scholarly journals Targeting the Prion-Like Aggregation of Mutant p53 to Combat Cancer

2021 ◽  
pp. 198-236
Author(s):  
Elena Locci ◽  
Silvia Raymond
Keyword(s):  
Cancer Cells ◽  
P53 Mutation ◽  
Lead Author ◽  
Protein Accumulation ◽  
Cancer Therapies ◽  
Protein Mimics ◽  
Wide Range ◽  
Keywords Cancer ◽  
New Cancer Therapies

The team first screened a set of protein mimics originally designed to target Alzheimer's disease and type 2 diabetes. The results identify a mimicry of the protein that potentially isolates the mutated p53 material and prevents further protein accumulation. The researchers then showed that segregation of mutated p53 grains by protein mimicking restored the suppressive function of the p53 tumor, leading to the death of a wide range of cancer cells. Importantly, protein mimicry therapy effectively reduces tumors that contain mutated p53 while showing no significant toxins for healthy tissue, resulting in significantly longer survival. "As the prevalence of cancer increases worldwide, there is an urgent need for new cancer therapies to complement or replace existing therapies," said the study's lead author. Here we show the first successful use of a small molecule amyloid inhibitor as an anticancer agent. We believe that this will have a far-reaching impact, as it effectively bridges the gap between amyloid disease and cancer and is the basis for passing on information approaches in the design of new and robust cancer mutation therapies for the p53 mutation. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management

scholarly journals Identification of a Mimicry of the Protein that Potentially Isolates the Mutated p53 Material and Prevents Further Protein Accumulation

2021 ◽  
pp. 182-222
Author(s):  
Ricardo Gobato ◽  
Abhijit Mitra
Keyword(s):  
Cancer Cells ◽  
P53 Mutation ◽  
Lead Author ◽  
Protein Accumulation ◽  
Cancer Therapies ◽  
Protein Mimics ◽  
Wide Range ◽  
Keywords Cancer ◽  
New Cancer Therapies

The team first screened a set of protein mimics originally designed to target Alzheimer's disease and type 2 diabetes. The results identify a mimicry of the protein that potentially isolates the mutated p53 material and prevents further protein accumulation. The researchers then showed that segregation of mutated p53 grains by protein mimicking restored the suppressive function of the p53 tumor, leading to the death of a wide range of cancer cells. Importantly, protein mimicry therapy effectively reduces tumors that contain mutated p53 while showing no significant toxins for healthy tissue, resulting in significantly longer survival. "As the prevalence of cancer increases worldwide, there is an urgent need for new cancer therapies to complement or replace existing therapies," said the study's lead author. Here we show the first successful use of a small molecule amyloid inhibitor as an anticancer agent. We believe that this will have a far-reaching impact, as it effectively bridges the gap between amyloid disease and cancer and is the basis for passing on information approaches in the design of new and robust cancer mutation therapies for the p53 mutation. Keywords: Cancer; Cells; Tissues; Tumors; Prevention; Prognosis; Diagnosis; Imaging; Screening, Treatment; Management

scholarly journals Stage-specific embryonic antigen-3 (SSEA-3) and β3GalT5 are cancer specific and significant markers for breast cancer stem cells

2015 ◽  
Vol 113 (4) ◽  
pp. 960-965 ◽  
Author(s):  
Sarah K. C. Cheung ◽  
Po-Kai Chuang ◽  
Han-Wen Huang ◽  
Wendy W. Hwang-Verslues ◽  
Candy Hsin-Hua Cho ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Embryonic Stem ◽  
Cancer Therapies ◽  
New Cancer Therapies ◽  
Globo Series

The discovery of cancer stem cells (CSCs), which are responsible for self-renewal and tumor growth in heterogeneous cancer tissues, has stimulated interests in developing new cancer therapies and early diagnosis. However, the markers currently used for isolation of CSCs are often not selective enough to enrich CSCs for the study of this special cell population. Here we show that the breast CSCs isolated with CD44+CD24-/loSSEA-3+ or ESAhiPROCRhiSSEA-3+ markers had higher tumorigenicity than those with conventional markers in vitro and in vivo. As few as 10 cells with CD44+CD24-/loSSEA-3+ formed tumor in mice, compared with more than 100 cells with CD44+CD24-/lo. Suppression of SSEA-3 expression by knockdown of the gene encoding β-1,3-galactosyltransferase 5 (β3GalT5) in the globo-series pathway, led to apoptosis in cancer cells specifically but had no effect on normal cells. This finding is further supported by the analysis of SSEA-3 and the two related globo-series epitopes SSEA4 and globo-H in stem cells (embryonic stem cells and induced pluripotent stem cells) and various normal and cancer cells, and by the antibody approach to target the globo-series glycans and the late-stage clinical trials of a breast cancer vaccine.

scholarly journals Engineering T-Cell Activation for Immunotherapy by Mechanical Forces

2021 ◽  
pp. 553-591
Author(s):  
Elena Locci ◽  
Silvia Raymond
Keyword(s):  
T Cells ◽  
Immune System ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cytotoxic T Cells ◽  
Cancer Therapies ◽  
Physical Barriers ◽  
Keywords Cancer ◽  
New Cancer Therapies

A groundbreaking study led by engineering and medical researchers at the California South University (CSU) shows how immune cells engineered in new cancer therapies can overcome physical barriers so that the patient's own immune system can fight tumors. This research could improve the future of millions of cancer patients worldwide. Immunotherapy, instead of using chemicals or radiation, is a type of cancer treatment that helps the patient's immune system fight cancer. T cells are a type of white blood cell that is essential for the body's immune system. Cytotoxic T cells are like soldiers searching for and destroying target invading cells. Although there has been success in using immunotherapy for some types of cancer in the blood or blood-producing organs, T cell work is much more difficult in solid tumors. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management

scholarly journals Structure of PDE3A-SLFN12 complex reveals requirements for activation of SLFN12 RNase

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Colin W. Garvie ◽  
Xiaoyun Wu ◽  
Malvina Papanastasiou ◽  
Sooncheol Lee ◽  
James Fuller ◽  
...  
Keyword(s):  
Cell Death ◽  
Complex Formation ◽  
Cancer Cells ◽  
Active Site ◽  
Alpha Helix ◽  
Rnase Activity ◽  
Cancer Therapies ◽  
Cancer Cell Death ◽  
New Cancer Therapies ◽  
Related Compounds

AbstractDNMDP and related compounds, or velcrins, induce complex formation between the phosphodiesterase PDE3A and the SLFN12 protein, leading to a cytotoxic response in cancer cells that express elevated levels of both proteins. The mechanisms by which velcrins induce complex formation, and how the PDE3A-SLFN12 complex causes cancer cell death, are not fully understood. Here, we show that PDE3A and SLFN12 form a heterotetramer stabilized by binding of DNMDP. Interactions between the C-terminal alpha helix of SLFN12 and residues near the active site of PDE3A are required for complex formation, and are further stabilized by interactions between SLFN12 and DNMDP. Moreover, we demonstrate that SLFN12 is an RNase, that PDE3A binding increases SLFN12 RNase activity, and that SLFN12 RNase activity is required for DNMDP response. This new mechanistic understanding will facilitate development of velcrin compounds into new cancer therapies.

scholarly journals Metabolic Relationship Between Cancer-Associated Fibroblasts and Cancer Cells

2021 ◽  
pp. 189-204 ◽  
Author(s):  
Christos Sazeides ◽  
Anne Le
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Cell Interactions ◽  
Cancer Therapies ◽  
Cancer Associated Fibroblasts ◽  
Physical Support ◽  
Activated State ◽  
Cancer Initiation ◽  
New Cancer Therapies ◽  
The Way

AbstractCancer-associated fibroblasts (CAFs), a major component of the tumor microenvironment (TME), play an important role in cancer initiation, progression, and metastasis. Recent findings have demonstrated that the TME not only provides physical support for cancer cells but also directs cell-to-cell interactions (in this case, the interaction between cancer cells and CAFs). As cancer progresses, the CAFs also coevolve, transitioning from an inactivated state to an activated state. The elucidation and understanding of the interaction between cancer cells and CAFs will pave the way for new cancer therapies [1–3].

scholarly journals Process of Converting Glucose to Energy, Single Endothelial Cells and Blood Vessel Cells

2021 ◽  
pp. 261-300
Author(s):  
Ricardo Gobato ◽  
Abhijit Mitra
Keyword(s):  
Artificial Intelligence ◽  
Endothelial Cells ◽  
Blood Vessel ◽  
Cancer Cells ◽  
Single Cell Level ◽  
Cell Level ◽  
Wide Range ◽  
Keywords Cancer ◽  
Glycolysis Process ◽  
Genetically Encoded Biosensor

Understanding cellular metabolism (how cells use energy) can be key in treating a wide range of diseases, including vascular disease and cancer. Although many techniques can measure these processes in tens of thousands of cells, researchers have not been able to measure them at the single-cell level. Researchers have used a genetically encoded biosensor with artificial intelligence to measure glycolysis. (Process of converting glucose to energy, single endothelial cells, blood vessel cells). Keywords: Cancer; Cells; Tissues; Tumors; Prevention; Prognosis; Diagnosis; Imaging; Screening, Treatment; Management

scholarly journals Searching Cytotoxic T Cells for Destroying Target Invading Cells

2021 ◽  
pp. 544-583
Author(s):  
Alireza Heidari ◽  
Ricardo Gobato ◽  
Abhijit Mitra
Keyword(s):  
T Cells ◽  
Immune System ◽  
Blood Cell ◽  
Immune Cells ◽  
Cytotoxic T Cells ◽  
Cancer Therapies ◽  
Medical Researchers ◽  
Physical Barriers ◽  
Keywords Cancer ◽  
New Cancer Therapies

A groundbreaking study led by engineering and medical researchers at the California South University (CSU) shows how immune cells engineered in new cancer therapies can overcome physical barriers so that the patient's own immune system can fight tumors. This research could improve the future of millions of cancer patients worldwide. Immunotherapy, instead of using chemicals or radiation, is a type of cancer treatment that helps the patient's immune system fight cancer. T cells are a type of white blood cell that is essential for the body's immune system. Cytotoxic T cells are like soldiers searching for and destroying target invading cells. Although there has been success in using immunotherapy for some types of cancer in the blood or blood-producing organs, T cell work is much more difficult in solid tumors Keywords: Cancer; Cells; Tissues; Tumors; Prevention; Prognosis; Diagnosis; Imaging; Screening, Treatment; Management

scholarly journals Novel cancer therapies and their association with diabetes

2019 ◽  
Vol 62 (2) ◽  
pp. R187-R199 ◽  
Author(s):  
Afreen Idris Shariff ◽  
Sohail Syed ◽  
Rebecca A Shelby ◽  
Jeremy Force ◽  
Jeffrey Melson Clarke ◽  
...  
Keyword(s):  
Great Part ◽  
Cancer Therapies ◽  
Normal Tissues ◽  
Autoimmune Destruction ◽  
Clinical Presentations ◽  
New Cancer Therapies ◽  
New Diagnosis ◽  
The Impact

Over the last decade, there has been a shift in the focus of cancer therapy from conventional cytotoxic drugs to therapies more specifically directed to cancer cells. These novel therapies include immunotherapy, targeted therapy and precision medicine, each developed in great part with a goal of limiting collateral destruction of normal tissues, while enhancing tumor destruction. Although this approach is sound in theory, even new, specific therapies have some undesirable, ‘off target effects’, in great part due to molecular pathways shared by neoplastic and normal cells. One such undesirable effect is hyperglycemia, which results from either the loss of immune tolerance and autoimmune destruction of pancreatic β-cells or dysregulation of the insulin signaling pathway resulting in insulin resistance. These distinct pathogenic mechanisms lead to clinical presentations similar to type 1 (T1DM) and type 2 (T2DM) diabetes mellitus. Both types of diabetes have been reported in patients across clinical trials, and data on the mechanism(s) for developing hyperglycemia, prevalence, prognosis and effect on cancer mortality is still emerging. With the rapidly expanding list of clinical indications for new cancer therapies, it is essential to understand the impact of their adverse effects. In this review, we focus on hyperglycemia and diabetes related to cancer therapies, describe what is known about mechanism(s) leading to dysregulated glucose metabolism and provide a guide to management of complex oncology patients with a new diagnosis of diabetes.

Potential of Mesenchymal Stem Cells in Anti-Cancer Therapies

2020 ◽  
Vol 15 (6) ◽  
pp. 482-491 ◽  
Author(s):  
Milena Kostadinova ◽  
Milena Mourdjeva
Keyword(s):  
Cancer Cells ◽  
Small Population ◽  
Tumor Formation ◽  
Bioactive Molecules ◽  
Cancer Therapies ◽  
New Methods ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Blocking Mechanisms

Mesenchymal stem/stromal cells (MSCs) are localized throughout the adult body as a small population in the stroma of the tissue concerned. In injury, tissue damage, or tumor formation, they are activated and leave their niche to migrate to the site of injury, where they release a plethora of growth factors, cytokines, and other bioactive molecules. With the accumulation of data about the interaction between MSCs and tumor cells, the dualistic role of MSCs remains unclear. However, a large number of studies have demonstrated the natural anti-tumor properties inherent in MSCs, so this is the basis for intensive research for new methods using MSCs as a tool to suppress cancer cell development. This review focuses specifically on advanced approaches in modifying MSCs to become a powerful, precision- targeted tool for killing cancer cells, but not normal healthy cells. Suppression of tumor growth by MSCs can be accomplished by inducing apoptosis or cell cycle arrest, suppressing tumor angiogenesis, or blocking mechanisms mediating metastasis. In addition, the chemosensitivity of cancer cells may be increased so that the dose of the chemotherapeutic agent used could be significantly reduced.

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