Cancer research

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Cancer research is research into cancer to identify causes and develop strategies for prevention, diagnosis, treatment, and cure.

Contents

Cancer research ranges from epidemiology, molecular bioscience to the performance of clinical trials to evaluate and compare applications of the various cancer treatments. These applications include surgery, radiation therapy, chemotherapy, hormone therapy, immunotherapy and combined treatment modalities such as chemo-radiotherapy. Starting in the mid-1990s, the emphasis in clinical cancer research shifted towards therapies derived from biotechnology research, such as cancer immunotherapy and gene therapy.

Cancer research is done in academia, research institutes, and corporate environments, and is largely government funded.[ citation needed ]

History

Sidney Farber is regarded as the father of modern chemotherapy. Sidney Farber nci-vol-1926-300.jpg
Sidney Farber is regarded as the father of modern chemotherapy.

Cancer research has been ongoing for centuries. Early research focused on the causes of cancer. [1] Percivall Pott identified the first environmental trigger (chimney soot) for cancer in 1775 and cigarette smoking was identified as a cause of lung cancer in 1950. Early cancer treatment focused on improving surgical techniques for removing tumors. Radiation therapy took hold in the 1900s. Chemotherapeutics were developed and refined throughout the 20th century.

The U.S. declared a "War on Cancer" in the 1970s, and increased the funding and support for cancer research. [2]

Seminal papers

Some of the most highly cited and most influential research reports include:

Types of research

Cancer research encompasses a variety of types and interdisciplinary areas of research. Scientists involved in cancer research may be trained in areas such as chemistry, biochemistry, molecular biology, physiology, medical physics, epidemiology, and biomedical engineering. Research performed on a foundational level is referred to as basic research and is intended to clarify scientific principles and mechanisms. Translational research aims to elucidate mechanisms of cancer development and progression and transform basic scientific findings into concepts that can be applicable to the treatment and prevention of cancer. Clinical research is devoted to the development of pharmaceuticals, surgical procedures, and medical technologies for the eventual treatment of patients.

Prevention and epidemiology

Epidemiologic analysis indicates that at least 35% of all cancer deaths in the world could now be avoided by primary prevention. [3] According to a newer GBD systematic analysis, in 2019, ~44% of all cancer deaths — or ~4.5 million deaths or ~105 million lost disability-adjusted life years — were due to known clearly preventable risk factors , led by smoking, alcohol use and high BMI. [4]

However, one 2015 study suggested that between ~70% and ~90% of cancers are due to environmental factors and therefore potentially preventable. [5] [ contradictory ] Furthermore, it is estimated that with further research cancer death rates could be reduced by 70% around the world even without the development of any new therapies. [3] Cancer prevention research receives only 2–9% of global cancer research funding, [3] albeit many of the options for prevention are already well-known without further cancer-specific research but are not reflected in economics and policy. Mutational signatures of various cancers, for example, could reveal further causes of cancer and support causal attribution. [6] [ additional citation(s) needed ]

Detection

Prompt detection of cancer is important, since it is usually more difficult to treat in later stages. Accurate detection of cancer is also important because false positives can cause harm from unnecessary medical procedures. Some screening protocols are currently not accurate (such as prostate-specific antigen testing). Others such as a colonoscopy or mammogram are unpleasant and as a result some patients may opt out. Active research is underway to address all these problems, to develop novel ways of cancer screening and to increase detection rates.[ citation needed ][ further explanation needed ]

For example:

Treatment

Emerging topics of cancer treatment research include:

Cause and development of cancer

Numerous cell signaling pathways are disrupted in the development of cancer. Signal transduction v1.png
Numerous cell signaling pathways are disrupted in the development of cancer.

Research into the cause of cancer involves many different disciplines including genetics, diet, environmental factors (i.e. chemical carcinogens). In regard to investigation of causes and potential targets for therapy, the route used starts with data obtained from clinical observations, enters basic research, and, once convincing and independently confirmed results are obtained, proceeds with clinical research, involving appropriately designed trials on consenting human subjects, with the aim to test safety and efficiency of the therapeutic intervention method. An important part of basic research is characterization of the potential mechanisms of carcinogenesis, in regard to the types of genetic and epigenetic changes that are associated with cancer development. The mouse is often used as a mammalian model for manipulation of the function of genes that play a role in tumor formation, while basic aspects of tumor initiation, such as mutagenesis, are assayed on cultures of bacteria and mammalian cells.

Genes involved in cancer

The goal of oncogenomics is to identify new oncogenes or tumor suppressor genes that may provide new insights into cancer diagnosis, predicting clinical outcome of cancers, and new targets for cancer therapies. As the Cancer Genome Project stated in a 2004 review article, "a central aim of cancer research has been to identify the mutated genes that are causally implicated in oncogenesis (cancer genes)." [32] The Cancer Genome Atlas project is a related effort investigating the genomic changes associated with cancer, while the COSMIC cancer database documents acquired genetic mutations from hundreds of thousands of human cancer samples. [33]

These large scale projects, involving about 350 different types of cancer, have identified ~130,000 mutations in ~3000 genes that have been mutated in the tumors. The majority occurred in 319 genes, of which 286 were tumor suppressor genes and 33 oncogenes.

Several hereditary factors can increase the chance of cancer-causing mutations, including the activation of oncogenes or the inhibition of tumor suppressor genes. The functions of various onco- and tumor suppressor genes can be disrupted at different stages of tumor progression. Mutations in such genes can be used to classify the malignancy of a tumor.

In later stages, tumors can develop a resistance to cancer treatment. The identification of oncogenes and tumor suppressor genes is important to understand tumor progression and treatment success. The role of a given gene in cancer progression may vary tremendously, depending on the stage and type of cancer involved. [34]

Cancer epigenetics

These paragraphs are an excerpt from Cancer epigenetics.[ edit ]
Cancer epigenetics is the study of epigenetic modifications to the DNA of cancer cells that do not involve a change in the nucleotide sequence, but instead involve a change in the way the genetic code is expressed. Epigenetic mechanisms are necessary to maintain normal sequences of tissue specific gene expression and are crucial for normal development. [35] They may be just as important, if not even more important, than genetic mutations in a cell's transformation to cancer. The disturbance of epigenetic processes in cancers, can lead to a loss of expression of genes that occurs about 10 times more frequently by transcription silencing (caused by epigenetic promoter hypermethylation of CpG islands) than by mutations. As Vogelstein et al. points out, in a colorectal cancer there are usually about 3 to 6 driver mutations and 33 to 66 hitchhiker or passenger mutations. [36] However, in colon tumors compared to adjacent normal-appearing colonic mucosa, there are about 600 to 800 heavily methylated CpG islands in the promoters of genes in the tumors while these CpG islands are not methylated in the adjacent mucosa. [37] [38] [39] Manipulation of epigenetic alterations holds great promise for cancer prevention, detection, and therapy. [40] [41] In different types of cancer, a variety of epigenetic mechanisms can be perturbed, such as the silencing of tumor suppressor genes and activation of oncogenes by altered CpG island methylation patterns, histone modifications, and dysregulation of DNA binding proteins. There are several medications which have epigenetic impact, that are now used in a number of these diseases.

Diet and cancer

This section is an excerpt from Diet and cancer.[ edit ]
Advertisement suggesting that a healthy diet helps prevent cancer. Make healthy choices poster.jpg
Advertisement suggesting that a healthy diet helps prevent cancer.

Many dietary recommendations have been proposed to reduce the risk of cancer, few have significant supporting scientific evidence. [42] [43] [44] Obesity and drinking alcohol have been correlated with the incidence and progression of some cancers. [42] Lowering the consumption of sweetened beverages is recommended as a measure to address obesity. [45]

Some specific foods are linked to specific cancers. There is strong evidence that processed meat and red meat intake increases risk of colorectal cancer. [46] [47] [48] [49] Aflatoxin B1, a frequent food contaminant, increases risk of liver cancer, [50] while drinking coffee is associated with a reduced risk. [51] Betel nut chewing causes oral cancer. [50] Stomach cancer is more common in Japan due to its high-salt diet. [50] [52]

Dietary recommendations for cancer prevention typically include weight management and eating a healthy diet, consisting mainly of "vegetables, fruit, whole grains and fish, and a reduced intake of red meat, animal fat, and refined sugar." [42] A healthy dietary pattern may lower cancer risk by 10–20%. [53] There is no clinical evidence that diets or specific foods can cure cancer. [54] [55]

Periods of intermittent fasting (time-restricted feeding which may not include caloric restriction) is investigated for potential usefulness in cancer prevention and treatment and as of 2021 additional trials are needed to elucidate the risks and benefits. [56] [57] [58] [59] In some cases, "caloric restrictions could hinder both cancer growth and progression, besides enhancing the efficacy of chemotherapy and radiation therapy". [60] Caloric restriction mimetics, including some present in foods like spermidine, are also investigated for these or similar reasons. [61] [62] Such and similar dietary supplements may contribute to prevention or treatment, with candidate substances including apigenin, [63] [64] [65] berberine, [66] [67] [68] [69] [70] jiaogulan, [71] and rhodiola rosea. [72] [73]

Research funding

Cancer research is funded by government grants, charitable foundations and pharmaceutical and biotechnology companies. [74]

In the early 2000s, most funding for cancer research came from taxpayers and charities, rather than from corporations. In the US, less than 30% of all cancer research was funded by commercial researchers such as pharmaceutical companies. [75] Per capita, public spending on cancer research by taxpayers and charities in the US was five times as much in 2002–03 as public spending by taxpayers and charities in the 15 countries that were full members of the European Union. [75] As a percentage of GDP, the non-commercial funding of cancer research in the US was four times the amount dedicated to cancer research in Europe. [75] Half of Europe's non-commercial cancer research is funded by charitable organizations. [75]

The National Cancer Institute is the major funding institution in the United States. In the 2023 fiscal year, the NCI funded $7.1 billion in cancer research. [76]

Difficulties

Difficulties inherent to cancer research are shared with many types of biomedical research.

Cancer research processes have been criticised. These include, especially in the US, for the financial resources and positions required to conduct research. Other consequences of competition for research resources appear to be a substantial number of research publications whose results cannot be replicated. [77] [78] [79] [80]

Replicability

This section is an excerpt from Replication crisis § In medicine.[ edit ]
Results from The Reproducibility Project: Cancer Biology suggest most studies of the cancer research sector may not be replicable. Barriers to conducting replications of experiment in cancer research.jpg
Results from The Reproducibility Project: Cancer Biology suggest most studies of the cancer research sector may not be replicable.
In a 2012 paper, C. Glenn Begley, a biotech consultant working at Amgen, and Lee Ellis, a medical researcher at the University of Texas, found that only 11% of 53 pre-clinical cancer studies had replications that could confirm conclusions from the original studies. [81] In late 2021, The Reproducibility Project: Cancer Biology examined 53 top papers about cancer published between 2010 and 2012 and showed that among studies that provided sufficient information to be redone, the effect sizes were 85% smaller on average than the original findings. [82] [83] A survey of cancer researchers found that half of them had been unable to reproduce a published result. [84] Another report estimated that almost half of randomized controlled trials contained flawed data (based on the analysis of anonymized individual participant data (IPD) from more than 150 trials). [85]

Public participation

Distributed computing

One can share computer time for distributed cancer research projects like Help Conquer Cancer. [86] World Community Grid also had a project called Help Defeat Cancer. Other related projects include the Folding@home and Rosetta@home projects, which focus on groundbreaking protein folding and protein structure prediction research. Vodafone has also partnered with the Garvan Institute to create the DreamLab Project, which uses distributed computing via an app on cellphones to perform cancer research.

Clinical trials

MatchMiner overview of data flow and modes of use MatchMiner overview of data flow and modes of use.webp
MatchMiner overview of data flow and modes of use

Members of the public can also join clinical trials as healthy control subjects or for methods of cancer detection.

There could be software and data-related procedures that increase participation in trials and make them faster and less expensive. One open source platform matches genomically profiled cancer patients to precision medicine drug trials. [88] [87]

MD Anderson Cancer Center is ranked as one of the top cancer research institutions. MDACC.jpg
MD Anderson Cancer Center is ranked as one of the top cancer research institutions.

Organizations

Breast cancer awareness ribbon statue in Kentucky Breast Cancer Awareness (263497131).jpg
Breast cancer awareness ribbon statue in Kentucky

Organizations exist as associations for scientists participating in cancer research, such as the American Association for Cancer Research and American Society of Clinical Oncology, and as foundations for public awareness or raising funds for cancer research, such as Relay For Life and the American Cancer Society.

Awareness campaigns

Supporters of different types of cancer have adopted different colored awareness ribbons and promote months of the year as being dedicated to the support of specific types of cancer. [89] The American Cancer Society began promoting October as Breast Cancer Awareness Month in the United States in the 1980s. Pink products are sold to both generate awareness and raise money to be donated for research purposes. This has led to pinkwashing, or the selling of ordinary products turned pink as a promotion for the company.

See also

Related Research Articles

Experimental cancer treatments are mainstream medical therapies intended to treat cancer by improving on, supplementing or replacing conventional methods. However, researchers are still trying to determine whether these treatments are safe and effective treatments. Experimental cancer treatments are normally available only to people who participate in formal research programs, which are called clinical trials. Occasionally, a seriously ill person may be able to access an experimental drug through an expanded access program. Some of the treatments have regulatory approval for treating other conditions. Health insurance and publicly funded health care programs normally refuse to pay for experimental cancer treatments.

<span class="mw-page-title-main">Tumor suppressor gene</span> Gene that inhibits expression of the tumorigenic phenotype

A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication. If the cell grows uncontrollably, it will result in cancer. When a tumor suppressor gene is mutated, it results in a loss or reduction in its function. In combination with other genetic mutations, this could allow the cell to grow abnormally. The loss of function for these genes may be even more significant in the development of human cancers, compared to the activation of oncogenes.

<span class="mw-page-title-main">Cancer</span> Group of diseases involving cell growth

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread. Possible signs and symptoms include a lump, abnormal bleeding, prolonged cough, unexplained weight loss, and a change in bowel movements. While these symptoms may indicate cancer, they can also have other causes. Over 100 types of cancers affect humans.

<span class="mw-page-title-main">Colorectal cancer</span> Cancer of the colon or rectum

Colorectal cancer (CRC), also known as bowel cancer, colon cancer, or rectal cancer, is the development of cancer from the colon or rectum. Signs and symptoms may include blood in the stool, a change in bowel movements, weight loss, abdominal pain and fatigue. Most colorectal cancers are due to lifestyle factors and genetic disorders. Risk factors include diet, obesity, smoking, and lack of physical activity. Dietary factors that increase the risk include red meat, processed meat, and alcohol. Another risk factor is inflammatory bowel disease, which includes Crohn's disease and ulcerative colitis. Some of the inherited genetic disorders that can cause colorectal cancer include familial adenomatous polyposis and hereditary non-polyposis colon cancer; however, these represent less than 5% of cases. It typically starts as a benign tumor, often in the form of a polyp, which over time becomes cancerous.

<span class="mw-page-title-main">Glioma</span> Tumour of the glial cells of the brain or spine

A glioma is a type of primary tumor that starts in the glial cells of the brain or spinal cord. They are cancerous but some are extremely slow to develop. Gliomas comprise about 30 percent of all brain tumors and central nervous system tumours, and 80 percent of all malignant brain tumours.

<span class="mw-page-title-main">Glioblastoma</span> Aggressive type of brain cancer

Glioblastoma, previously known as glioblastoma multiforme (GBM), is the most aggressive and most common type of cancer that originates in the brain, and has a very poor prognosis for survival. Initial signs and symptoms of glioblastoma are nonspecific. They may include headaches, personality changes, nausea, and symptoms similar to those of a stroke. Symptoms often worsen rapidly and may progress to unconsciousness.

<span class="mw-page-title-main">Neuroblastoma</span> Genetically inherited cancer of certain nerve tissues

Neuroblastoma (NB) is a type of cancer that forms in certain types of nerve tissue. It most frequently starts from one of the adrenal glands but can also develop in the head, neck, chest, abdomen, or spine. Symptoms may include bone pain, a lump in the abdomen, neck, or chest, or a painless bluish lump under the skin.

<span class="mw-page-title-main">Non-small-cell lung cancer</span> Any type of epithelial lung cancer other than small-cell lung carcinoma

Non-small-cell lung cancer (NSCLC), or non-small-cell lung carcinoma, is any type of epithelial lung cancer other than small-cell lung cancer (SCLC). NSCLC accounts for about 85% of all lung cancers. As a class, NSCLCs are relatively insensitive to chemotherapy, compared to small-cell carcinoma. When possible, they are primarily treated by surgical resection with curative intent, although chemotherapy has been used increasingly both preoperatively and postoperatively.

<span class="mw-page-title-main">Oncogenomics</span> Sub-field of genomics

Oncogenomics is a sub-field of genomics that characterizes cancer-associated genes. It focuses on genomic, epigenomic and transcript alterations in cancer.

<span class="mw-page-title-main">KRAS</span> Protein-coding gene in humans

KRAS is a gene that provides instructions for making a protein called K-Ras, a part of the RAS/MAPK pathway. The protein relays signals from outside the cell to the cell's nucleus. These signals instruct the cell to grow and divide (proliferate) or to mature and take on specialized functions (differentiate). It is called KRAS because it was first identified as a viral oncogene in the KirstenRAt Sarcoma virus. The oncogene identified was derived from a cellular genome, so KRAS, when found in a cellular genome, is called a proto-oncogene.

<span class="mw-page-title-main">Liver cancer</span> Medical condition

Liver cancer, also known as hepatic cancer, primary hepatic cancer, or primary hepatic malignancy, is cancer that starts in the liver. Liver cancer can be primary in which the cancer starts in the liver, or it can be liver metastasis, or secondary, in which the cancer spreads from elsewhere in the body to the liver. Liver metastasis is the more common of the two liver cancers. Instances of liver cancer are increasing globally.

<span class="mw-page-title-main">CDKN2A</span> Protein-coding gene in humans

CDKN2A, also known as cyclin-dependent kinase inhibitor 2A, is a gene which in humans is located at chromosome 9, band p21.3. It is ubiquitously expressed in many tissues and cell types. The gene codes for two proteins, including the INK4 family member p16 and p14arf. Both act as tumor suppressors by regulating the cell cycle. p16 inhibits cyclin dependent kinases 4 and 6 and thereby activates the retinoblastoma (Rb) family of proteins, which block traversal from G1 to S-phase. p14ARF activates the p53 tumor suppressor. Somatic mutations of CDKN2A are common in the majority of human cancers, with estimates that CDKN2A is the second most commonly inactivated gene in cancer after p53. Germline mutations of CDKN2A are associated with familial melanoma, glioblastoma and pancreatic cancer. The CDKN2A gene also contains one of 27 SNPs associated with increased risk of coronary artery disease.

Somatic evolution is the accumulation of mutations and epimutations in somatic cells during a lifetime, and the effects of those mutations and epimutations on the fitness of those cells. This evolutionary process has first been shown by the studies of Bert Vogelstein in colon cancer. Somatic evolution is important in the process of aging as well as the development of some diseases, including cancer.

Synthetic lethality is defined as a type of genetic interaction where the combination of two genetic events results in cell death or death of an organism. Although the foregoing explanation is wider than this, it is common when referring to synthetic lethality to mean the situation arising by virtue of a combination of deficiencies of two or more genes leading to cell death, whereas a deficiency of only one of these genes does not. In a synthetic lethal genetic screen, it is necessary to begin with a mutation that does not result in cell death, although the effect of that mutation could result in a differing phenotype, and then systematically test other mutations at additional loci to determine which, in combination with the first mutation, causes cell death arising by way of deficiency or abolition of expression.

<span class="mw-page-title-main">Cancer treatment</span> Overview of various treatment possibilities for cancer

Cancer treatments are a wide range of treatments available for the many different types of cancer, with each cancer type needing its own specific treatment. Treatments can include surgery, chemotherapy, radiation therapy, hormonal therapy, targeted therapy including small-molecule drugs or monoclonal antibodies, and PARP inhibitors such as olaparib. Other therapies include hyperthermia, immunotherapy, photodynamic therapy, and stem-cell therapy. Most commonly cancer treatment involves a series of separate therapies such as chemotherapy before surgery. Angiogenesis inhibitors are sometimes used to enhance the effects of immunotherapies.

Embryonal rhabdomyosarcoma (EMRS) is a rare histological form of cancer in the connective tissue wherein the mesenchymally-derived cells (rhabdomyoblasts) resemble the primitive developing skeletal muscle of the embryo. It is the most common soft tissue sarcoma occurring in children. Embryonal rhabdomyosarcoma is also known as PAX-fusion negative or fusion-negative rhabdomyosarcoma, as tumors of this subtype are unified by their lack of a PAX3-FOXO1 fusion oncogene. Fusion status refers to the presence or absence of a fusion gene, which is a gene formed from joining two different genes together through DNA rearrangements. These types of tumors are classified as embryonal rhabdomyosarcoma "because of their remarkable resemblance to developing embryonic and fetal skeletal muscle."

<span class="mw-page-title-main">Cancer biomarker</span> Substance or process that is indicative of the presence of cancer in the body

A cancer biomarker refers to a substance or process that is indicative of the presence of cancer in the body. A biomarker may be a molecule secreted by a tumor or a specific response of the body to the presence of cancer. Genetic, epigenetic, proteomic, glycomic, and imaging biomarkers can be used for cancer diagnosis, prognosis, and epidemiology. Ideally, such biomarkers can be assayed in non-invasively collected biofluids like blood or serum.

<span class="mw-page-title-main">Cancer epigenetics</span> Field of study in cancer research

Cancer epigenetics is the study of epigenetic modifications to the DNA of cancer cells that do not involve a change in the nucleotide sequence, but instead involve a change in the way the genetic code is expressed. Epigenetic mechanisms are necessary to maintain normal sequences of tissue specific gene expression and are crucial for normal development. They may be just as important, if not even more important, than genetic mutations in a cell's transformation to cancer. The disturbance of epigenetic processes in cancers, can lead to a loss of expression of genes that occurs about 10 times more frequently by transcription silencing than by mutations. As Vogelstein et al. points out, in a colorectal cancer there are usually about 3 to 6 driver mutations and 33 to 66 hitchhiker or passenger mutations. However, in colon tumors compared to adjacent normal-appearing colonic mucosa, there are about 600 to 800 heavily methylated CpG islands in the promoters of genes in the tumors while these CpG islands are not methylated in the adjacent mucosa. Manipulation of epigenetic alterations holds great promise for cancer prevention, detection, and therapy. In different types of cancer, a variety of epigenetic mechanisms can be perturbed, such as the silencing of tumor suppressor genes and activation of oncogenes by altered CpG island methylation patterns, histone modifications, and dysregulation of DNA binding proteins. There are several medications which have epigenetic impact, that are now used in a number of these diseases.

Pharmacoepigenetics is an emerging field that studies the underlying epigenetic marking patterns that lead to variation in an individual's response to medical treatment.

<span class="mw-page-title-main">Epigenetic priming</span> Type of modification to a cells epigenome

Epigenetic priming is the modification to a cell's epigenome whereby specific chromatin domains within a cell are converted from a closed state to an open state, usually as the result of an external biological trigger or pathway, allowing for DNA access by transcription factors or other modification mechanisms. The action of epigenetic priming for a certain region of DNA dictates how other gene regulation mechanisms will be able to act on the DNA later in the cell’s life. Epigenetic priming has been chiefly investigated in neuroscience and cancer research, as it has been found to play a key role in memory formation within neurons and tumor-suppressor gene activation in cancer treatment respectively.

References

  1. ↑ "Early Theories about Cancer Causes". American Cancer Society. Archived from the original on 9 May 2018. Retrieved 9 May 2018.
  2. ↑ "Milestone (1971): President Nixon declares war on cancer". dtp.cancer.gov. Archived from the original on 3 December 2017. Retrieved 9 May 2018.
  3. 1 2 3 Song M, Vogelstein B, Giovannucci EL, Willett WC, Tomasetti C (September 2018). "Cancer prevention: Molecular and epidemiologic consensus". Science. 361 (6409): 1317–8. doi:10.1126/science.aau3830. PMC   6260589 . PMID   30262488.
  4. ↑ Tran, Khanh Bao; Lang, Justin J.; Compton, Kelly; Xu, Rixing; Acheson, Alistair R.; Henrikson, Hannah Jacqueline; Kocarnik, Jonathan M.; Penberthy, Louise; Aali, Amirali; Abbas, Qamar; et al. (20 August 2022). "The global burden of cancer attributable to risk factors, 2010–19: a systematic analysis for the Global Burden of Disease Study 2019". The Lancet. 400 (10352): 563–591. doi: 10.1016/S0140-6736(22)01438-6 . PMC   9395583 . PMID   35988567.
  5. ↑ Wu S, Powers S, Zhu W, Hannun YA (January 2016). "Substantial contribution of extrinsic risk factors to cancer development". Nature. 529 (7584): 43–7. Bibcode:2016Natur.529...43W. doi:10.1038/nature16166. PMC   4836858 . PMID   26675728.
  6. ↑ Degasperi, Andrea; Zou, Xueqing; Dias Amarante, Tauanne; Martinez-Martinez, Andrea; et al. (22 April 2022). "Substitution mutational signatures in whole-genome–sequenced cancers in the UK population". Science. 376 (6591): abl9283. doi:10.1126/science.abl9283. PMC   7613262 . PMID   35949260. S2CID   248334490.
  7. ↑ Quach, Katyanna. "Harvard boffins build multimodal AI system to predict cancer". The Register. Retrieved 16 September 2022.
  8. ↑ Chen, Richard J.; Lu, Ming Y.; Williamson, Drew F. K.; Chen, Tiffany Y.; Lipkova, Jana; Noor, Zahra; Shaban, Muhammad; Shady, Maha; Williams, Mane; Joo, Bumjin; Mahmood, Faisal (8 August 2022). "Pan-cancer integrative histology-genomic analysis via multimodal deep learning". Cancer Cell. 40 (8): 865–878.e6. doi: 10.1016/j.ccell.2022.07.004 . PMC   10397370 . PMID   35944502. S2CID   251456162.
  9. ↑ Zimmer, Carl (29 September 2022). "A New Approach to Spotting Tumors: Look for Their Microbes". The New York Times. Retrieved 19 October 2022.
  10. ↑ Dohlman, Anders B.; Klug, Jared; Mesko, Marissa; Gao, Iris H.; Lipkin, Steven M.; Shen, Xiling; Iliev, Iliyan D. (29 September 2022). "A pan-cancer mycobiome analysis reveals fungal involvement in gastrointestinal and lung tumors". Cell. 185 (20): 3807–22. doi:10.1016/j.cell.2022.09.015. PMC   9564002 . PMID   36179671.
  11. ↑ Narunsky-Haziza, Lian; Sepich-Poore, Gregory D.; Livyatan, Ilana; Asraf, Omer; Martino, Cameron; Nejman, Deborah; Gavert, Nancy; Stajich, Jason E.; Amit, Guy; González, Antonio; Wandro, Stephen; Perry, Gili; Ariel, Ruthie; Meltser, Arnon; Shaffer, Justin P.; Zhu, Qiyun; Balint-Lahat, Nora; Barshack, Iris; Dadiani, Maya; Gal-Yam, Einav N.; Patel, Sandip Pravin; Bashan, Amir; Swafford, Austin D.; Pilpel, Yitzhak; Knight, Rob; Straussman, Ravid (29 September 2022). "Pan-cancer analyses reveal cancer-type-specific fungal ecologies and bacteriome interactions". Cell. 185 (20): 3789–3806.e17. doi: 10.1016/j.cell.2022.09.005 . PMC   9567272 . PMID   36179670.
  12. ↑ Piqueret, Baptiste; Montaudon, Élodie; Devienne, Paul; Leroy, Chloé; Marangoni, Elisabetta; Sandoz, Jean-Christophe; d'Ettorre, Patrizia (25 January 2023). "Ants act as olfactory bio-detectors of tumours in patient-derived xenograft mice". Proceedings of the Royal Society B: Biological Sciences. 290 (1991): 20221962. doi:10.1098/rspb.2022.1962. PMC   9874262 . PMID   36695032.
  13. ↑ di Pietro A, Tosti G, Ferrucci PF, Testori A (December 2008). "Oncophage: step to the future for vaccine therapy in melanoma". Expert Opinion on Biological Therapy. 8 (12): 1973–84. doi:10.1517/14712590802517970. PMID   18990084. S2CID   83589014.
  14. ↑ Chen, Kok-Siong; Reinshagen, Clemens; Van Schaik, Thijs A.; Rossignoli, Filippo; Borges, Paulo; Mendonca, Natalia Claire; Abdi, Reza; Simon, Brennan; Reardon, David A.; Wakimoto, Hiroaki; Shah, Khalid (4 January 2023). "Bifunctional cancer cell–based vaccine concomitantly drives direct tumor killing and antitumor immunity". Science Translational Medicine. 15 (677): eabo4778. doi:10.1126/scitranslmed.abo4778. PMC   10068810 . PMID   36599004. S2CID   255416438.
  15. ↑ "Gene Therapy, Cancer-Killing Viruses And New Drugs Highlight Novel Approaches To Cancer Treatment". Medical News Today. Retrieved 24 April 2007.
  16. ↑ "World first gene therapy trial for leukaemia". LLR. Archived from the original on 2 August 2013. Retrieved 23 July 2013.
  17. ↑ Chinese scientists to pioneer first human CRISPR trial
  18. ↑ Schmidt, Christine K.; Medina-Sánchez, Mariana; Edmondson, Richard J.; Schmidt, Oliver G. (5 November 2020). "Engineering microrobots for targeted cancer therapies from a medical perspective". Nature Communications. 11 (1): 5618. Bibcode:2020NatCo..11.5618S. doi: 10.1038/s41467-020-19322-7 . ISSN   2041-1723. PMC   7645678 . PMID   33154372.
  19. ↑ Gwisai, T.; Mirkhani, N.; Christiansen, M. G.; Nguyen, T. T.; Ling, V.; Schuerle, S. (26 October 2022). "Magnetic torque–driven living microrobots for increased tumor infiltration". Science Robotics. 7 (71): eabo0665. bioRxiv   10.1101/2022.01.03.473989 . doi:10.1126/scirobotics.abo0665. ISSN   2470-9476. PMID   36288270. S2CID   253160428.
  20. ↑ Kishore, Chandra; Bhadra, Priyanka (July 2021). "Targeting Brain Cancer Cells by Nanorobot, a Promising Nanovehicle: New Challenges and Future Perspectives". CNS & Neurological Disorders Drug Targets. 20 (6): 531–9. doi:10.2174/1871527320666210526154801. PMID   34042038. S2CID   235217854.
  21. ↑ Contreras-Llano, Luis E.; Liu, Yu-Han; Henson, Tanner; Meyer, Conary C.; Baghdasaryan, Ofelya; Khan, Shahid; Lin, Chi-Long; Wang, Aijun; Hu, Che-Ming J.; Tan, Cheemeng (11 January 2023). "Engineering Cyborg Bacteria Through Intracellular Hydrogelation". Advanced Science. 10 (9): 2204175. doi: 10.1002/advs.202204175 . ISSN   2198-3844. PMC   10037956 . PMID   36628538.
  22. ↑ Lawler, Sean E.; Speranza, Maria-Carmela; Cho, Choi-Fong; Chiocca, E. Antonio (1 June 2017). "Oncolytic Viruses in Cancer Treatment: A Review". JAMA Oncology. 3 (6): 841–9. doi: 10.1001/jamaoncol.2016.2064 . PMID   27441411. S2CID   39321536.
  23. ↑ Harrington, Kevin; Freeman, Daniel J.; Kelly, Beth; Harper, James; Soria, Jean-Charles (September 2019). "Optimizing oncolytic virotherapy in cancer treatment". Nature Reviews Drug Discovery. 18 (9): 689–706. doi:10.1038/s41573-019-0029-0. ISSN   1474-1784. PMID   31292532. S2CID   256745869.
  24. ↑ Osborne, Margaret. "Small Cancer Trial Resulted in Complete Remission for All Participants". Smithsonian Magazine. Retrieved 21 July 2022.
  25. ↑ Cercek, Andrea; Lumish, Melissa; Sinopoli, Jenna; Weiss, Jill; Shia, Jinru; Lamendola-Essel, Michelle; El Dika, Imane H.; Segal, Neil; Shcherba, Marina; Sugarman, Ryan; Stadler, Zsofia; Yaeger, Rona; Smith, J. Joshua; Rousseau, Benoit; Argiles, Guillem; Patel, Miteshkumar; Desai, Avni; Saltz, Leonard B.; Widmar, Maria; Iyer, Krishna; Zhang, Janie; Gianino, Nicole; Crane, Christopher; Romesser, Paul B.; Pappou, Emmanouil P.; Paty, Philip; Garcia-Aguilar, Julio; Gonen, Mithat; Gollub, Marc; Weiser, Martin R.; Schalper, Kurt A.; Diaz, Luis A. (23 June 2022). "PD-1 Blockade in Mismatch Repair–Deficient, Locally Advanced Rectal Cancer". New England Journal of Medicine. 386 (25): 2363–76. doi:10.1056/NEJMoa2201445. ISSN   0028-4793. PMC   9492301 . PMID   35660797. S2CID   249395846.
  26. ↑ "Trastuzumab Deruxtecan Leads to Longer PFS and OS Compared with Chemotherapy in Previously Treated HER2-Low Unresectable or Metastatic Breast Cancer". www.esmo.org. Retrieved 21 July 2022.
  27. ↑ Modi, Shanu; Jacot, William; Yamashita, Toshinari; Sohn, Joohyuk; Vidal, Maria; Tokunaga, Eriko; Tsurutani, Junji; Ueno, Naoto T.; Prat, Aleix; Chae, Yee Soo; Lee, Keun Seok; Niikura, Naoki; Park, Yeon Hee; Xu, Binghe; Wang, Xiaojia; Gil-Gil, Miguel; Li, Wei; Pierga, Jean-Yves; Im, Seock-Ah; Moore, Halle C. F.; Rugo, Hope S.; Yerushalmi, Rinat; Zagouri, Flora; Gombos, Andrea; Kim, Sung-Bae; Liu, Qiang; Luo, Ting; Saura, Cristina; Schmid, Peter; Sun, Tao; Gambhire, Dhiraj; Yung, Lotus; Wang, Yibin; Singh, Jasmeet; Vitazka, Patrik; Meinhardt, Gerold; Harbeck, Nadia; Cameron, David A. (5 June 2022). "Trastuzumab Deruxtecan in Previously Treated HER2-Low Advanced Breast Cancer". New England Journal of Medicine. 387 (1): 9–20. doi:10.1056/NEJMoa2203690. hdl: 2445/197309 . PMC   10561652 . PMID   35665782. S2CID   249418284.
  28. ↑ "Scientists harness light therapy to target and kill cancer cells in world first". The Guardian. 17 June 2022. Retrieved 21 June 2022.
  29. ↑ Mączyńska, Justyna; Raes, Florian; Da Pieve, Chiara; Turnock, Stephen; Boult, Jessica K. R.; Hoebart, Julia; Niedbala, Marcin; Robinson, Simon P.; Harrington, Kevin J.; Kaspera, Wojciech; Kramer-Marek, Gabriela (21 January 2022). "Triggering anti-GBM immune response with EGFR-mediated photoimmunotherapy". BMC Medicine. 20 (1): 16. doi: 10.1186/s12916-021-02213-z . ISSN   1741-7015. PMC   8780306 . PMID   35057796.
  30. 1 2 Cerwenka A, Lanier LL (February 2016). "Natural killer cell memory in infection, inflammation and cancer". Nature Reviews. Immunology. 16 (2): 112–123. doi:10.1038/nri.2015.9. PMID   26806484. S2CID   361806.
  31. ↑ Zhu, Shaoming; Zhang, Tian; Zheng, Lei; Liu, Hongtao; Song, Wenru; Liu, Delong; Li, Zihai; Pan, Chong-xian (December 2021). "Combination strategies to maximize the benefits of cancer immunotherapy". Journal of Hematology & Oncology. 14 (1): 156. doi: 10.1186/s13045-021-01164-5 . PMC   8475356 . PMID   34579759.
  32. ↑ Futreal PA, Coin L, Marshall M, Down T, Hubbard T, Wooster R, Rahman N, Stratton MR (March 2004). "A census of human cancer genes". Nature Reviews. Cancer. 4 (3): 177–183. doi:10.1038/nrc1299. PMC   2665285 . PMID   14993899.
  33. ↑ Forbes S, Clements J, Dawson E, Bamford S, Webb T, Dogan A, Flanagan A, Teague J, Wooster R, Futreal PA, Stratton MR (January 2006). "COSMIC 2005". British Journal of Cancer. 94 (2): 318–322. doi:10.1038/sj.bjc.6602928. PMC   2361125 . PMID   16421597.
  34. ↑ Vlahopoulos SA, Logotheti S, Mikas D, Giarika A, Gorgoulis V, Zoumpourlis V.The role of ATF-2 in oncogenesis" Bioessays 2008 Apr;30(4) 314-27.
  35. ↑ Sharma S, Kelly TK, Jones PA (January 2010). "Epigenetics in cancer". Carcinogenesis. 31 (1): 27–36. doi:10.1093/carcin/bgp220. PMC   2802667 . PMID   19752007.
  36. ↑ Vogelstein B, Papadopoulos N, Velculescu VE, Zhou S, Diaz LA, Kinzler KW (March 2013). "Cancer genome landscapes". Science. 339 (6127): 1546–1558. Bibcode:2013Sci...339.1546V. doi:10.1126/science.1235122. PMC   3749880 . PMID   23539594.
  37. ↑ Illingworth RS, Gruenewald-Schneider U, Webb S, Kerr AR, James KD, Turner DJ, et al. (September 2010). "Orphan CpG islands identify numerous conserved promoters in the mammalian genome". PLOS Genetics. 6 (9): e1001134. doi: 10.1371/journal.pgen.1001134 . PMC   2944787 . PMID   20885785.
  38. ↑ Wei J, Li G, Dang S, Zhou Y, Zeng K, Liu M (2016). "Discovery and Validation of Hypermethylated Markers for Colorectal Cancer". Disease Markers. 2016: 2192853. doi: 10.1155/2016/2192853 . PMC   4963574 . PMID   27493446.
  39. ↑ Beggs AD, Jones A, El-Bahrawy M, El-Bahwary M, Abulafi M, Hodgson SV, Tomlinson IP (April 2013). "Whole-genome methylation analysis of benign and malignant colorectal tumours". The Journal of Pathology. 229 (5): 697–704. doi:10.1002/path.4132. PMC   3619233 . PMID   23096130.
  40. ↑ Novak K (December 2004). "Epigenetics changes in cancer cells". MedGenMed. 6 (4): 17. PMC   1480584 . PMID   15775844.
  41. ↑ Banno K, Kisu I, Yanokura M, Tsuji K, Masuda K, Ueki A, et al. (September 2012). "Epimutation and cancer: a new carcinogenic mechanism of Lynch syndrome (Review)". International Journal of Oncology. 41 (3): 793–797. doi:10.3892/ijo.2012.1528. PMC   3582986 . PMID   22735547.
  42. 1 2 3 Wicki A, Hagmann J (9 September 2011). "Diet and cancer". Swiss Medical Weekly . 141: w13250. doi: 10.4414/smw.2011.13250 . PMID   21904992.
  43. ↑ Papadimitriou N, Markozannes G, Kanellopoulou A, Critselis E, Alhardan S, Karafousia V, Kasimis JC, Katsaraki C, Papadopoulou A, Zografou M, Lopez DS, Chan DS, Kyrgiou M, Ntzani E, Cross AJ, Marrone MT, Platz EA, Gunter MJ, Tsilidis KK (2021). "An umbrella review of the evidence associating diet and cancer risk at 11 anatomical sites". Nature Communications. 12 (1): 4579. Bibcode:2021NatCo..12.4579P. doi:10.1038/s41467-021-24861-8. PMC   8319326 . PMID   34321471.
  44. ↑ Jabbari M, Pourmoradian S, Eini-Zinab H, Mosharkesh E, Hosseini Balam F, Yaghmaei Y, Yadegari A, Amini B, Arman Moghadam D, Barati M, Hekmatdoost A (2022). "Levels of evidence for the association between different food groups/items consumption and the risk of various cancer sites: an umbrella review". Int J Food Sci Nutr. 73 (7): 861–874. doi:10.1080/09637486.2022.2103523. PMID   35920747. S2CID   251280745.
  45. ↑ Stewart BW, Wild CP, eds. (2014). "Ch. 2: Cancer Etiology § 6 Diet, obesity and physical activity". World Cancer Report 2014. World Health Organization. pp. 124–33. ISBN   978-92-832-0429-9.
  46. ↑ Vieira AR, Abar L, Chan DSM, Vingeliene S, Polemiti E, Stevens C, Greenwood D, Norat T. (2017). "Foods and beverages and colorectal cancer risk: a systematic review and meta-analysis of cohort studies, an update of the evidence of the WCRF-AICR Continuous Update Project". Annals of Oncology. 28 (8): 1788–1802. doi:10.1093/annonc/mdx171. hdl: 10044/1/48313 . PMID   28407090.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  47. ↑ "Meat, fish, dairy and cancer risk". wcrf.org. Retrieved 24 April 2023.
  48. ↑ "Red Meat and Processed Meat Consumption". progressreport.cancer.gov. Retrieved 24 April 2023.
  49. ↑ "Red Meat (Beef, Pork, Lamb): Increases Risk of Colorectal Cancer". aicr.org. Retrieved 24 April 2023.
  50. 1 2 3 Park S, Bae J, Nam BH, Yoo KY (2008). "Aetiology of cancer in Asia" (PDF). Asian Pacific Journal of Cancer Prevention. 9 (3): 371–380. PMID   18990005.
  51. ↑ Yu C, Cao Q, Chen P, Yang S, Deng M, Wang Y, Li L (December 2016). "An updated dose-response meta-analysis of coffee consumption and liver cancer risk". Scientific Reports. 6 (1): 37488. Bibcode:2016NatSR...637488Y. doi:10.1038/srep37488. PMC   5133591 . PMID   27910873.
  52. ↑ Brenner H, Rothenbacher D, Arndt V (2009). "Epidemiology of Stomach Cancer". In Mukesh V (ed.). Cancer Epidemiology. Methods in Molecular Biology. Vol. 472. pp. 467–477. doi:10.1007/978-1-60327-492-0_23. ISBN   978-1-60327-491-3. PMC   2166976 . PMID   19107449.
  53. ↑ "Preventing Cancer". hsph.harvard.edu. Retrieved 24 April 2023.
  54. ↑ "A healthy diet alone will not cure cancer". National Academies of Sciences, Engineering, and Medicine. 2024. Archived from the original on 28 April 2024.
  55. ↑ Ilerhunmwuwa NP, Abdul Khader AHS, Smith C, Cliff ERS, Booth CM, Hottel E, Aziz M, Lee-Smith W, Goodman A, Chakraborty R, Mohyuddin GR. (2024). "Dietary interventions in cancer: a systematic review of all randomized controlled trials". Journal of the National Cancer Institute. 116 (7): 1026–1034. doi:10.1093/jnci/djae051. PMC   11223872 . PMID   38429997.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  56. ↑ Clifton, Katherine K.; Ma, Cynthia X.; Fontana, Luigi; Peterson, Lindsay L. (November 2021). "Intermittent fasting in the prevention and treatment of cancer". CA: A Cancer Journal for Clinicians. 71 (6): 527–546. doi:10.3322/caac.21694. ISSN   0007-9235. PMID   34383300. S2CID   236989849.
  57. ↑ Manoogian, Emily N. C.; Panda, Satchidananda (1 October 2017). "Circadian rhythms, time-restricted feeding, and healthy aging". Ageing Research Reviews. 39: 59–67. doi:10.1016/j.arr.2016.12.006. ISSN   1568-1637. PMC   5814245 . PMID   28017879.
  58. ↑ Brandhorst, Sebastian; Longo, Valter D. (2016). "Fasting and Caloric Restriction in Cancer Prevention and Treatment". Metabolism in Cancer. Recent Results in Cancer Research. Vol. 207. Springer. pp. 241–266. doi:10.1007/978-3-319-42118-6_12. ISBN   978-3-319-42116-2. PMC   7476366 . PMID   27557543. S2CID   42198775.
  59. ↑ Alidadi, Mona; Banach, Maciej; Guest, Paul C.; Bo, Simona; Jamialahmadi, Tannaz; Sahebkar, Amirhossein (1 August 2021). "The effect of caloric restriction and fasting on cancer". Seminars in Cancer Biology. 73: 30–44. doi:10.1016/j.semcancer.2020.09.010. ISSN   1044-579X. PMID   32977005. S2CID   221938415.
  60. ↑ Ibrahim, Ezzeldin M.; Al-Foheidi, Meteb H.; Al-Mansour, Mubarak M. (1 May 2021). "Energy and caloric restriction, and fasting and cancer: a narrative review". Supportive Care in Cancer. 29 (5): 2299–2304. doi:10.1007/s00520-020-05879-y. PMC   7981322 . PMID   33190181. S2CID   226945778.
  61. ↑ Hofer, Sebastian J.; Davinelli, Sergio; Bergmann, Martina; Scapagnini, Giovanni; Madeo, Frank (2021). "Caloric Restriction Mimetics in Nutrition and Clinical Trials". Frontiers in Nutrition. 8: 717343. doi: 10.3389/fnut.2021.717343 . PMC   8450594 . PMID   34552954.
  62. ↑ Madeo, Frank; Eisenberg, Tobias; Pietrocola, Federico; Kroemer, Guido (26 January 2018). "Spermidine in health and disease". Science. 359 (6374): eaan2788. doi: 10.1126/science.aan2788 . ISSN   0036-8075. PMID   29371440. S2CID   206659415.
  63. ↑ Imran, Muhammad; Aslam Gondal, Tanweer; Atif, Muhammad; Shahbaz, Muhammad; Batool Qaisarani, Tahira; Hanif Mughal, Muhammad; Salehi, Bahare; Martorell, Miquel; Sharifi-Rad, Javad (August 2020). "Apigenin as an anticancer agent". Phytotherapy Research. 34 (8): 1812–28. doi:10.1002/ptr.6647. ISSN   0951-418X. PMID   32059077. S2CID   211122428.
  64. ↑ Shukla, Sanjeev; Gupta, Sanjay (1 June 2010). "Apigenin: A Promising Molecule for Cancer Prevention". Pharmaceutical Research. 27 (6): 962–978. doi:10.1007/s11095-010-0089-7. PMC   2874462 . PMID   20306120.
  65. ↑ Shankar, Eswar; Goel, Aditi; Gupta, Karishma; Gupta, Sanjay (1 December 2017). "Plant Flavone Apigenin: an Emerging Anticancer Agent". Current Pharmacology Reports. 3 (6): 423–446. doi:10.1007/s40495-017-0113-2. PMC   5791748 . PMID   29399439.
  66. ↑ Samadi, Parisa; Sarvarian, Parisa; Gholipour, Elham; Asenjan, Karim Shams; Aghebati-Maleki, Leili; Motavalli, Roza; Hojjat-Farsangi, Mohammad; Yousefi, Mehdi (October 2020). "Berberine: A novel therapeutic strategy for cancer". IUBMB Life. 72 (10): 2065–79. doi: 10.1002/iub.2350 . ISSN   1521-6543. PMID   32735398. S2CID   220893166.
  67. ↑ Zhong, Xiao-Dan; Chen, Li-Juan; Xu, Xin-Yang; Liu, Yan-Jun; Tao, Fan; Zhu, Ming-Hui; Li, Chang-Yun; Zhao, Dan; Yang, Guan-Jun; Chen, Jiong (2022). "Berberine as a potential agent for breast cancer therapy". Frontiers in Oncology. 12: 993775. doi: 10.3389/fonc.2022.993775 . PMC   9480097 . PMID   36119505.
  68. ↑ Wang, Ye; Liu, Yanfang; Du, Xinyang; Ma, Hong; Yao, Jing (30 January 2020). "The Anti-Cancer Mechanisms of Berberine: A Review". Cancer Management and Research. 12: 695–702. doi: 10.2147/CMAR.S242329 . PMC   6996556 . PMID   32099466.
  69. ↑ Vlavcheski, Filip; O’Neill, Eric J.; Gagacev, Filip; Tsiani, Evangelia (January 2022). "Effects of Berberine against Pancreatitis and Pancreatic Cancer". Molecules. 27 (23): 8630. doi: 10.3390/molecules27238630 . PMC   9738201 . PMID   36500723.
  70. ↑ Guamán Ortiz, Luis Miguel; Lombardi, Paolo; Tillhon, Micol; Scovassi, Anna Ivana (August 2014). "Berberine, an Epiphany Against Cancer". Molecules. 19 (8): 12349–67. doi: 10.3390/molecules190812349 . PMC   6271598 . PMID   25153862.
  71. ↑ Su, Chao; Li, Nan; Ren, Ruru; Wang, Yingli; Su, Xiaojuan; Lu, Fangfang; Zong, Rong; Yang, Lingling; Ma, Xueqin (January 2021). "Progress in the Medicinal Value, Bioactive Compounds, and Pharmacological Activities of Gynostemma pentaphyllum". Molecules. 26 (20): 6249. doi: 10.3390/molecules26206249 . PMC   8540791 . PMID   34684830.
  72. ↑ Pu, Wei-ling; Zhang, Meng-ying; Bai, Ru-yu; Sun, Li-kang; Li, Wen-hua; Yu, Ying-li; Zhang, Yue; Song, Lei; Wang, Zhao-xin; Peng, Yan-fei; Shi, Hong; Zhou, Kun; Li, Tian-xiang (1 January 2020). "Anti-inflammatory effects of Rhodiola rosea L.: A review". Biomedicine & Pharmacotherapy. 121: 109552. doi: 10.1016/j.biopha.2019.109552 . ISSN   0753-3322. PMID   31715370. S2CID   207938536.
  73. ↑ Magani, Sri Krishna Jayadev; Mupparthi, Sri Durgambica; Gollapalli, Bhanu Prakash; Shukla, Dhananjay; Tiwari, A. K.; Gorantala, Jyotsna; Yarla, Nagendra Sastry; Tantravahi, Srinivasan (2020). "Salidroside — Can it be a Multifunctional Drug?". Current Drug Metabolism. 21 (7): 512–524. doi:10.2174/1389200221666200610172105. PMID   32520682. S2CID   219588131.
  74. ↑ "Federally Funded Cancer Research". asco.org. 8 February 2016. Archived from the original on 23 April 2018. Retrieved 9 May 2018.
  75. 1 2 3 4 Eckhouse S, Sullivan R (July 2006). "A survey of public funding of cancer research in the European union". PLOS Medicine. 3 (7): e267. doi: 10.1371/journal.pmed.0030267 . PMC   1513045 . PMID   16842021.
  76. ↑ "NCI Budget Fact Book". National Cancer Institute.
  77. ↑ Alberts B, Kirschner MW, Tilghman S, Varmus H (April 2014). "Rescuing US biomedical research from its systemic flaws". Proceedings of the National Academy of Sciences of the United States of America. 111 (16): 5773–7. Bibcode:2014PNAS..111.5773A. doi: 10.1073/pnas.1404402111 . PMC   4000813 . PMID   24733905.
  78. ↑ Kolata G (23 April 2009). "Advances Elusive in the Drive to Cure Cancer". The New York Times. Archived from the original on 14 January 2012. Retrieved 29 December 2009.
  79. ↑ Kolata G (27 June 2009). "Grant System Leads Cancer Researchers to Play It Safe". The New York Times. Archived from the original on 8 June 2011. Retrieved 29 December 2009.
  80. ↑ Leaf C (22 March 2004). "Why We're Losing The War on Cancer". Fortune Magazine (CNN Money). Archived from the original on 2 May 2014.
  81. ↑ Begley CG, Ellis LM (March 2012). "Drug development: Raise standards for preclinical cancer research". Nature (Comment article). 483 (7391): 531–533. Bibcode:2012Natur.483..531B. doi: 10.1038/483531a . PMID   22460880. S2CID   4326966. (Erratum:  doi:10.1038/485041e)
  82. ↑ Haelle T (7 December 2021). "Dozens of major cancer studies can't be replicated". Science News. Retrieved 19 January 2022.
  83. ↑ "Reproducibility Project: Cancer Biology". www.cos.io. Center for Open Science . Retrieved 19 January 2022.
  84. ↑ Mobley A, Linder SK, Braeuer R, Ellis LM, Zwelling L (2013). Arakawa H (ed.). "A survey on data reproducibility in cancer research provides insights into our limited ability to translate findings from the laboratory to the clinic". PLOS ONE. 8 (5): e63221. Bibcode:2013PLoSO...863221M. doi: 10.1371/journal.pone.0063221 . PMC   3655010 . PMID   23691000.
  85. ↑ Van Noorden R (July 2023). "Medicine is plagued by untrustworthy clinical trials. How many studies are faked or flawed?". Nature. 619 (7970): 454–458. Bibcode:2023Natur.619..454V. doi: 10.1038/d41586-023-02299-w . PMID   37464079.
  86. ↑ "Help Conquer Cancer". 19 November 2007. Archived from the original on 16 November 2007. Retrieved 19 November 2007.
  87. 1 2 Klein, Harry; Mazor, Tali; Siegel, Ethan; Trukhanov, Pavel; Ovalle, Andrea; Vecchio Fitz, Catherine Del; Zwiesler, Zachary; Kumari, Priti; Van Der Veen, Bernd; Marriott, Eric; Hansel, Jason; Yu, Joyce; Albayrak, Adem; Barry, Susan; Keller, Rachel B.; MacConaill, Laura E.; Lindeman, Neal; Johnson, Bruce E.; Rollins, Barrett J.; Do, Khanh T.; Beardslee, Brian; Shapiro, Geoffrey; Hector-Barry, Suzanne; Methot, John; Sholl, Lynette; Lindsay, James; Hassett, Michael J.; Cerami, Ethan (6 October 2022). "MatchMiner: an open-source platform for cancer precision medicine". npj Precision Oncology. 6 (1): 69. doi: 10.1038/s41698-022-00312-5 . PMC   9537311 . PMID   36202909.
  88. ↑ "Researchers report genomic profiling from more than 110,000 tumors". News-Medical.net. 19 July 2022. Retrieved 20 November 2022.
  89. ↑ "Cancer Awareness Dates". cancer.net. 19 December 2013. Archived from the original on 9 December 2017. Retrieved 9 May 2018.
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