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Primary liver cancers (PLC), including hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), are among the leading causes of cancer-related mortality worldwide. Bi-dimensional in vitro models are unable to recapitulate the key features of PLC; consequently, recent advancements in three-dimensional in vitro systems, such as organoids, opened up new avenues for the development of innovative models for studying tumour's pathological mechanisms. Liver organoids show self-assembly and self-renewal capabilities, retaining essential aspects of their respective in vivo tissue and allowing modelling diseases and personalized treatment development. In this review, we will discuss the current advances in the field of liver organoids focusing on existing development protocols and possible applications in regenerative medicine and drug discovery. [ABSTRACT FROM AUTHOR]

Prostate cancer (PCa) affects millions of men worldwide and is a major cause of cancer-related mortality. Race-associated PCa health disparities are also common and are of both social and clinical concern. Most PCa is diagnosed early due to PSA-based screening, but it fails to discern between indolent and aggressive PCa. Androgen or androgen receptor-targeted therapies are standard care of treatment for locally advanced and metastatic disease, but therapy resistance is common. Mitochondria, the powerhouse of cells, are unique subcellular organelles that have their own genome. A large majority of mitochondrial proteins are, however, nuclear-encoded and imported after cytoplasmic translation. Mitochondrial alterations are common in cancer, including PCa, leading to their altered functions. Aberrant mitochondrial function affects nuclear gene expression in retrograde signaling and promotes tumor-supportive stromal remodeling. In this article, we discuss mitochondrial alterations that have been reported in PCa and review the literature related to their roles in PCa pathobiology, therapy resistance, and racial disparities. We also discuss the translational potential of mitochondrial alterations as prognostic biomarkers and as effective targets for PCa therapy. [ABSTRACT FROM AUTHOR]

Although tremendous progress has been made in treating childhood cancer, it is still one of the leading causes of death in children worldwide. Because cancer symptoms overlap with those of other diseases, it is difficult to predict a tumor early enough, which causes cancers in children to be more aggressive and progress more rapidly than in adults. Therefore, early and accurate detection methods are urgently needed to effectively treat children with cancer therapy. Identification and detection of cancer biomarkers serve as non-invasive tools for early cancer screening, prevention, and treatment. Biosensors have emerged as a potential technology for rapid, sensitive, and cost-effective biomarker detection and monitoring. In this review, we provide an overview of important biomarkers for several common childhood cancers. Accordingly, we have enumerated the developed biosensors for early detection of pediatric cancer or related biomarkers. This review offers a restructured platform for ongoing research in pediatric cancer diagnostics that can contribute to the development of rapid biosensing techniques for early-stage diagnosis, monitoring, and treatment of children with cancer and reduce the mortality rate. [ABSTRACT FROM AUTHOR]

Cancer is considered as one of the main causes of human deaths globally. Despite the recent progresses in therapeutic modalities, there is still a high rate of mortality among cancer patients. Late diagnosis in advanced tumor stages is one of the main reasons for treatment failure in cancer patients. Therefore, it is required to suggest the novel strategies for the early tumor detection. MicroRNAs (miRNAs) have critical roles in neoplastic transformation by regulation of cell proliferation, migration, and apoptosis. They are always considered as non-invasive markers due to their high stability in body fluids. Since, all of the miRNAs have tissue-specific functions in different tumors as tumor suppressor or oncogene; it is required to investigate the molecular mechanisms of every miRNA in different tumors to introduce that as a suitable non-invasive diagnostic marker in cancer patients. For the first time in the present review, we discussed the role of miR-377 during tumor progression. It has been reported that miR-377 mainly functions as a tumor suppressor through the regulation of signaling pathways and transcription factors. This review is an important step toward introducing the miR-377 as a novel diagnostic marker as well as a therapeutic target in cancer patients. [ABSTRACT FROM AUTHOR]

Esophageal cancer is one of the most common cancers with high mortality rate around the world. Although the treatment strategy of this disease has made great progress, the prognosis of advanced patients is not ideal. Ferroptosis, a novel regulatory cell death model, that is different from traditional apoptosis and characterized by increased Fenton reaction mediated by intracellular free iron and lipid peroxidation of cell membrane. Ferroptosis has been proved to be closely linked to a variety of diseases, especially cancer. This review aims to summarize the core mechanism of ferroptosis in esophageal cancer, the regulation of ferroptosis signaling pathway and its current application. At the same time, we emphasize the potential and prospect of ferroptosis in the treatment of esophageal cancer. Collectively, targeting ferroptosis pathway may provide new insights into the diagnosis, treatment and prognosis of esophageal cancer. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is the world's third most prevalent cancer and the main cause of cancer-related mortality. A lot of work has been put into improving CRC patients' clinical care, including the development of more effective methods and wide biomarkers variety for prognostic, and diagnostic purposes. MicroRNAs (miRNAs) regulate a variety of cellular processes and play a significant role in the CRC progression and spread via controlling their target gene expression by translation inhibition or mRNA degradation. Consequently, dysregulation and disruption in their function, miRNAs are linked to CRC malignant pathogenesis by controlling several cellular processes involved in the CRC. These cellular processes include increased proliferative and invasive capacity, cell cycle aberration, evasion of apoptosis, enhanced EMT, promotion of angiogenesis and metastasis, and decreased sensitivity to major treatments. The miRNAs control cellular processes in CRC via regulation of pathways such as Wnt/β-catenin signaling, PTEN/AKT/mTOR axis, KRAS, TGFb signaling, VEGFR, EGFR, and P53. Hence, the goal of this review was to review miRNA biogenesis and present an updated summary of oncogenic and tumor suppressor (TS) miRNAs and their potential implication in CRC pathogenesis and responses to chemotherapy and radiotherapy. We also summarise the biological importance and clinical applications of miRNAs in the CRC. [Display omitted] • We describe an updated summary of oncogenic and tumor suppressor miRNAs in CRC. • miRNAs serve a critical role in the regulation of many biological processes in CRC. • miRNAs have appeared as novel CRC biomarkers and a possible therapeutic target. [ABSTRACT FROM AUTHOR]

Considerable controversy exists regarding the association between milk and dairy consumption and mortality risk. The present systematic review and meta-analysis of prospective studies was undertaken to examine the association of high vs. low-fat dairy and milk consumption with mortality. We searched PubMed/Medline, ISI Web of Science, and Scopus databases through February 2020 for prospective cohort studies that reported the association between milk and dairy consumption and mortality risk. High-fat milk consumption was significantly associated with a greater risk of all-cause (Pooled ES: 1.15; 95% CI: 1.09-1.20, I2=24.5%, p = 0.22), CVD (Pooled ES: 1.09; 95% CI: 1.02-1.16, I2=4.5%, p = 0.38) and cancer mortality (Pooled ES: 1.17; 95% CI: 1.08-1.28, I2=30.1%, p = 0.19). However, total dairy consumption was associated with a lower risk of CVD mortality (Pooled ES: 0.93; 95% CI: 0.88-0.98, I2=59.7%, p = 0.001). Dose-response analysis revealed a significant non-linear association of total dairy consumption with all-cause and CVD mortality. Moreover, high-fat milk consumption was significantly associated with risk of cancer mortality in linear and non-linear dose-response analysis. In conclusion, we found high-fat milk consumption was associated with a higher risk of all-cause, CVD, and cancer mortality. However, total dairy consumption was associated with a lower risk of CVD mortality. [ABSTRACT FROM AUTHOR]

Background: Cancer patients are more vulnerable to Coronavirus disease-2019 (COVID-19) and have a higher risk of adverse outcomes than the general population. Therefore, it is necessary to evaluate whether anti-cancer therapies such as surgery, chemotherapy, immunotherapy, and targeted therapy will increase the severity and mortality of cancer patients with COVID-19. Methods: Relevant articles were retrieved from PubMed, Embase, Web of Science, Cochrane Library and China National Knowledge Infrastructure (CNKI). The search time was from December 1, 2019 to January 23, 2021. Meta-analysis was conducted using Revman 5.3 statistical software. Results: A total of 26 studies were included in this meta-analysis, involving 5571 cancer patients infected with SARS-CoV-2. Meta-analysis showed that surgery, chemotherapy, immunotherapy and targeted therapy were not associated with disease severity or mortality (107/688, OR =1.30, 95% CI[0.79, 2.13], P =0.30; 1956/2674, OR =1.27, 95% CI [0.95, 1.69], P =0.10; 342/1455, OR =1.20, 95% CI [0.90, 1.61], P =0.21; 503/1378, OR =0.92, 95% CI [0.72, 1.19], P =0.54, respectively). Conclusion: In cancer patients with COVID-19, anti-cancer therapy had no adverse effect on disease severity or mortality. Further research is necessary to determine the complex interrelationship between anti-cancer therapy, particularly chemotherapy, and COVID-19. [ABSTRACT FROM AUTHOR]

Colorectal cancer is the third most common neoplasm in the world and the third leading cause of cancer-related deaths in the USA. A safer and more effective therapeutic intervention against this malignant carcinoma is called for given the limitations and toxicities associated with the currently available treatment modalities. Immuno-oncolytic or oncolytic virotherapy, the use of viruses to selectively or preferentially kill cancer cells, has emerged as a potential anticancer treatment modality. Oncolytic viruses act as double-edged swords against the tumors through the direct cytolysis of cancer cells and the induction of antitumor immunity. A number of such viruses have been tested against colorectal cancer, in both preclinical and clinical settings, and many have produced promising results. Oncolytic virotherapy has also shown synergistic antitumor efficacy in combination with conventional treatment regimens. In this review, we describe the status of this therapeutic approach against colorectal cancer at both preclinical and clinical levels. Successes with and the challenges of using oncolytic viruses, both as monotherapy and in combination therapy, are also highlighted. [ABSTRACT FROM AUTHOR]

Cancer is the leading cause of mortality in the world. The major therapies for cancer treatment are chemotherapy, surgery, and radiation therapy. All these therapies expensive, toxic and show resistance. The plant‐derived compounds are considered safe, cost‐effective and target cancer through different pathways. In these pathways include oxidative stress, mitochondrial dependent and independent, STAT3, NF‐kB, MAPKs, cell cycle, and autophagy pathways. One of the new plants derived compounds is Polyphyllin VII (PPVII), which target cancer through different molecular mechanisms. In literature, there is a review gap of studies on PPVII; therefore in the current review, we summarized the available studies on PPVII to provide a base for future research. [ABSTRACT FROM AUTHOR]

The incidence of obesity and type 2 diabetes (T2DM) in the Western world has increased dramatically during the recent decades. According to the American Cancer Society, pancreatic cancer (PC) is the fourth leading cause of cancer‐related death in the United States. The relationship among obesity, T2DM and PC is complex. Due to increase in obesity, diabetes, alcohol consumption and sedentary lifestyle, the mortality due to PC is expected to rise significantly by year 2040. The underlying mechanisms by which diabetes and obesity contribute to pancreatic tumorigenesis are not well understood. Furthermore, metabolism and microenvironment within the pancreas can also modulate pancreatic carcinogenesis. The risk of PC on a population level may be reduced by modifiable lifestyle risk factors. In this review, the interactions of diabetes and obesity to PC development were summarized, and novel strategies for the prevention and treatment of diabetes and PC were discussed. [ABSTRACT FROM AUTHOR]

In 1971, President Nixon declared war on cancer. Thirty years later, many declared this war a failure: the age-adjusted mortality rate from cancer in 2000 was essentially the same as in the early 1970s. Meanwhile the age-adjusted mortality rate from cardiovascular disease fell dramatically. Since the causes that underlie cancer and cardic, vascular disease arc likely dependent, the decline in mortality rates from cardiovascular disease may partially explain the lack of progress in cancer mortality. Because competing risks models (used to model mortality from multiple causes) are fundamentally unidentified, it is difficult to estimate cancer trends. We derive bounds for aspects of the underlying distributions without assuming that the underlying risks are independent. We then estimate changes in cancer and cardiovascular mortality since 1970. The bounds for the change in duration until death for either cause are fairly tight and suggest much larger improvements in cancer than previously estimated. [ABSTRACT FROM AUTHOR]

Reviews the book "What Remains: A Memoir of Fate, Friendship & Love," by Carole Radziwill.

The article reviews the book "A Scattering," by Christopher Reid.

The article reviews the book "Cancer Mortality and Morbidity Patterns in the U.S. Population," by Kenneth G. Manton, Igor Akushevich, and Julia Kravchenko.

The article reviews the book "Atlas of Cancer Mortality in the United States (1950-1994)," edited by Susan S. Devesa.

Reviews the book 'Cancer Mortality in the United States: 1950-1977.'

Reviews the book 'Reducing Cancer Mortality: A Geographical Perspective,' by Harold D. Foster.

The article reviews the book "Cancer Mortality and Morbidity Patterns in the U.S. Population: An Interdisciplinary Approach," by Kenneth G. Manton, Igor Akuschevich and Julia Kravchenko.

The article reviews the book "Cancer Mortality and Morbidity Patterns in the U.S. Population: An Interdisciplinary Approach," by K. G. Manton, I. Akushevich and J. Kravchenko.

The article reviews the book "Atlas of Cancer Mortality in England and Wales 1968-1978," by M. J. Gardner et al.