PurposeThis study reports the cancer statistics and temporal trends in Korea on a nationwide scale, including incidence, survival, prevalence, and mortality in 2017.Materials and MethodsThe incidence, survival, and prevalence rates of cancer were evaluated using data from the Korea National Cancer Incidence Database from 1999 to 2017 with follow-up until December 31, 2018. Deaths from cancer were assessed using cause-of-death data from 1983 to 2017, obtained from Statistics Korea. Crude and age-standardized rates (ASRs) for incidence, mortality, and prevalence, and 5-year relative survival rates were calculated and trend analysis was performed.ResultsIn 2017, newly diagnosed cancer cases and deaths from cancer numbered 232,255 (ASR, 264.4 per 100,000) and 78,863 (ASR, 76.6 per 100,000), respectively. The overall cancer incidence rates increased annually by 3.5% from 1999 to 2011 and decreased by 2.7% annually thereafter. Cancer mortality rates have been decreasing since 2002, by 2.8% annually. The 5-year relative survival rate for all patients diagnosed with cancer between 2013 and 2017 was 70.4%, which contributed to a prevalence of approximately 1.87 million cases by the end of 2017.ConclusionThe burden of cancer measured by incidence and mortality rates have improved in Korea, with the exception of a few particular cancers that are associated with increasing incidence or mortality rates. However, cancer prevalence is increasing rapidly, with the dramatic improvement in survival during the past several years. Comprehensive cancer control strategies and efforts should continue, based on the changes of cancer statistics.

Zn 1−x Co x O  (x⩽0.22) films were prepared on (0001)-oriented Al2O3 substrates by rf magnetron sputtering. The alloys show wurtzite crystal structure with the c-axis lattice constant increasing with increasing x. The optical properties of the samples were measured by spectroscopic ellipsometry at room temperature in the 1.5–5 eV photon energy region. As x increases, the optical band gap absorption edge (E0) of the alloys shows a redshift from that of pure ZnO, reaching 350 meV for x=0.22. The excitonic character of the E0 edge is gradually reduced as x increases and is replaced by the three-dimensional critical-point shape. Optical absorption structures are also observed below the E0 edge near 2 eV and interpreted as due to the transitions between the crystal-field-split 3d levels of tetrahedral Co2+ ions substituting Zn2+ ions.

Using the full-potential linearized augmented plane wave method, we have investigated the oxygen vacancy defect induced ferromagnetism in both rutile and anatase TiO(2). It has been found that the oxygen vacancy induces lattice distortion in rutile TiO(2), whereas there is no such meaningful change in the anatase structure. Interestingly, the lattice distorted rutile TiO(2) shows an oxygen vacancy induced ferromagnetic state with a magnetic moment of 0.22 µ(B) in the Ti atom neighboring the vacancy site, while only 0.06 µ(B) is observed in the Ti atom in anatase TiO(2). We attribute the sizable magnetic moment due to the oxygen vacancy in rutile TiO(2) to the charge redistribution owing to lattice distortion. Experimentally measured magnetic hysteresis curves for undoped rutile and anatase TiO(2) films clearly display ferromagnetic behavior at room temperature. The observed magnetic strength of the rutile sample turns out to be larger than that of the anatase sample, in accordance with the theoretical calculations.

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Optical absorption properties of n-type In-doped ZnO films were investigated by spectroscopic ellipsometry for varying carrier concentration. The fundamental optical band gap (E0) edge of the compound showed a blueshift below the carrier concentration n0=5×1019 cm−3, which can be explained in terms of the Burstein–Moss band-filling effect. An abrupt jump of the E0 edge from blue- to redshift was observed as the carrier concentration increased beyond n0. It is interpreted as due to a merging of the donor and conduction bands of the compound near n0. The redshift increases quite linearly with the carrier concentration, reaching 600 meV for n=1.2×1020 cm−3. Such linear increase is interpreted as mainly due to a band gap narrowing caused by impurity-induced potential fluctuations.

Transmembrane-4-L6 family 1 (TM4SF1) is upregulated in colorectal carcinoma (CRC). However, the mechanism leading to inhibition of the TM4SF1 is not known. In the present study, we investigated the regulation of TM4SF1 and function of microRNAs (miRNAs) in CRC invasion and metastasis. We analyzed 60 colon cancers and paired normal specimens for TM4SF1 and miRNA-9 (miR-9) expression using quantitative real-time PCR. A bioinformatics analysis identified a putative miR-9 binding site within the 3'-UTR of TM4SF1. We also found that TM4SF1 was upregulated in CRC tissues and CRC cell lines. The expression of TM4SF1 was positively correlated with clinical advanced stage and lymph node metastasis. Moreover, a luciferase assay revealed that miR-9 directly targeted 3'-UTR-TM4SF1. Overexpression of miR-9 inhibited expression of TM4SF1 mRNA and protein, wound healing, transwell migration and invasion of SW480 cells, whereas, overexpression of anti-miR-9 and siRNA-TM4SF1 inversely regulated the TM4SF1 mRNA and protein level in HCT116 cells. Furthermore, miR-9 suppressed not only TM4SF1 expression but also MMP-2, MMP-9 and VEGF expression. In clinical specimens, miR-9 was generally down-regulated in CRC and inversely correlated with TM4SF1 expression. These results suggest that miR-9 functions as a tumor-suppressor in CRC, and that its suppressive effects mediate invasion and metastasis by inhibition of TM4SF1 expression. Our results also indicate that miR-9 might be a novel target for the treatment of CRC invasion and metastasis.

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