癌症最新文献

ABCC10, also known as multidrug-resistant protein 7 (MRP7), is the tenth member of the C subfamily of the ATP-binding cassette (ABC) superfamily. ABCC10 mediates multidrug resistance (MDR) in cancer cells by preventing the intracellular accumulation of certain antitumor drugs. The ABCC10 transporter is a 171-kDa protein that is localized on the basolateral cell membrane. ABCC10 is a broad-specificity transporter of xenobiotics, including antitumor drugs, such as taxanes, epothilone B, vinca alkaloids, and cytarabine, as well as modulators of the estrogen pathway, such as tamoxifen. In recent years, ABCC10 inhibitors, including cepharanthine, lapatinib, erlotinib, nilotinib, imatinib, sildenafil, and vardenafil, have been reported to overcome ABCC10-mediated MDR. This review discusses some recent and clinically relevant aspects of the ABCC10 drug efflux transporter from the perspective of current chemotherapy, particularly its inhibition by tyrosine kinase inhibitors and phosphodiesterase type 5 inhibitors.

Muscular dystrophies (MD) comprise a heterogeneous group of hereditary myopathic diseases. In this group, myotonic MD is associated with an increased cancer risk. However, the cancer risk in other types of MD is unclear. To address this gap in knowledge, we assessed data obtained from the Taiwan Health Insurance Program database. A total of 1,272 patients with MD diagnosed between 1997 and 2009 were enrolled. They were followed up for cancer during the same period by record linkage with the cancer certification in Taiwan. Age- and sex-standardized incidence ratios (SIRs) of overall and site-specific cancers were calculated. For congenital and progressive hereditary MD, there were 685 and 505 cases (males: 69.5% and 80.6%), the median ages at diagnosis were 16 and 13 years, and the mean follow-up durations were 7.12 and 5.06 years, respectively. In addition, cancers were developed in 10 patients with congenital MD and 3 patients with progressive hereditary MD. Female MD patients exhibited an increased cancer risk, yielding an SIR of 3.37 [95% confidence interval (CI) = 1.38-8.25] in congenital MD and 2.95 (95% CI = 0.95-9.19) in hereditary progressive MD. Site-specific cancer SIRs were not powered to be significantly different. In conclusion, genetic defects in hereditary MD may increase cancer risks in females and a sex difference should be further investigated.

Erythropoietin-producing hepatoma (EPH) receptors are considered the largest family of receptor tyrosine kinases and play key roles in physiological and pathologic processes in development and disease. EPH receptors are often overexpressed in human malignancies and are associated with poor prognosis. However, the functions of EPH receptors in epithelial-mesenchymal transition (EMT) remain largely unknown. This review depicts the relationship between EPH receptors and the EMT marker E-cadherin as well as the crosstalk between EPH receptors and the signaling pathways involved EMT. Further discussion is focused on the clinical significance of EPH receptors as candidates for targeting in cancer therapeutics. Finally, we summarize how targeted inhibition of both EPH receptors and EMT-related signaling pathways represents a novel strategy for cancer treatment.

Although several models have been developed to predict the probability of Gleason sum upgrading between biopsy and radical prostatectomy specimens, most of these models are restricted to prostate-specific antigen screening-detected prostate cancer. This study aimed to build a nomogram for the prediction of Gleason sum upgrading in clinically diagnosed prostate cancer. The study cohort comprised 269 Chinese prostate cancer patients who underwent prostate biopsy with a minimum of 10 cores and were subsequently treated with radical prostatectomy. Of all included patients, 220 (81.8%) were referred with clinical symptoms. The prostate-specific antigen level, primary and secondary biopsy Gleason scores, and clinical T category were used in a multivariate logistic regression model to predict the probability of Gleason sum upgrading. The developed nomogram was validated internally. Gleason sum upgrading was observed in 90 (33.5%) patients. Our nomogram showed a bootstrap-corrected concordance index of 0.789 and good calibration using 4 readily available variables. The nomogram also demonstrated satisfactory statistical performance for predicting significant upgrading. External validation of the nomogram published by Chun et al. in our cohort showed a marked discordance between the observed and predicted probabilities of Gleason sum upgrading. In summary, a new nomogram to predict Gleason sum upgrading in clinically diagnosed prostate cancer was developed, and it demonstrated good statistical performance upon internal validation.

Malnutrition occurs frequently in patients with cancer. Indeed, a variety of nutritional and tumor-related factors must be taken into account in these patients. Recognizing this relationship, we aimed to prospectively evaluate the risk factors that influence weight loss in patients undergoing radiotherapy with oral nutritional supplementation and dietetic counseling. Weight loss of 74 patients during radiotherapy and 1 month after treatment was analyzed. Parameters such as age, gender, tumor location, tumor stage, Eastern Cooperative Oncology Group performance status (ECOG PS) score, and the use of chemotherapy were analyzed to evaluate their influence on weight loss. All patients underwent oral nutritional supplementation and dietetic counseling. Forty-six (65.7%) patients lost weight, with a mean weight loss of (4.73 ± 3.91) kg, during radiotherapy. At 1 month after treatment, 45 (66.2%) patients lost weight, presenting a mean weight loss of (4.96 ± 4.04) kg, corresponding to a (6.84 ± 5.24)% net reduction from their baseline weight. Head and neck cancer patients had a mean weight loss of (3.25 ± 5.30) kg, whereas the remaining patients had a mean weight loss of (0.64 ± 2.39) kg (P = 0.028) during radiotherapy. In the multivariate analysis, the head and neck tumor location (P = 0.005), use of chemotherapy (P = 0.011), and ECOG PS score of 2-3 (P = 0.026) were considered independent risk factors. Nutritional status and parameters, such as tumor location (especially the head and neck), the use of chemotherapy, and the ECOG PS score, should be evaluated before radiotherapy because these factors can influence weight loss during radiotherapy and 1 month after treatment.

Once considered a taboo topic or stigma, cancer is the number one public health enemy in the world. Once a product of an almost untouchable industry, tobacco is indisputably recognized as a major cause of cancer and a target for anticancer efforts. With the emergence of new economic powers in the world, especially in highly populated countries such as China, air pollution has rapidly emerged as a smoking gun for cancer and has become a hot topic for public health debate because of the complex political, economic, scientific, and technologic issues surrounding the air pollution problem. This editorial and the referred articles published in this special issue of the Chinese Journal of Cancer discuss these fundamental questions. Does air pollution cause a wide spectrum of cancers? Should air pollution be considered a necessary evil accompanying economic transformation in developing countries? Is an explosion of cancer incidence coming to China and how soon will it arrive? What must be done to prevent this possible human catastrophe? Finally, the approaches for air pollution control are also discussed.

Recently, the International Agency for Research on Cancer (IARC) has classified outdoor air pollution and the particulate matter component of outdoor air pollution as class I carcinogen. Air pollution is consistently associated with lung cancer in epidemiologic and experimental studies. The IARC assessment is specifically designed as hazard identification, and it does not quantify the magnitude of the cancer risk. This article addresses the magnitude of the lung cancer risk in the population due to ambient air pollution exposure.

The International Agency for Research on Cancer (IARC) has classified outdoor air pollution and the particulate matter (PM) in outdoor air pollution as carcinogenic to humans, as based on sufficient evidence of carcinogenicity in humans and experimental animals and strong support by mechanistic studies. The data with important contributions to the evaluation are reviewed, highlighting the data with particular relevance to China, and implications of the evaluation with respect to China are discussed. The air pollution levels in Chinese cities are among the highest observed in the world today and frequently exceed health-based national and international guidelines. Data from high-quality epidemiologic studies in Asia, Europe, and North America consistently show positive associations between lung cancer and PM exposure and other indicators of air pollution, which persist after adjustment for important lung cancer risk factors, such as tobacco smoking. Epidemiologic data from China are limited but nevertheless indicate an increased risk of lung cancer associated with several air pollutants. Excess cancer risk is also observed in experimental animals exposed to polluted outdoor air or extracted PM. The exposure of several species to outdoor air pollution is associated with markers of genetic damage that have been linked to increased cancer risk in humans. Numerous studies from China, especially genetic biomarker studies in exposed populations, support that the polluted air in China is genotoxic and carcinogenic to humans. The evaluation by IARC indicates both the need for further research into the cancer risks associated with exposure to air pollution in China and the urgent need to act to reduce exposure to the population.

In 2013, at the congress of the European CanCer Organization and the European Society for Medical Oncology, colorectal cancer was the subject of various oral presentations and posters. In this article, we have selected the most innovative studies that are likely to change our daily practice.

Air pollution in China comes from multiple sources, including coal consumption, construction and industrial dust, and vehicle exhaust. Coal consumption in particular directly determines the emissions of three major air pollutants: dust, sulfur dioxide (SO(2)), and nitrogen oxide (NOx). The rapidly increasing number of civilian vehicles is expected to bring NOx emission to a very high level. Contrary to expectations, however, existing data show that the concentrations of major pollutants [particulate matter-10 (PM10), SO(2), and nitrogen dioxide (NO(2))] in several large Chinese cities have declined during the past decades, though they still exceed the national standards of ambient air quality. Archived data from China does not fully support that the concentrations of pollutants directly depend on local emissions, but this is likely due to inaccurate measurement of pollutants. Analyses on the cancer registry data show that cancer burden related to air pollution is on the rise in China and will likely increase further, but there is a lack of data to accurately predict the cancer burden. Past experience from other countries has sounded alarm of the link between air pollution and cancer. The quantitative association requires dedicated research as well as establishment of needed monitoring infrastructures and cancer registries. The air pollution-cancer link is a serious public health issue that needs urgent investigation.