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Journal ArticleDOI

Global cancer statistics, 2012

TL;DR: A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.
Abstract: Cancer constitutes an enormous burden on society in more and less economically developed countries alike. The occurrence of cancer is increasing because of the growth and aging of the population, as well as an increasing prevalence of established risk factors such as smoking, overweight, physical inactivity, and changing reproductive patterns associated with urbanization and economic development. Based on GLOBOCAN estimates, about 14.1 million new cancer cases and 8.2 million deaths occurred in 2012 worldwide. Over the years, the burden has shifted to less developed countries, which currently account for about 57% of cases and 65% of cancer deaths worldwide. Lung cancer is the leading cause of cancer death among males in both more and less developed countries, and has surpassed breast cancer as the leading cause of cancer death among females in more developed countries; breast cancer remains the leading cause of cancer death among females in less developed countries. Other leading causes of cancer death in more developed countries include colorectal cancer among males and females and prostate cancer among males. In less developed countries, liver and stomach cancer among males and cervical cancer among females are also leading causes of cancer death. Although incidence rates for all cancers combined are nearly twice as high in more developed than in less developed countries in both males and females, mortality rates are only 8% to 15% higher in more developed countries. This disparity reflects regional differences in the mix of cancers, which is affected by risk factors and detection practices, and/or the availability of treatment. Risk factors associated with the leading causes of cancer death include tobacco use (lung, colorectal, stomach, and liver cancer), overweight/obesity and physical inactivity (breast and colorectal cancer), and infection (liver, stomach, and cervical cancer). A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.

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Citations
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Journal ArticleDOI
TL;DR: This paper aims to provide new ideas for TNBC treatment by summarizing existing treatment regimens, therapeutic drugs, and their efficacy for different TNBC subtypes and reviewing some new preclinical studies and targeted treatment regimen for T NBC.
Abstract: Triple-negative breast cancer (TNBC), a specific subtype of breast cancer that does not express estrogen receptor (ER), progesterone receptor (PR), or human epidermal growth factor receptor 2 (HER-2), has clinical features that include high invasiveness, high metastatic potential, proneness to relapse, and poor prognosis. Because TNBC tumors lack ER, PR, and HER2 expression, they are not sensitive to endocrine therapy or HER2 treatment, and standardized TNBC treatment regimens are still lacking. Therefore, development of new TNBC treatment strategies has become an urgent clinical need. By summarizing existing treatment regimens, therapeutic drugs, and their efficacy for different TNBC subtypes and reviewing some new preclinical studies and targeted treatment regimens for TNBC, this paper aims to provide new ideas for TNBC treatment.

731 citations

Journal ArticleDOI
TL;DR: The data indicate that sorafenib is not an effective intervention in the adjuvant setting for hepatocellular carcinoma following resection or ablation.
Abstract: Summary Background There is no standard of care for adjuvant therapy for patients with hepatocellular carcinoma. This trial was designed to assess the efficacy and safety of sorafenib versus placebo as adjuvant therapy in patients with hepatocellular carcinoma after surgical resection or local ablation. Methods We undertook this phase 3, double-blind, placebo-controlled study of patients with hepatocellular carcinoma with a complete radiological response after surgical resection (n=900) or local ablation (n=214) in 202 sites (hospitals and research centres) in 28 countries. Patients were randomly assigned (1:1) to receive 400 mg oral sorafenib or placebo twice a day, for a maximum of 4 years, according to a block randomisation scheme (block size of four) using an interactive voice-response system. Patients were stratified by curative treatment, geography, Child-Pugh status, and recurrence risk. The primary outcome was recurrence-free survival assessed after database cut-off on Nov 29, 2013. We analysed efficacy in the intention-to-treat population and safety in randomly assigned patients receiving at least one study dose. The final analysis is reported. This study is registered with ClinicalTrials.gov, number NCT00692770. Findings We screened 1602 patients between Aug 15, 2008, and Nov 17, 2010, and randomly assigned 1114 patients. Of 556 patients in the sorafenib group, 553 (>99%) received the study treatment and 471 (85%) terminated treatment. Of 558 patients in the placebo group, 554 (99%) received the study treatment and 447 (80%) terminated treatment. Median duration of treatment and mean daily dose were 12·5 months (IQR 2·6–35·8) and 577 mg per day (SD 212·8) for sorafenib, compared with 22·2 months (8·1–38·8) and 778·0 mg per day (79·8) for placebo. Dose modification was reported for 497 (89%) of 559 patients in the sorafenib group and 206 (38%) of 548 patients in the placebo group. At final analysis, 464 recurrence-free survival events had occurred (270 in the placebo group and 194 in the sorafenib group). Median follow-up for recurrence-free survival was 8·5 months (IQR 2·9–19·5) in the sorafenib group and 8·4 months (2·9–19·8) in the placebo group. We noted no difference in median recurrence-free survival between the two groups (33·3 months in the sorafenib group vs 33·7 months in the placebo group; hazard ratio [HR] 0·940; 95% CI 0·780–1·134; one-sided p=0·26). The most common grade 3 or 4 adverse events were hand-foot skin reaction (154 [28%] of 559 patients in the sorafenib group vs four [ vs five [ Interpretation Our data indicate that sorafenib is not an effective intervention in the adjuvant setting for hepatocellular carcinoma following resection or ablation. Funding Bayer HealthCare Pharmaceuticals and Onyx Pharmaceuticals.

721 citations

Journal ArticleDOI
TL;DR: The findings show that radionuclide treatment with Lutetium-177 [177Lu]-PSMA-617 has high response rates, low toxic effects, and reduction of pain in men with metastatic castration-resistant prostate cancer who have progressed after conventional treatments.
Abstract: Summary Background Progressive metastatic castration-resistant prostate cancer is a highly lethal disorder and new effective therapeutic agents that improve patient outcomes are urgently needed. Lutetium-177 [ 177 Lu]-PSMA-617, a radiolabelled small molecule, binds with high affinity to prostate-specific membrane antigen (PSMA) enabling beta particle therapy targeted to metastatic castration-resistant prostate cancer. We aimed to investigate the safety, efficacy, and effect on quality of life of [ 177 Lu]-PSMA-617 in men with metastatic castration-resistant prostate cancer who progressed after standard treatments. Methods In this single-arm, single-centre, phase 2 trial, we recruited men (aged 18 years and older) with metastatic castration-resistant prostate cancer and progressive disease after standard treatments, including taxane-based chemotherapy and second-generation anti-androgens, from the Peter MacCallum Cancer Centre, Melbourne, VIC, Australia. Patients underwent a screening PSMA and FDG-PET/CT to confirm high PSMA-expression. Eligible patients had progressive disease defined by imaging (according to Response Evaluation Criteria In Solid Tumours [RECIST] or bone scan) or new pain in an area of radiographically evident disease, and were required to have an Eastern Cooperative Oncology Group (ECOG) performance status score of 2 or lower. Eligible patients received up to four cycles of intravenous [ 177 Lu]-PSMA-617, at six weekly intervals. The primary endpoint was PSA response according to Prostate Cancer Clinical Trial Working Group criteria defined as a greater than 50% PSA decline from baseline and toxicity according to CTCAE. Additional primary endpoints were imaging responses (as measured by bone scan, CT, PSMA, and FDG PET/CT) and quality of life (assessed with the EORTC-Q30 and Brief Pain Inventory-Short Form questionnaires), all measured up to 3 months post completion of treatment. This trial is registered with the Australian New Zealand Clinical Trials Registry, number 12615000912583. Findings Between Aug 26, 2015, and Dec 8, 2016, 43 men were screened to identify 30 patients eligible for treatment. 26 (87%) had received at least one line of previous chemotherapy (80% docetaxel and 47% cabazitaxel) and 25 (83%) received prior abiraterone acetate, enzalutamide, or both. The mean administered radioactivity was 7·5 GBq per cycle. 17 (57%) of 30 patients (95% CI 37–75) achieved a PSA decline of 50% or more. There were no treatment-related deaths. The most common toxic effects related to [ 177 Lu]-PSMA-617 were grade 1 dry mouth recorded in 26 (87%) patients, grade 1 and 2 transient nausea in 15 (50%), and G1–2 fatigue in 15 (50%). Grade 3 or 4 thrombocytopenia possibly attributed to [ 177 Lu]-PSMA-617 occurred in four (13%) patients. Objective response in nodal or visceral disease was reported in 14 (82%) of 17 patients with measurable disease. Clinically meaningful improvements in pain severity and interference scores were recorded at all timepoints. 11 (37%) patients experienced a ten point or more improvement in global health score by the second cycle of treatment. Interpretation Our findings show that radionuclide treatment with [ 177 Lu]-PSMA-617 has high response rates, low toxic effects, and reduction of pain in men with metastatic castration-resistant prostate cancer who have progressed after conventional treatments. This evidence supports the need for randomised controlled trials to further assess efficacy compared with current standards of care. Funding None.

717 citations

Journal ArticleDOI
Liisa M. Pelttari1, Sofia Khan1, Mikko Vuorela2, Johanna I. Kiiski1, Sara Vilske1, Viivi Nevanlinna1, Salla Ranta1, Johanna Schleutker3, Johanna Schleutker4, Johanna Schleutker5, Robert Winqvist2, Anne Kallioniemi3, Thilo Dörk6, Natalia Bogdanova6, Jonine Figueroa, Paul D.P. Pharoah7, Marjanka K. Schmidt8, Alison M. Dunning7, Montserrat Garcia-Closas9, Manjeet K. Bolla7, Joe Dennis7, Kyriaki Michailidou7, Qin Wang7, John L. Hopper10, Melissa C. Southey10, Efraim H. Rosenberg8, Peter A. Fasching11, Peter A. Fasching12, Matthias W. Beckmann12, Julian Peto13, Isabel dos-Santos-Silva13, Elinor J. Sawyer14, Ian Tomlinson15, Barbara Burwinkel16, Barbara Burwinkel17, Harald Surowy17, Harald Surowy16, Pascal Guénel18, Thérèse Truong18, Stig E. Bojesen19, Stig E. Bojesen20, Børge G. Nordestgaard20, Børge G. Nordestgaard19, Javier Benitez, Anna González-Neira, Susan L. Neuhausen21, Hoda Anton-Culver22, Hermann Brenner16, Volker Arndt16, Alfons Meindl23, Rita K. Schmutzler24, Hiltrud Brauch16, Hiltrud Brauch25, Hiltrud Brauch26, Thomas Brüning27, Annika Lindblom28, Sara Margolin28, Arto Mannermaa29, Jaana M. Hartikainen29, Georgia Chenevix-Trench30, kConFab10, kConFab30, Aocs Investigators31, Laurien Van Dyck31, Hilde Janssen32, Hilde Janssen16, Jenny Chang-Claude16, Anja Rudolph, Paolo Radice, Paolo Peterlongo33, Emily Hallberg33, Janet E. Olson10, Janet E. Olson34, Graham G. Giles10, Graham G. Giles34, Roger L. Milne35, Christopher A. Haiman35, Fredrick Schumacher36, Jacques Simard36, Martine Dumont37, Martine Dumont38, Vessela N. Kristensen37, Vessela N. Kristensen38, Anne Lise Børresen-Dale39, Wei Zheng39, Alicia Beeghly-Fadiel40, Mervi Grip41, Mervi Grip42, Irene L. Andrulis41, Gord Glendon43, Peter Devilee44, Caroline Seynaeve44, Maartje J. Hooning45, Margriet Collée46, Angela Cox46, Simon S. Cross7, Mitul Shah7, Robert Luben16, Ute Hamann16, Ute Hamann47, Diana Torres48, Anna Jakubowska48, Jan Lubinski33, Fergus J. Couch, Drakoulis Yannoukakos9, Nick Orr9, Anthony J. Swerdlow28, Hatef Darabi28, Jingmei Li28, Kamila Czene28, Per Hall7, Douglas F. Easton1, Johanna Mattson1, Carl Blomqvist1, Kristiina Aittomäki1, Heli Nevanlinna 
05 May 2016-PLOS ONE
TL;DR: It is suggested that loss-of-function mutations in RAD 51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk.
Abstract: Common variation on 14q24.1, close to RAD51B, has been associated with breast cancer: rs999737 and rs2588809 with the risk of female breast cancer and rs1314913 with the risk of male breast cancer. The aim of this study was to investigate the role of RAD51B variants in breast cancer predisposition, particularly in the context of familial breast cancer in Finland. We sequenced the coding region of RAD51B in 168 Finnish breast cancer patients from the Helsinki region for identification of possible recurrent founder mutations. In addition, we studied the known rs999737, rs2588809, and rs1314913 SNPs and RAD51B haplotypes in 44,791 breast cancer cases and 43,583 controls from 40 studies participating in the Breast Cancer Association Consortium (BCAC) that were genotyped on a custom chip (iCOGS). We identified one putatively pathogenic missense mutation c.541C>T among the Finnish cancer patients and subsequently genotyped the mutation in additional breast cancer cases (n = 5259) and population controls (n = 3586) from Finland and Belarus. No significant association with breast cancer risk was seen in the meta-analysis of the Finnish datasets or in the large BCAC dataset. The association with previously identified risk variants rs999737, rs2588809, and rs1314913 was replicated among all breast cancer cases and also among familial cases in the BCAC dataset. The most significant association was observed for the haplotype carrying the risk-alleles of all the three SNPs both among all cases (odds ratio (OR): 1.15, 95% confidence interval (CI): 1.11-1.19, P = 8.88 x 10-16) and among familial cases (OR: 1.24, 95% CI: 1.16-1.32, P = 6.19 x 10-11), compared to the haplotype with the respective protective alleles. Our results suggest that loss-of-function mutations in RAD51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk.

715 citations

References
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Journal ArticleDOI
TL;DR: The GLOBOCAN series of the International Agency for Research on Cancer (IARC) as mentioned in this paper provides estimates of the worldwide incidence and mortality from 27 major cancers and for all cancers combined for 2012.
Abstract: Estimates of the worldwide incidence and mortality from 27 major cancers and for all cancers combined for 2012 are now available in the GLOBOCAN series of the International Agency for Research on Cancer. We review the sources and methods used in compiling the national cancer incidence and mortality estimates, and briefly describe the key results by cancer site and in 20 large “areas” of the world. Overall, there were 14.1 million new cases and 8.2 million deaths in 2012. The most commonly diagnosed cancers were lung (1.82 million), breast (1.67 million), and colorectal (1.36 million); the most common causes of cancer death were lung cancer (1.6 million deaths), liver cancer (745,000 deaths), and stomach cancer (723,000 deaths).

24,414 citations

Journal ArticleDOI
TL;DR: This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists, and it is concluded that hepatitis D virus cannot be classified as a human carcinogen.
Abstract: Viral hepatitis in all its forms is a major public health problem throughout the world, affecting several hundreds of millions of people. Viral hepatitis is a cause of considerable morbidity and mortality both from acute infection and chronic sequelae which include, in the case of hepatitis B, C and D, chronic active hepatitis and cirrhosis. Hepatocellular carcinoma, which is one of the 10 commonest cancers worldwide, is closely associated with hepatitis B and, at least in some regions of the world, with hepatitis C virus. This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists. (It is interesting to note in passing that some 5000 papers on viral hepatitis are published annually in the world literature.) The epidemiological, clinical and experimental data on the association between infection with hepatitis B virus and primary liver cancer in humans are reviewed in a readable and succinct format. The available information on hepatitis C and progression to chronic infection is also evaluated and it is concluded (perhaps a little prematurely) that hepatitis C virus is carcinogenic. However, it is concluded that hepatitis D virus, an unusual virus with a number of similarities to certain plant viral satellites and viroids, cannot be classified as a human carcinogen. There are some minor criticisms: there are few illustrations and some complex tabulations (for example, Table 6) and no subject index. A cumulative cross index to IARC Monographs is of little value and occupies nearly 30 pages. This small volume is a useful addition to the overwhelming literature on viral hepatitis, and the presentation is similar to the excellent World Health Organisation Technical Reports series on the subject published in the past. It is strongly recommended as a readable up-to-date summary of a complex subject; and at a cost of 65 Sw.fr (approximately £34) is excellent value. A J ZUCKERMAN

11,533 citations

Book
31 Dec 1997
TL;DR: The aim of this study was to establish a database of histological groups and to provide a level of consistency and quality of data that could be applied in the design of future registries.
Abstract: 1. Techniques of registration 2. Classification and coding 3. Histological groups 4. Comparability and quality of data 5. Data processing 6. Age-standardization 7. Incidence data by site and sex for each registry 8. Summary tables presenting age-standardized rates 9. Data on histological type for selected sites

10,160 citations


"Global cancer statistics, 2012" refers background in this paper

  • ...in many countries in South America, Africa, and Asia.(25) The reasons are not completely understood but likely reflect changing reproductive patterns, increasing obesity, decreasing physical activity,(26) and some breast cancer screening activity....

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  • ...Rates are low in Africa and South-Central Asia....

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  • ...Nearly 90% of cervical cancer deaths occurred in developing parts of the world: 60,100 deaths in Africa, 28,600 in Latin America and the Caribbean, and 144,400 in Asia....

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  • ...Global Cancer Statistics, 2012 92 CA: A Cancer Journal for Clinicians in many countries in South America, Africa, and Asia.25 The reasons are not completely understood but likely reflect changing reproductive patterns, increasing obesity, decreasing physical activity,26 and some breast cancer screening activity.14 Mortality rates in these countries are also increasing,27 most likely due to lifestyle changes associated with westernization compounded by the delayed introduction of effective breast cancer screening programs and, in some cases, limited access to treatment.27,28 Maintaining a healthy body weight, increasing physical activity, and minimizing alcohol intake are the best available strategies to reduce the risk of developing breast cancer.29 Mammography can often detect breast cancer at an early stage, when treatment is more effective and a cure is more likely....

    [...]

  • ...In the highest-risk area, often referred to as the “esophageal cancer belt,” which stretches from Northern Iran through the Central Asian republics to North-Central China, 90% of cases are squamous cell carcinomas, compared with about 26% in the United States (among white individuals).83,99,100 In high-risk areas such as Golestan (Iran) and Linxan (China), contributing risk factors are not well understood, but are thought to include poor nutritional status, low intake of fruits and vegetables, and drinking beverages at high temperatures.101-104 HPV infection has been detected in squamous cell carcinomas, particularly in highrisk areas in Asia....

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Journal ArticleDOI
TL;DR: Screening with the use of low-dose CT reduces mortality from lung cancer, as compared with the radiography group, and the rate of death from any cause was reduced.
Abstract: Background The aggressive and heterogeneous nature of lung cancer has thwarted efforts to reduce mortality from this cancer through the use of screening. The advent of low-dose helical computed tomography (CT) altered the landscape of lung-cancer screening, with studies indicating that low-dose CT detects many tumors at early stages. The National Lung Screening Trial (NLST) was conducted to determine whether screening with low-dose CT could reduce mortality from lung cancer. Methods From August 2002 through April 2004, we enrolled 53,454 persons at high risk for lung cancer at 33 U.S. medical centers. Participants were randomly assigned to undergo three annual screenings with either low-dose CT (26,722 participants) or single-view posteroanterior chest radiography (26,732). Data were collected on cases of lung cancer and deaths from lung cancer that occurred through December 31, 2009. Results The rate of adherence to screening was more than 90%. The rate of positive screening tests was 24.2% with low-dose CT and 6.9% with radiography over all three rounds. A total of 96.4% of the positive screening results in the low-dose CT group and 94.5% in the radiography group were false positive results. The incidence of lung cancer was 645 cases per 100,000 person-years (1060 cancers) in the low-dose CT group, as compared with 572 cases per 100,000 person-years (941 cancers) in the radiography group (rate ratio, 1.13; 95% confidence interval [CI], 1.03 to 1.23). There were 247 deaths from lung cancer per 100,000 person-years in the low-dose CT group and 309 deaths per 100,000 person-years in the radiography group, representing a relative reduction in mortality from lung cancer with low-dose CT screening of 20.0% (95% CI, 6.8 to 26.7; P=0.004). The rate of death from any cause was reduced in the low-dose CT group, as compared with the radiography group, by 6.7% (95% CI, 1.2 to 13.6; P=0.02). Conclusions Screening with the use of low-dose CT reduces mortality from lung cancer. (Funded by the National Cancer Institute; National Lung Screening Trial ClinicalTrials.gov number, NCT00047385.).

7,710 citations

Trending Questions (3)
Cancer statistics in the world

In 2012, there were approximately 14.1 million new cancer cases and 8.2 million deaths worldwide, with a shift towards less developed countries in terms of cancer burden.

Which are the current statistics for cancer worldwide?

The current statistics for cancer worldwide in 2012 were approximately 14.1 million new cases and 8.2 million deaths. Less developed countries accounted for 57% of cases and 65% of cancer deaths.

What is factors that lead to cancer rate increasing nowadays?

The factors that lead to the increasing cancer rate nowadays include the growth and aging of the population, prevalence of risk factors such as smoking, overweight, physical inactivity, and changing reproductive patterns associated with urbanization and economic development.