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The Lancet. Public Health Dec 2023Cancer has been the leading cause of death since 2010 in China, with increasing incidence, mortality, and burden. We aimed to assess national and subnational changes in...
BACKGROUND
Cancer has been the leading cause of death since 2010 in China, with increasing incidence, mortality, and burden. We aimed to assess national and subnational changes in the cancer burden from 2005 to 2020 in China using data from the National Mortality Surveillance System.
METHODS
We extracted data on cancer-related deaths from the National Mortality Surveillance System, which accounts for 24·3% of the country's population with national and provincial representativeness. Data for the surveillance population stratified by age and sex were extracted from the National Bureau of Statistics of China. We estimated mortality and years of life lost (YLLs) for all cancers and for 23 cancer groups by age and sex, nationally, and for 31 provinces in China between 2005 and 2020. We calculated age-standardised mortality and YLL rates using the China 2020 census as the reference population. Average annual percent changes in age-standardised rates for mortality and YLLs were calculated to assess trends over the study period. Decomposition analysis was used to assess the drivers of changes in cancer-related death due to three explanatory components: population growth, population ageing, and age-specific mortality rates in China.
FINDINGS
The total number of cancer-related deaths increased by 21·6% to 2 397 772 and YLLs increased by 5·0% to 56 598 975 between 2005 and 2020. The three leading fatal cancer types remained stable for both sexes over the study period: tracheal, bronchus, and lung cancer; liver cancer; and stomach cancer. The fourth and fifth leading cancers also remained stable among males (oesophageal, and colon and rectum), while colon and rectum cancer replaced oesophageal cancer as the fourth and breast cancer replaced colon and rectum cancer as the fifth leading cause of cancer-related death among females. Age-standardised mortality rates and age-standardised YLL rates for almost all cancer types (except for prostate for male and multiple myeloma for female) decreased significantly in both sexes in urban areas. Age-standardised YLL rates increased for about half of all cancers for both sexes in rural areas. Leading fatal types were leukaemia and brain and nervous system cancer in younger groups (aged 0-19 years); liver, tracheal, bronchus, and lung, or breast cancers in middle-aged groups (aged 40-59 years); and tracheal, bronchus, and lung, liver, or stomach cancers in older adults (aged ≥60 years) in 2020. The leading causes of cancer-related mortality varied for each province, with tracheal, bronchus, and lung or liver cancer at the top in 30 provinces.
INTERPRETATION
The cancer burden in China appeared to be shifting towards that in high-income countries from 2005 to 2020. Adjustments to existing health plans and actions are needed to reduce the burdens of tracheal, bronchus, and lung cancer or other leading and emerging cancers.
FUNDING
National Key Research and Development Program of China.
Topics: Middle Aged; Humans; Male; Female; Aged; Cause of Death; Breast Neoplasms; Lung Neoplasms; Liver Neoplasms; Rectal Neoplasms; Stomach Neoplasms
PubMed: 38000889
DOI: 10.1016/S2468-2667(23)00211-6 -
Nature Dec 2023Four endemic seasonal human coronaviruses causing common colds circulate worldwide: HKU1, 229E, NL63 and OC43 (ref. ). After binding to cellular receptors, coronavirus...
Four endemic seasonal human coronaviruses causing common colds circulate worldwide: HKU1, 229E, NL63 and OC43 (ref. ). After binding to cellular receptors, coronavirus spike proteins are primed for fusion by transmembrane serine protease 2 (TMPRSS2) or endosomal cathepsins. NL63 uses angiotensin-converting enzyme 2 as a receptor, whereas 229E uses human aminopeptidase-N. HKU1 and OC43 spikes bind cells through 9-O-acetylated sialic acid, but their protein receptors remain unknown. Here we show that TMPRSS2 is a functional receptor for HKU1. TMPRSS2 triggers HKU1 spike-mediated cell-cell fusion and pseudovirus infection. Catalytically inactive TMPRSS2 mutants do not cleave HKU1 spike but allow pseudovirus infection. Furthermore, TMPRSS2 binds with high affinity to the HKU1 receptor binding domain (Kd 334 and 137 nM for HKU1A and HKU1B genotypes) but not to SARS-CoV-2. Conserved amino acids in the HKU1 receptor binding domain are essential for binding to TMPRSS2 and pseudovirus infection. Newly designed anti-TMPRSS2 nanobodies potently inhibit HKU1 spike attachment to TMPRSS2, fusion and pseudovirus infection. The nanobodies also reduce infection of primary human bronchial cells by an authentic HKU1 virus. Our findings illustrate the various evolution strategies of coronaviruses, which use TMPRSS2 to either directly bind to target cells or prime their spike for membrane fusion and entry.
Topics: Humans; Betacoronavirus; Bronchi; Common Cold; Membrane Fusion; Receptors, Virus; SARS-CoV-2; Serine Endopeptidases; Single-Domain Antibodies; Species Specificity; Spike Glycoprotein, Coronavirus; Virus Internalization
PubMed: 37879362
DOI: 10.1038/s41586-023-06761-7