angiogenesis offers a theoretically selective target for anticancer therapy, since it is only required for wound healing, endometrial proliferation, and pregnancy in healthy individuals. Antiangiogenic cancer treatment is still largely experimental and its clinical potential is currently being studied in clinical trials. Thalidomide, a drug with antiangiogenic properties, has shown significant efficacy in patients with relapsed or refractory multiple myeloma. In addition, an anti-VEGF monoclonal antibody prolonged survival in patients with advanced colorectal and renal cell carcinoma. Although these results are encouraging, selection of patients is essential in order to target populations most likely to benefit from antiangiogenic therapy.     

Thrombophilia in cancer

Malignancy is an acquired thrombophilic condition associated with a significant risk of thrombosis. Venous and arterial thromboembolism is a common complication for patients with cancer, who also present with a hypercoagulable state, even in the absence of manifest thrombosis. Furthermore, clotting activation may play a role in tumor progression. The pathogenesis of thrombosis in cancer is multifactorial; however, a relevant role is attributed to the tumor cell capacity to interact with and activate the host hemostatic system. Among other factors, the prothrombotic action of antitumor therapies is also important. Thrombotic events can influence the morbidity and mortality of the underlying disease. Therefore, preventing these complications in cancer patients is a clinically relevant issue. Recently, new approaches to the prevention and cure of thrombosis in cancer have been investigated, and the hypothesis that strategies to inhibit clotting mechanism may favorably affect malignant disease is gaining increasing interest. In this article, the various aspects of the complex relationship between thrombosis and cancer, from pathophysiology to therapy, are reviewed.     

Synchronous gastric cancer in primary sporadic colorectal cancer patients in Korea

Background and aims Colorectal cancer has been reported to be the malignancy most frequently associated with gastric cancer in Korea. The aim of this study was to define the frequency and clinical characteristics of synchronous gastric cancer detected at preoperative esophagogastroduodenoscopy (EGD) in colorectal cancer patients. Materials and methods This prospective study analyzed the EGD results from 1,542 consecutive colorectal cancer patients who underwent surgery from January 2003 to December 2005 at the Center for Colorectal Cancer, National Cancer Center, Korea. Results Of the 1,542 cases, 1,155 (74.9%) underwent EGD at our center and 387 underwent EGD at other hospitals within 6 months before surgery. Of the 1,542 cases, synchronous gastric cancers were detected in 31 cases (2.0%). Of these 31 cases, 26 had early gastric cancer (EGC; 83.9%) and 5 had advanced gastric cancer. Ten (38.5%) of the 26 EGC cases were managed using endoscopic mucosal resection. Compared to colorectal cancer patients without synchronous gastric cancer, the group of patients with synchronous gastric cancer was older (65.5 ± 9.6 vs 58.4 ± 11.3 years, p = 0.001) and had a greater proportion of males (77.4 vs 59.4%, p = 0.043). Conclusion This study found that 2% of Korean sporadic colorectal cancer patients had synchronous gastric cancer. A preoperative EGD for colorectal cancer patients is likely to greatly assist in the diagnosis of synchronous gastric cancer at an early stage and the implementation of appropriate minimally invasive treatment. Presented at the Tenth Congress of Asian Federation of Coloproctology, Singapore, March 24–26, 2005.     

Intraperitoneal exfoliated cancer cells in patients with colorectal cancer

PURPOSE: The aims of this study were to evaluate potential predictors of exfoliated free cancer cells in the peritoneal cavity and to assess intraoperative peritoneal lavage cytology as a prognostic indicator in patients with colorectal cancer. METHODS: From 1985 to 1987, intraoperative peritoneal lavage cytology was performed in 140 patients with colorectal cancer. Among them, 88 patients underwent curative resection and 52 patients had noncurative surgery. Cytology was examined twice,i.e., immediately after opening the peritoneal cavity (precytology) and just before closing the abdomen (postcytology). One hundred milliliters of saline was poured into the peritoneal cavity and it was retrieved by suction after irrigation. Cytologic examination was performed after staining with Papanicolaou, Giemsa, periodic acid-Schiff, and Alcian blue stains. RESULTS: Among the 140 patients examined, the incidence of positive cytology in the prelavage was 15 percent, and that in the postlavage was 9 percent, although it was 16 percent in either lavage. Among patients with curative resection, 10 percent had positive cytology. Seven characteristics were identified as features of tumors which are prone to exfoliate cells into the peritoneal cavity: 1) macroscopic peritoneal dissemination, 2) liver metastasis, 3) more than 20 ml of ascites, 4) ulcerated tumors without definite borders, 5) invasion of the serosal surface or beyond, 6) semiannular or annular shape, and 7) moderate or marked lymphatic invasion. In patients undergoing curative surgery, among these features, circumferential involvement was the only one correlated closely with positive cytology (P<0.02). Positive cytology was associated with a worse outcome. In patients who were resected curatively, the postcytology had a stronger influence on local recurrence than the precytology; the local recurrence rate in patients with positive postcytology was higher than in those with negative postcytology, regardless of the precytology. All patients with cancer cells in the peritoneal cavity at the end of surgery had recurrence. CONCLUSIONS: Seven characteristics were identified as risk factors for exfoliation of cancer cells into the peritoneal cavity in patients with colorectal cancer. These findings may be helpful for the choice of laparoscopic surgery in this era of increasing port-site metastases after laparoscopic procedure. The results of peritoneal lavage cytology at the end of surgery were correlated with the long-term postoperative outcome of colorectal cancer. Thus, meticulous follow-up and possibly adjuvant chemotherapy may be beneficial for patients with free cancer cells in lavage fluid, even after curative surgery.     

Survival outcomes in esophageal cancer patients with a prior cancer

To achieve a deeper understanding of patients who developed esophageal cancer (EC) as a second primary malignancy, which may help guide in clinical practice for these patients in the future.In the primary cohort, EC patients with a prior malignancy were identified from the surveillance, epidemiology, and end result 18 database. The 5 most common types of prior cancers were picked out based on the frequency of occurrence. In addition, Kaplan–Meier and log-rank tests were performed to investigate the survival impacts of prior cancers on EC patients. Besides, a competing-risk model was constructed to explore the relationship between EC-treatment and EC-specific mortality. In the secondary cohort, patients with stage I–III (N0M0) EC from 2004 to 2014 were enrolled. After propensity score matching, univariate and multivariate Cox analyses were developed to determine the prognostic factors for EC patients.A total of 1199 EC patients with a prior cancer were identified in the primary cohort. The 5 most common sites of prior cancers were prostate, female breast, bladder, lung and bronchus, and larynx. Kaplan–Meier analyses revealed that EC patients with prior prostate cancer and bladder cancer had the best overall survival (OS), while those with prior cancers of larynx and lung and bronchus had the worst OS. Fine and Gray competing risks analysis indicated that the administration of surgery was closely associated with better EC-specific survival (P < .001). In the secondary cohort, multivariate Cox analyses found that age at diagnosis, race, tumor grade, tumor extent, nodal status and metastasis stage, histology, and the administration of surgery were prognostic factors for OS and cancer-specific survival in EC patients. Besides, the existence of a prior cancer was an independent prognostic factor for cancer-specific survival.EC remains to be the most important cause of death in EC patients with a prior cancer. EC related treatment should be actively adopted in patients with a prior cancer, as they were more likely to die from EC than the prior cancer. EC patients with a prior cancer had comparable OS than those without.     

大肠癌相关基因对大肠癌的筛检

随着人们生活水平的提高和医疗条件的改善,诸多急性传染病均得到了有效的控制.然而,一些与环境因素密切相关的慢性非传染性疾病,如心、脑血管疾病和恶性肿瘤的发病率有了明显上升.大肠癌便是一个突出的例子.欧美和日本等大肠癌高发国家的研究证明,长年的高蛋白、高脂肪和低纤维素饮食习惯是促发大肠癌的重要环境因素(外因),患者遗传上的缺陷,如多种病相关基因的突变又是大肠癌发病的内在因素,这些相关的内外因素结合在一起可能也是近年我国大肠癌发病率上升的重要原因之一.预防为主是我国一贯的卫生工作方针,也是大肠癌防治工作的重点,纠正不良的饮食习惯,深入研究大肠癌发病的分子机制,从病因上着手防病是大肠癌预防工作的一级预防,而提高早癌和癌前疾病的检出率则是大肠癌的二级预防.众所周知,大肠癌有两个特点:一是有明确的癌前病变(93％的大肠癌来源于腺瘤);二是从癌前病变发展为癌有一较长的过程(平均7a).我们可以利用这些特点,通过普查发现癌前病变和早期癌,经过内镜的微创治疗,预防大肠癌的发生,提高早癌治愈率.下面几篇论文将围绕大肠癌早诊、早治的问题进行初步讨论,希望能引起同行专家的兴趣,提出更深入的见解.     

Erythropoietin in thyroid cancer

Erythropoietin (Epo) and the epo-receptor (EpoR) have been implicated in tumor growth, invasion and metastasis. We previously demonstrated Epo and EpoR expression in a small group of archived papillary thyroid cancers (PTC), but were unable to examine functional integrity using formalin-fixed tissues. In the present study, we examined the in vitro expression, induction and function of Epo and EpoR in papillary (NPA), follicular (WRO) and anaplastic (ARO-81) thyroid cancer cells. We found that all three cell lines expressed Epo and EpoR mRNA and that the hypoxia-mimetic cobalt induced Epo expression in all cell lines. None of the growth factors we examined (thyrotropin, vascular endothelial growth factor, IGF-I, or human Epo) altered Epo or EpoR gene expression. Importantly, however, administration of Epo to NPA but not WRO cells resulted in significant alterations in the expression of several mitogenic genes including cyclooxygenase-2 (COX-2), beta-casein (CSN2), wild type p53-induced gene-1 (WIG1) and cathepsin D (CTSD). Epo treated ARO-81 cells only had an increase in CSN2 expression. We conclude that Epo and EpoR are expressed by thyroid cancers and that stimulation of the Epo/EpoR signal pathway results in changes that could impact on the clinical behavior of thyroid cancers.