Describes the place of death from cancer in Scotland, by demographic characteristics including deprivation. Locations of death are home, hospice, NHS Acute hospital, other institution; covers the four major cancers of lung, breast, colorectal and prostate. Ten year trends are also presented. As from May 2010 these statistics can be designated as National Statistics products. Source agency: ISD Scotland (part of NHS National Services Scotland) Designation: National Statistics Language: English Alternative title: Place of Death from Cancer

This data shows premature deaths (Age under 75) from all Cancers, numbers and rates by gender, as 3-year moving-averages. Cancers are a major cause of premature deaths. Inequalities exist in cancer rates between the most deprived areas and the most affluent areas. Directly Age-Standardised Rates (DASR) are shown in the data (where numbers are sufficient) so that death rates can be directly compared between areas. The DASR calculation applies Age-specific rates to a Standard (European) population to cancel out possible effects on crude rates due to different age structures among populations, thus enabling direct comparisons of rates. A limitation on using mortalities as a proxy for prevalence of health conditions is that mortalities may give an incomplete view of health conditions in an area, as ill-health might not lead to premature death. Data source: Office for Health Improvement and Disparities (OHID), indicator ID 40501, E05a. This data is updated annually.

Directly age-standardised registration rate for oral cancer (ICD-10 C00-C14), in persons of all ages, per 100,000 2013 European Standard PopulationRationaleTobacco is a known risk factor for oral cancers (1). In England, 65% of hospital admissions (2014–15) for oral cancer and 64 % of deaths (2014) due to oral cancer were attributed to smoking (2). Oral cancer registration is therefore a direct measure of smoking-related harm. Given the high proportion of these registrations that are due to smoking, a reduction in the prevalence of smoking would reduce the incidence of oral cancer.Towards a Smokefree Generation: A Tobacco Control Plan for England states that tobacco use remains one of our most significant public health challenges and that smoking is the single biggest cause of inequalities in death rates between the richest and poorest in our communities (3).In January 2012 the Public Health Outcomes Framework was published, then updated in 2016. Smoking and smoking related death plays a key role in two of the four domains: Health Improvement and Preventing premature mortality (4).References:(1) GBD 2013 Risk Factors Collaborators. Global, regional and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risk factors in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. The Lancet 2015; 386:10010 2287–2323. (2) Statistics on smoking, England 2016, May 2016; http://content.digital.nhs.uk/catalogue/PUB20781 (3) Towards a Smokefree Generation: A Tobacco Control Plan for England, July 2017 https://www.gov.uk/government/publications/towards-a-smoke-free-generation-tobacco-control-plan-for-england (4) Public Health Outcomes Framework 2016 to 2019, August 2016; https://www.gov.uk/government/publications/public-health-outcomes-framework-2016-to-2019 Definition of numeratorCancer registrations for oral cancer (ICD-10, C00-C14) in the calendar years 2007-09 to 2017-2019. The National Cancer Registration and Analysis Service collects data relating to each new diagnosis of cancer that occurs in England. This does not include secondary cancers. Data are reported according to the calendar year in which the cancer was diagnosed.Definition of denominatorPopulation-years (ONS mid-year population estimates aggregated for the respective years) for people of all ages, aggregated into quinary age bands (0-4, 5-9,…, 85-89, 90+).CaveatsReviews of the quality of UK cancer registry data 1, 2 have concluded that registrations are largely complete, accurate and reliable. The data on cancer registration ‘quality indicators’ (mortality to incidence ratios, zero survival cases and unspecified site) demonstrate that although there is some variability, overall ascertainment and reliability is good. However cancer registrations are continuously being updated, so the number of registrations for each year may not be complete, as there is a small but steady stream of late registrations, some of which only come to light through death certification.1. Huggett C (1995). Review of the Quality and Comparability of Data held by Regional Cancer Registries. Bristol: Bristol Cancer Epidemiology Unit incorporating the South West Cancer Registry. 2. Seddon DJ, Williams EMI (1997). Data quality in population based cancer registration. British Journal of Cancer 76: 667-674.The data presented here replace versions previously published. Population data and the European Standard Population have been revised. ONS have provided an explanation of the change in standard population (available at http://www.ons.gov.uk/ons/guide-method/user-guidance/health-and-life-events/revised-european-standard-population-2013--2013-esp-/index.html )

Background: Lung cancer is the leading cause of cancer related death worldwide. Over the past 15 years no major improvement of survival rates could be accomplished. The recently discovered histone methyltransferase KMT9 as epigenetic regulator of prostate tumor growth has now raised hopes of enabling new cancer therapies. In this study we aimed to identify the function of KMT9 in lung cancer which has remained elusive so far. Methods: We linked full transcriptome and proteome analyses of A549 lung adenocarcinoma cells using RNA-Seq and mass spectrometry with functional cell culture, real-time proliferation and flow cytometry assays. Results: KMT9 is expressed in lung cancer tissue and cell lineswith high levels of KMT9 correlating with poor patient survival. We identified 460 overlapping genes and proteins that are deregulated upon knock-down of KMT9alpha in A549 cells. These genes cluster with proliferation, cell cycle and cell death gene sets as well as with subcellular organelles in gene ontology analysis. Knock-down of KMT9alpha inhibits lung cancer cell proliferation and induces non-apoptotic cell death in A549 cells. Conclusions: The novel histone methyltransferase KMT9 is crucial for proliferation and survival of lung cancer cells harboring various mutations. Small molecule inhibitors targeting KMT9 therefore should be further examined as potential milestones in modern epigenetic lung cancer therapy.

Results of logistic regression analysis: The younger group (

BackgroundTelomere length is an important indicator of tumor progression and survival for cancer patients. Previous work investigated the associations between genetically predicted telomere length and cancers; however, the types of cancers investigated in those studies were relatively limited or the telomere length-associated genetic variants employed often came from genome-wide association studies (GWASs) with small sample sizes.MethodsWe constructed the genetic risk score (GRS) for leukocyte telomere length based on 17 associated genetic variants available from the largest telomere length GWAS up to 78,592 individuals. Then, a comprehensive analysis was undertaken to evaluate the association between the constructed GRS and the risk or mortality of a wide range of cancers [i.e., 37 cancers in the UK Biobank and 33 cancers in The Cancer Genome Atlas (TCGA)]. We further applied the two-sample Mendelian randomization (MR) to estimate the causal effect of leukocyte telomere length on UK Biobank cancers via summary statistics.ResultsIn the UK Biobank dataset, we found that the GRS of leukocyte telomere length was associated with a decreased risk of nine types of cancer (i.e., significant association with multiple myeloma, chronic lymphocytic leukemia, kidney/renal cell cancer, bladder cancer, malignant melanoma, basal cell carcinoma, and prostate cancer and suggestive association with sarcoma/fibrosarcoma and Hodgkin’s lymphoma/Hodgkin’s disease). In addition, we found that the GRS was suggestively associated with an increased risk of leukemia. In the TCGA dataset, we observed suggestive evidence that the GRS was associated with a high death hazard of rectum adenocarcinoma (READ), sarcoma (SARC), and skin cutaneous melanoma (SKCM), while the GRS was associated with a low death hazard of kidney renal papillary cell carcinoma (KIRP). The results of MR further supported the association for leukocyte telomere length on the risk of malignant melanoma, Hodgkin’s lymphoma/Hodgkin’s disease, chronic lymphocytic leukemia and multiple myeloma.ConclusionOur study reveals that telomere played diverse roles in different types of cancers. However, further validations in large-scale prospective studies and deeper investigations of the biologic mechanisms are warranted.

Following a number of feasibility studies and pilot surveys carried out in 1978, the first Health and Lifestyle Survey (HALS1) (held at the UKDA under SN 2218), funded by the Health Promotion Research Trust, was carried out in 1984-1985 on a random sample of the population of England, Scotland and Wales. A follow-up survey, HALS2, was conducted in 1991-1992. Ethical approval for the initial pilot studies was obtained locally, and ethical approval for the main HALS surveys was received from the BMA Ethical Committee before the launch of each survey.

The first survey, HALS1, was designed as a unique attempt to describe the self-reported health, attitudes to health and beliefs about causes of disease in relation to measurements of health (e.g. blood pressure and lung function) and lifestyle in adults of all ages and circumstances living in their own homes in all parts of Great Britain. It also examined the distribution of, and the relationship between, physical and mental health, health-related behaviour (diet, exercise, smoking and alcohol consumption) and social circumstances. Following completion of HALS1, the respondents were 'flagged' with the Office for National Statistics (ONS) National Health Service register at Southport,so that notification of deaths and copies of death certificates of respondents were provided to the HALS1 team. (Note that at the time of HALS1 and 2, ONS was known as the Office of Population Censuses and Surveys (OPCS).)

At the time of HALS1, a repeat survey was not foreseen, so no attempt was made to retain contact with the respondents to HALS1. However, when funding again became available from the Health Promotion Research Trust, as many of the respondents to HALS1 were traced as possible, and re-surveyed for HALS2 (held under SN 3279), which was conducted in 1991-1992. The principal aims of HALS2 were to examine the changes over seven years in the health and circumstances of the surviving respondents of HALS1.

A further HALS dataset is held under SN 6339, which includes deaths and causes of death, and registrations of cancer morbidity and mortality for HALS respondents, currently up to June 2009.HALS Deaths and Cancer Data:
This file lists the original 9,003 respondents to HALS (1984-1985) and flags those found on the NHS Central Register at ONS Southport. This allows analysis of final outcome - death - to be correlated against previously reported medical history, physiological status and lifestyle behaviour. In addition, registrations for cancer morbidity and mortality for HALS respondents, taken from the various regional Cancer Registries' returns to ONS, are also included. Up to the beginning of July 2009, notification of some 2,883 deaths has been received, and 1,468 respondents have been coded for cancer. Further details may be found in the documentation.

This dataset comprises the 7th Listing (6th Update) of Deaths data, and the 4th Listing (3rd Update) of the Cancer data. Prior Listings/Updates of the Deaths and Cancer data were previously held under two separate studies, SN 3491, Health and Lifestyle Survey Deaths Data, and SN 4540, Health and Lifestyle Survey Cancer Data. As the Deaths and Cancer data are now included in one file, SNs 3491 and 4540 were combined into SN 6339 at the time the June 2009 updates were deposited, in November 2009.

Prostate cancer, a leading cause of cancer death, displays a broad range of clinical behavior from relatively indolent to aggressive metastatic disease. To explore potential molecular variation underlying this clinical heterogeneity, we profiled gene expression in 62 primary prostate tumors, as well as 41 normal prostate specimens and nine lymph node metastases, using cDNA microarrays containing approximately 26,000 genes. Unsupervised hierarchical clustering readily distinguished tumors from normal samples, and further identified three subclasses of prostate tumors based on distinct patterns of gene expression. High-grade and advanced stage tumors, as well as tumors associated with recurrence, were disproportionately represented among two of the three subtypes, one of which also included most lymph node metastases. To further characterize the clinical relevance of tumor subtypes, we evaluated as surrogate markers two genes differentially expressed among tumor subgroups by using immunohistochemistry on tissue microarrays representing an independent set of 225 prostate tumors. Positive staining for MUC1, a gene highly expressed in the subgroups with "aggressive" clinicopathological features, was associated with an elevated risk of recurrence (P = 0.003), whereas strong staining for AZGP1, a gene highly expressed in the other subgroup, was associated with a decreased risk of recurrence (P = 0.0008). In multivariate analysis, MUC1 and AZGP1 staining were strong predictors of tumor recurrence independent of tumor grade, stage, and preoperative prostate-specific antigen levels. Our results suggest that prostate tumors can be usefully classified according to their gene expression patterns, and these tumor subtypes may provide a basis for improved prognostication and treatment stratification. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Keywords: disease_state_design Using regression correlation

Ovarian cancer is the fifth most common malignancy in women and is the leading cause of death amongst gynecological cancers. Due to the nonspecific nature of disease symptoms, the majority of ovarian cancer patients are diagnosed with advanced-stage disease, at which point the prognosis is poor. Current standard of care therapies focus on debulking surgery and platinum-based chemotherapy, with carboplatin and paclitaxel being the gold standard. The majority of patients respond well to initial first-line therapy and enter into remission, however over 80% of patients will relapse and require multiple lines of therapy. Read More

Results of logistic regression analysis: The older group (50 years or older; 2,387 cases and 8,579 controls).

Liver cancer is the second leading cause of cancer related death in the world in men and the sixth leading cause of cancer death in women. Hepatocellular carcinoma (HCC) is the most dominant form of liver cancer, accounting for approximately 85% of liver cancer cases. The prognosis of HCC is dependent on the stage of the disease at diagnosis. However, even with treatments such as surgical resection, liver transplantation, and ablative therapies, which are only suitable for early-stage HCC patients, the majority of patients are likely to progress onto the advanced stages of the disease. Read More

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Cancer Biologics Market Size 2025-2029

The cancer biologics market size is valued to increase USD 84.5 billion, at a CAGR of 10.7% from 2024 to 2029. Rising global incidence of cancer will drive the cancer biologics market.

Major Market Trends & Insights

North America dominated the market and accounted for a 50% growth during the forecast period.
By Product - Monoclonal antibodies segment was valued at USD 76.00 billion in 2023
By Route Of Administration - Injectable segment accounted for the largest market revenue share in 2023

Market Size & Forecast

Market Opportunities: USD 112.60 billion
Market Future Opportunities: USD 84.50 billion
CAGR : 10.7%
North America: Largest market in 2023

Market Summary

The market encompasses a rapidly evolving landscape of technologies and applications, driven by the untapped potential in cancer treatment. Core technologies, such as monoclonal antibodies, immunotherapies, and gene therapies, continue to revolutionize oncology. Applications span from targeted therapies to immunomodulatory treatments, addressing various cancer types. Service types, including contract research organizations and clinical trial services, play a crucial role in advancing the market. Regulations, such as FDA approvals and reimbursement policies, significantly impact market dynamics. Despite the high cost of cancer biologics, their adoption rates continue to rise, fueled by the increasing global incidence of cancer. For instance, the World Health Organization estimates that approximately 19.3 million new cancer cases occurred worldwide in 2020. The evolving market landscape presents both opportunities and challenges, with ongoing research and development efforts shaping the future of cancer biologics.

What will be the Size of the Cancer Biologics Market during the forecast period?

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How is the Cancer Biologics Market Segmented and what are the key trends of market segmentation?

The cancer biologics industry research report provides comprehensive data (region-wise segment analysis), with forecasts and estimates in 'USD billion' for the period 2025-2029, as well as historical data from 2019-2023 for the following segments. ProductMonoclonal antibodiesCell and gene therapyVaccinesOthersRoute Of AdministrationInjectableOralTypeBreast cancerLung cancerColorectal cancerProstate cancerOthersDistribution ChannelHospitalsClinicsOthersGeographyNorth AmericaUSCanadaEuropeFranceGermanyItalyUKMiddle East and AfricaEgyptKSAOmanUAEAPACChinaIndiaJapanSouth AmericaArgentinaBrazilRest of World (ROW)

By Product Insights

The monoclonal antibodies segment is estimated to witness significant growth during the forecast period.

Monoclonal antibodies represent a significant segment of cancer therapeutics, targeting specific proteins involved in angiogenesis and altering cancer cell behavior. These targeted therapies prevent cancer progression and carcinogenesis, minimizing side-effects on healthy cells. In 2023, monoclonal antibodies accounted for 35% of the total cancer therapeutics market share. RNA interference, another burgeoning technology, silences disease-causing genes by introducing small RNA molecules. This approach has shown promise in cancer treatment, with a 30% market growth expectation in the next five years. Immunotherapy checkpoint inhibitors, such as PD-1 and CTLA-4 inhibitors, boost the immune system's response against cancer cells, accounting for 25% of the market share in 2023. Gene therapy vectors, including viral and non-viral, deliver therapeutic genes to cancer cells, triggering cell death or immune response. Clinical trials for gene therapy have shown a 27% success rate, with a projected 35% market expansion in the upcoming years. Tumor angiogenesis, tumor microenvironment, and cell cycle checkpoints are essential targets for cancer therapeutics, with ongoing research in biomarker discovery, therapeutic efficacy, and treatment response. Bispecific antibodies, antibody-drug conjugates, and CRISPR gene editing are innovative approaches to cancer treatment, addressing drug resistance mechanisms, personalized medicine, metastasis inhibitors, tumor suppressor genes, and DNA repair mechanisms. Toxicity profiles, immune cell engineering, and oncolytic viruses are crucial aspects of cancer therapeutics development, ensuring minimal side-effects and maximizing therapeutic efficacy. In the future, car T-cell therapy, progression-free survival, patient stratification, cancer stem cells, and targeted therapy will continue to shape the market, offering new opportunities and challenges for researchers and industry professionals.

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The Monoclonal antibodies segment was valued at USD 76.00 billion in 2019 and showed a gradual increase during the forecast period.

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Reg

Breast cancer is one of the most commonly diagnosed cancers among women and the leading cause of death in women under 50. The majority of breast cancers are estrogen receptor α-positive (ER+) and are most commonly treated with hormonal therapy that inhibits ER activity, such as tamoxifen. The TP53 tumor suppressor gene, encoding the p53 protein, is the most frequently mutated gene in breast cancer, and TP53 mutations are associated with diminished tamoxifen response and worse prognosis for breast cancer patients. Here, we report that in breast cancer cells p53 and ER cooperate to regulate the expression of a set of genes encoding chromatin modifiers. The net result is a global increase in H3K4me3 and decrease in H3K9me3 chromatin marks. The resultant “open” chromatin is associated with increased transcription of luminal cell identity genes and enhanced tamoxifen sensitivity. Conversely, diminished p53 control of these chromatin modulators is associated with the evolution of tamoxifen resistance and cancer stem cell properties.

Affymetrix-U133-plus2.0-based gene expression analysis of laser-captured epithelium from 128 cervical tissue specimens from women enrolled in SUCCEED Cervical cancer (CC) is the second most frequent cancer in women and the third leading cause of cancer death in women worldwide. Our analysis of normal, precancerous, and cancerous cervical tissue shows that progress of the disease is a cascade of increased DNA replication/repair and cell proliferation followed by substantial metabolic shifts. The data show a sharp decrease in estrogen receptor alpha (ER?) in tumor cells, and ranking tissue specimens by estrogen-responsive gene expression correlates remarkably closely with histological pathology. Johan, den Boon, Morgridge Institute for Research at University of Wisconsin-Madison Paul, Ahlquist, Howard Hughes Medical Institute and Morgridge Institute for Research at University of Wisconsin-Madison Nicolas, Wentzensen, National Cancer Institute 24 normal, 14 CIN1 lesions, 22 CIN2 lesions, 40 CIN3 lesions, and 28 cancers specimens were cryosecrtioned and used for laser-capture, RNA extraction, two rounds of T7-mediated amplification, and cRNA biotinylation. Bio-cRNA was hybridized to Affymetrix U133-Plus2.0 arrays, scanned signals were processed through GC-RMA

Liver cancer is one of the most common malignant tumors in the world and metastasis is the leading cause of death associated with liver cancer. Hypoxia is a common feature of solid tumors and enhances malignant character of cancer cells. However, the exact mechanisms involved in hypoxia-driven liver cancer progression and metastasis have not been well clarified so far. The aim of this study was to investigate the contribution of long non-coding RNA (lncRNA) in hypoxia promoting liver cancer progression. We screened and revealed LINC00839 as a novel hypoxia-responsive lncRNA in liver cancer. LINC00839 expression was up-regulated in liver cancer tissues and cell lines, and the patients with high LINC00839 expression had shortened overall survival. LINC00839 further overexpressed under hypoxia and promoted liver cancer cell proliferation, migration, and invasion. Mechanistically, LINC00839 bound multiple proteins that were primarily associated with the metabolism and RNA transport, and positively regulated the expression of Formin-like protein 2 (FMNL2). LINC00839 could promote hypoxia-mediated liver cancer progression, suggesting it may be a clinically valuable biomarker and serve as a molecular target for the diagnosis, prognosis, and therapy of liver cancer.

Prostate cancer (PCa) is the second most common cancer and fifth leading cause of cance death among men worldwide. Intriguingly, primary prostate tumors do not undergo a metabolic switch from oxidative phosphorylation to aerobic glycolysis to meet increased energetic and biosynthetic demand for cell growth and division. In contrast, PCa cells preferentially use fatty acids for metabolic fuel, and malignant transformation of prostate tissue is accompanied by a sustained increase in the activity of both lipogenic and oxidative enzymes. As peroxisomes (PO) play a key role in cellular lipid and redox metabolism, it may not come as a surprise that these organelles are increasingly recognized as being involved in the pathogenesis of PCa. However, many uncertainties and inadequacies in our understanding of how PO function in PCa progression remain. This project is intended to gain a more coherent picture of how alterations in PO metabolism contribute to PCa development, progression, and therapy response. Specifically, by employing cutting-edge technologies, we systematically inventory which peroxisomal parameters are affected in commonly used cell models of PCa.

Gastric cancer is still one of the most common causes of cancer-related death worldwide, which is mainly attributable to late diagnosis and poor treatment options. Infection with H. pylori, different environmental factors and genetic alterations are known to influence the risk of developing gastric tumors. However, the molecular mechanisms involved in gastric carcinogenesis are still not fully understood, making it difficult to design targeted therapeutic approaches. Aberrant expression of the specific gastric differentiation marker Sox2 (sry-related HMG box 2) has been observed in stomach cancer. However, the role of Sox2 in gastric tumors has not been well established to date. To elucidate the role of Sox2 in gastric tumorigenesis, Sox2 transcriptional activity was blocked in AZ521 cells. Interestingly, inhibition of Sox2 reduced cell proliferation and migration, increased apoptosis and induced changes in cell cycle. Blocking of Sox2 also reduced the tumorigenic potential of AZ521 cells in vivo. In addition, correlation of Sox2 expression and proliferation was observed in a subset of human gastric tumours. Finally, target genes of Sox2 were for the first time identified by RNA microarray in gastric cancer cells. Taken together, the results presented here indicate that Sox2 controls several aspects related to gastric cancer development and progression by regulating the expression of members of important signalling pathways. These findings could provide new therapeutic options for a subset of gastric cancers exhibiting Sox2 deregulation. Inducible dnSox2 in AZ521 cells, 4 timepoints with/without induction.

Results of logistic regression analysis: All cases and controls (2,585 cases and 9,362 controls).

Breast cancer remains one of the leading causes of death in women, being the chemotherapeutic agent doxorubicin (Dox) among the most widely standard chemotherapy options for its treatment. However, its effective use has been severely limited owing to its well-documented cardiotoxic side effect that can lead to heart failure in a subset of patients. We have previously shown that a specific population of mesenchymal stem cells (MSCs) present immunomodulatory and regenerative properties, mainly granted by its secretome (CM), whose potential was improved when produced under 3D conditions. In cancer, the role of MSCs is still contradictory, with literature reporting both cancer promoting and suppressive effects. Therefore, we aimed at determining the effect of concomitant exposure of Dox with CM from 3D (CM3D) and 2D (CM2D) MSC cultures in breast cancer cells (MDA-MB-231) and in non-tumour breast epithelial cells (MCF10A) and differentiated AC16 cardiomyocytes. As such, the whole secretome was obtained by collecting and concentrating the culture media conditioned by MSCs in 2D (CM2D) and 3D (CM3D). A Ge-LC-MS/MS proteomic analysis revealed that CM3D effects may be linked to MSC cytoprotection and tumour development, namely through regulation of cell proliferation (CAPN1, CST1, LAMC2, RANBP3), migration (CCN3, MMP-8, PDCD5), invasion (TIMP-1/2), oxidative stress (AIFM1, CD9, GSR) and inflammation (ANXA5, CDH13, GDF-15). Overall, MSC-derived CM3D decreased Dox-induced cytotoxic effects on non-tumour breast cells and cardiomyocytes, without compromising Dox chemotherapeutic nature, highlighting the potential use of CM3D as an adjuvant in chemotherapy to reduce off-target side effects.