scholarly journals The Ultimate Substance to Cause Cancer Is a Hydrogen Ion and Cancer Cells Stop its Division-Multiplication and Return to Normal Cells by Supplying Oxygen as Hydrogen Acceptor, from Theoretical Research

2021 ◽  
Author(s):  
Nobuo Tomizawa
Keyword(s):  
Theoretical Model ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Normal Cell ◽  
Medical Science ◽  
Theoretical Models ◽  
Theoretical Work ◽  
Theoretical Research ◽  
Hydrogen Ions ◽  
Normal Cells

(1)A fundamental viewpoint about cancer cellsAt the present time, methods of treatment for cancer base on the viewpoint that cancer cells make humans deaths, therefore a treatment destroys and kills cancer cells and saves patients. But this conception strikes against the limit on treatment. A cancer cell changed from a normal cell of a human, it does not invade from outside and harm a human like virus. A cancer cell is derived from a human cell, therefore when we aim to destroy cancer cells, this attack damages to other normal cells and weaken vital energy of a human. Here there is the limit of treatment for cancer.In opposition to these thoughts, this theory is based on the viewpoint that normal cells faced to critical situation to live and changed its system to survive under the situation and that are certainly cancer cells. The reason why a cancer cell has tough vitality to make a human death is the result to acquire the ability for existing under such a situation. Therefore a treatment for cancer is not to destroy and to kill but to remove factors that prevent normal cells from living orderly. Then cancer cells become unnecessary to derive a tough vitality. And its rapid division and multiplication will stop and return to normal cells.I built the theoretical model as follows. A cell becomes lack of oxygen that is necessary to live. Then hydrogen ions emerge in that cell. Hydrogen ions promote division and multiplication. Take these hydrogen ions out by supplying oxygen like a normal cell doing, and cancer cells will stop division and return to normal cells.This research intends to explain by facts already known and prove this model on,how hydrogen ions emerge in cells?how hydrogen ions promote cell division? Thenhow a treatment for cancer is possible?(2)The division of works of building theoretical models and experiments on biology and medical scienceSome historical discoveries on physics have walked on the process that a theoretical research predicts the existence of materials or the law and some experiments prove it. Physics is divided into two areas. One is theoretical physics that builds theoretical models and another is experimental physics that proves those models by experiments. In medical science and biology, usually one researcher builds a supposition and proves it by experiments. Theoretical work and verification by experimental work are not divided. A theoretical model without experimental proof is not enough recognized its medical or biological value.However more multiple researches will be possible by dividing theoretical work to build theoretical models and experimental work to verify it in the field of cancer that is not solved an ultimate cause and a mechanism to change from normal cells. And it should value theoretical researches that are not yet verified by experiments.This treatise is the theoretical model that is not proved by experiments. I illustrated specific ways for experiments to prove in Chapter 4, “The principle and practical methods of medical treatment for cancer of human beings, (1)Supply oxygen to cultured cancer cells, and multiplication of cancer cells will stop”.I hope that scientists of medical science and biology would prove it by experiments.

Investigation on penetration model of shaped charge jet in water

2016 ◽  
Vol 30 (02) ◽  
pp. 1550268 ◽  
Author(s):  
Jinwei Shi ◽  
Xingbai Luo ◽  
Jinming Li ◽  
Jianwei Jiang
Keyword(s):  
Numerical Simulation ◽  
Theoretical Model ◽  
Model Simulation ◽  
Theoretical Models ◽  
Theoretical Research ◽  
Water Medium ◽  
Simulation Results ◽  
Jet Penetration ◽  
The Impact ◽  
Penetration Velocity

To analyze the process of jet penetration in water medium quantitatively, the properties of jet penetration spaced target with water interlayer were studied through test and numerical simulation. Two theoretical models of jet penetration in water were proposed. The theoretical model 1 was established considering the impact of the shock wave, combined with the shock equation Rankine–Hugoniot and the virtual origin calculation method. The theoretical model 2 was obtained by fitting theoretical analysis and numerical simulation results. The effectiveness and universality of the two theoretical models were compared through the numerical simulation results. Both the models can reflect the relationship between the penetration velocity and the penetration distance in water well, and both the deviation and stability of theoretical model 1 are better than 2, the lower penetration velocity, and the larger deviation of the theoretical model 2. Therefore, the theoretical model 1 can reflect the properties of jet penetration in water effectively, and provide the reference of model simulation and theoretical research.

Anticancer Activity of Novel Platinum Complex as DNA Binders

2013 ◽  
Vol 781-784 ◽  
pp. 1107-1110
Author(s):  
Xu Jian Luo ◽  
Qi Pin Qin ◽  
Yu Lan Li ◽  
Yan Cheng Liu
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Normal Cell ◽  
Platinum Complex ◽  
Cancer Cell Lines ◽  
Cytotoxic Activities ◽  
Element Analysis ◽  
Normal Cells ◽  
Dna Binders ◽  
Ct Dna

A new phenanthroimidazole platinum (II) complex has been synthesized and characterized by IR, NMR, ESI-MS, element analysis. The affinities of the complex toward ct-DNA was determined by circular dichroism absorption (CD), UV-Vis absorption. Results indicate that the complex interact with ct-DNA by classical intercalating mode. The cytotoxicities of the complex was screened against four cancer cell lines and normal cells of HL-7702 in comparison to cisplatin and it showed a higher activity than cisplatin, with IC50 values in the range 8.7417.11 μmol/L. Furthermore, the complex displayed lower cytotoxic activities to HL-7702 (normal cell) compared with the cancer cell lines.

scholarly journals Pulsed Magnetic Fields Cause hes1 and hsa-Circ-0068530 Expression Changes in Gastric Cancer Cell Line and Human Normal Fibroblast Cell Line

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Fereshteh Mansoury ◽  
Soheila Abdi ◽  
Nahid Babaei ◽  
Maliheh Entezari ◽  
Abbas Doosti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Magnetic Flux ◽  
Cancer Cells ◽  
Cell Line ◽  
Electromagnetic Fields ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Normal Cells

Background: In recent years, the relationship between cancer cells and electromagnetic radiation has received much attention. Objectives: The present study aimed to evaluate the effects of different intensities of electromagnetic fields on gastric cancer cell lines (AGS). Methods: After preparing AGS and Hu02 (normal) cell lines, they were exposed to magnetic flux densities of 0.25, 0.5, 1, and 2 millitesla (mT) for 18 h. The cell viability was studied by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression levels of hes1 and hsa-circ-0068530 RNAs were studied by the quantitative Real-time-PCR technique. Results: The inhibition of gastric cancer cell line growth was observed under the influence of electromagnetic fields at different intensities. However, they did not affect the viability of normal cells. A sharp increase in the expression of hes1 and hsa-circ-0068530 genes was observed in normal cells exposed to 2 mT electromagnetic fields. Conclusions: In general, it can be concluded that the effect of electromagnetic fields on gastric cancer cells depends on their intensity. Magnetic flux densities of 0.25 and 0.5 mT had anti-cancer effects and magnetic flux density of 2 mT showed carcinogenic effects.

scholarly journals Overview on the Side Effects of Doxorubicin

2020 ◽  
Author(s):  
Chittipolu Ajaykumar
Keyword(s):  
Side Effects ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Cytotoxic Effect ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Preventive Strategies ◽  
Normal Cells ◽  
Dna Strand

Doxorubicin is an anthracycline antibiotic extracted from the bacterium Streptomyces peucetius. Its cytotoxic effect produced by intercalating with DNA causing breakdown of DNA strand which causes cancer cell apoptosis. Despite being an effective anticancer agent it causes several crucial side effects like carditoxicity, neuropathy, hepatotoxicity, nephrotoxicity, alopecia, typhlitis, myelosuppression, neutropenia, anaemia, thrombocytopenia, nausea, and diarrhoea were caused mainly due to the inability to distinguish between cancer cells and normal cells. This chapter mainly focuses on doxorubicin’s side effects, current understanding of the molecular mechanisms, and management and preventive strategies of doxorubicin’s cardiotoxicity during the treatment of various type of cancer.

Targeting Y397 FAK scaffolding compared with FAK kinase inhibition: Efficacy and specificity for tumor cells.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e13547-e13547 ◽  
Author(s):  
Vita Golubovskaya ◽  
Baotran Ho ◽  
Adam Stright ◽  
Maria Zajac-Kaye ◽  
Steven N. Hochwald ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Kinase Domain ◽  
Normal Cells ◽  
Atp Binding Site ◽  
Survival Signaling ◽  
Student’S T

e13547 Background: Focal Adhesion Kinase is a non-receptor kinase which is highly overexpressed and activated or autophosphorylated in many types of tumors and plays a major role in survival signaling and metastasis. Recently, our group developed a highly specific allosteric scaffolding FAK autophosphorylation inhibitor, Y15, that blocked FAK Y397 autophosphorylation, decreased cancer cell viability, and significantly decreased breast, neuroblastoma, pancreatic and glioblastoma tumor growth. In addition, Y15 was not toxic in mice. In this study, we compared side by side efficacy of Y15 with two other FAK inhibitors in clinical trials, Pfizer PF-04554878 and Glaxo GSK-2256098. Methods: MTT, clonogenicity and Western blotting assays were used to detect the effect of FAK inhibitors on different cancer and normal cells. Student’s t-test was used for statistical analysis and p<0.05 was considered significant. Results: We tested different cancer cell lines: kidney 293T, colon SW620 and LoVo; lung A549; glioblastoma U251 and U87; breast: BT474, MDA-231, MDA-361, MDA-453, MDA-468 and T47D and pancreatic PANC-1 cancer cells with different doses of Y15, PF and GSK inhibitors by MTT assay and found that Y15 was the most effective at decreasing cancer cell viability in most cancer cell lines, with higher efficacy than PF and much higher efficacy than GSK inhibitor. The same was observed for clonogenicity assay. In addition, we found that Y15 did not significantly affect viability of normal colon (CCD-112) cells, while viability of these cells with PF and GSK decreased to 54% and 57% at a 2 microM dose, respectively, from 100% in untreated cells. In addition, Y15 significantly decreased Y397-FAK, Y418-Src, phospho- Ser 473-AKT and phospho-ERK1/2, while PF had less effect and GSK only a minimal effect in four different cancer cell lines: U251, A549, 293T and Lovo at 10 microM and 100 microM doses, showing high potency of the FAK Y397 scaffolding inhibitor. Conclusions: These data show that Y15, which inhibits the Y397 site of FAK, is more potent against cancer cells and less toxic to normal cells than FAK inhibitors that target the conserved ATP-binding site in the kinase domain.

Dual-targeted activatable photosensitizers with aggregation-induced emission (AIE) characteristics for image-guided photodynamic cancer cell ablation

2016 ◽  
Vol 4 (1) ◽  
pp. 169-176 ◽  
Author(s):  
Youyong Yuan ◽  
Shidang Xu ◽  
Chong-Jing Zhang ◽  
Ruoyu Zhang ◽  
Bin Liu
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Normal Cell ◽  
Aggregation Induced Emission ◽  
Image Guided ◽  
Cell Ablation

The currently available photosensitizers (PSs) for photodynamic therapy (PDT) can easily lead to undesirable normal cell death due to their intrinsic photo-toxicity and lack of selectivity for cancer cells.

scholarly journals Fundamental mechanisms of telomerase action in yeasts and mammals: understanding telomeres and telomerase in cancer cells

Open Biology ◽  
2017 ◽  
Vol 7 (3) ◽  
pp. 160338 ◽  
Author(s):  
Christine A. Armstrong ◽  
Kazunori Tomita
Keyword(s):  
Transcriptional Regulation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Current Knowledge ◽  
Model Systems ◽  
Cancer Treatments ◽  
Normal Cells ◽  
Telomere Homeostasis ◽  
Multiple Levels

Aberrant activation of telomerase occurs in 85–90% of all cancers and underpins the ability of cancer cells to bypass their proliferative limit, rendering them immortal. The activity of telomerase is tightly controlled at multiple levels, from transcriptional regulation of the telomerase components to holoenzyme biogenesis and recruitment to the telomere, and finally activation and processivity. However, studies using cancer cell lines and other model systems have begun to reveal features of telomeres and telomerase that are unique to cancer. This review summarizes our current knowledge on the mechanisms of telomerase recruitment and activation using insights from studies in mammals and budding and fission yeasts. Finally, we discuss the differences in telomere homeostasis between normal cells and cancer cells, which may provide a foundation for telomere/telomerase targeted cancer treatments.

scholarly journals Terrein Inhibits Aggressive Phenotype of A549 Human Lung Cancer Cell through Suppression of HIF-1α

2021 ◽  
Vol 18 (11) ◽  
Author(s):  
Paiwan BUACHAN ◽  
Maneekarn NAMSA-AID ◽  
Wanlaya TANECHPONGTAMB
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
A549 Cells ◽  
Specific Effect ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Normal Cells ◽  
Aggressive Phenotype

Terrein is a fungal metabolite that has already been reported with anticancer properties. However, the effect on the aggressive phenotype of cancer cells has not been elucidated yet.  In the present study, the cytotoxicity of terrein was first determined against lung cancer cells (A549) model and compared with several normal cell lines (Vero, L6, and H9C2 cells). The data demonstrated that terrein had a specific effect on A549 cells relative to normal cells with high selectivity index values. Then, the hypoxic model that recognized to induce aggressive abilities was established in A549 cells by cobalt chloride (CoCl2) stimulation. With this model, terrein could reduce HIF-1α, a marker of hypoxia, and inhibit both migration and invasion of which the effect on invasion is more explicit. Our results demonstrated that terrein has a potential new role as the anti-aggressive phenotype by inhibiting cancer cell migration and invasion through HIF-1α reduction. HIGHLIGHTS Terrein, a secondary bioactive metabolite extracted from Aspergillus terreus, demonstrates anticancer effect on lung cancer cells with less cytotoxic on normal cells CoCl2 treatment was successfully used for creating hypoxic model which resulting in HIF-1a augmentation and aggressive abilities enhancement in lung cancer cells Terrein could reduce HIF-1a expression and invasive ability of lung cancer cells demonstrated the potential role as anti-metastatic agent for lung cancer GRAPHICAL ABSTRACT

scholarly journals IDENTIFIKASI PERUBAHAN STRUKTUR DNA TERHADAP PEMBENTUKAN SEL KANKER MENGGUNAKAN DEKOMPOSISI GRAF

2017 ◽  
Vol 17 (2) ◽  
pp. 153
Author(s):  
Rondo V.S.A Morihito ◽  
Stephanie E Chungdinata ◽  
Timboeleng A Nazareth ◽  
M Iqbal Pulukadang ◽  
Roy A.M Makalew ◽  
...  
Keyword(s):  
Cell Division ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Control Cell ◽  
Hamilton Cycle ◽  
Graph Decomposition ◽  
Cancer Cell Growth ◽  
Normal Cells ◽  
Dna Structures ◽  
Control Cell Division

IDENTIFIKASI PERUBAHAN STRUKTUR DNA TERHADAP PEMBENTUKAN  SEL KANKER MENGGUNAKAN DEKOMPOSISI GRAFABSTRAKKerusakan DNA adalah salah satu penyebab yang dapat mebuat sel normal bertumbuh menjadi sel kanker. Hal ini dikarenakan DNA yang rusak dapat menyebabkan mutasi di gen vital yang mengontrol pembelahan sel sampai terjadi pembelahan sel yang tidak terkendali dan memicu pertumbuhan sel kanker. Beberapa mutasi dibutuhkan untuk mengubah sel normal menjadi sel kanker. Dalam hal ini, teori dekomposisi graf digunakan untuk menganalisa proses terjadinya pertumbuhan sel kanker yang dimulai dari kerusakan DNA yang menyebabkan terjadinya mutasi gen. Dengan teori dekomposisi graf, sebuah graf bisa difaktorkan ke dalam beberapa subgraf. Pemfaktoran ini dapat digunakan untuk melihat pola perubahan hubungan antar objek. Tujuan dari penelitian ini untuk mengidentifikasi struktur DNA terhadap pembentukan sek kanker dengan menggunakan dekomposisi graf. Yang  diidenfikasi adalah mutasi delesi, addisi, dan substitusi dimana dari mutasi-mutasi ini dilihat hasil dekomposisi graf dan apakah dari ketiga mutasi ini dapat membentuk sel kanker.Kata Kunci : Struktur DNA, Sel Kanker, Dekomposisi Graf, Perfect Matching, Hamilton cycle IDENTIFICATION OF CHANGES OF DNA STRUCTURES ON CANCER CELL FORM USING GRAPH DECOMPOSITIONABSTRACTDNA damage is one of the causes that can make normal cells grow into cancer cells. This is because damaged DNA can cause mutations in vital genes that control cell division until uncontrolled cell division and trigger the growth of cancer cells. Some mutations are needed to convert normal cells into cancer cells. In this case theory of graph decomposition will be used to analyze the process of cancer cell growth that starts from the DNA damage that causes gene mutation. With the graph decomposition theory, a graph can be factored into several subgraphs. This factoring can be used to see patterns of relationship changes between objects. The purpose of this study was to identify the structure of DNA against the formation of cancer cells by using decomposition graph. What will be identified are the deletion mutations, additions, and substitutions from which these mutations are seen in the decomposition of the graph and whether these three mutations can form cancer cells.Keywords :  Structure of DNA, Cancer Sel, Dekomposition Graph, Perfect Maching, Hamilton cycle

scholarly journals Mathematical Modeling of Locoregional Recurrence Caused by Premalignant Lesions Formed Before Initial Treatment

2021 ◽  
Vol 11 ◽  
Author(s):  
Mitsuaki Takaki ◽  
Hiroshi Haeno
Keyword(s):  
Mathematical Model ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Locoregional Recurrence ◽  
Branching Processes ◽  
Cancer Recurrence ◽  
Disease Free Survival ◽  
Premalignant Lesions ◽  
Cancer Type ◽  
Normal Cells

Locoregional recurrence after surgery is a major unresolved issue in cancer treatment. Premalignant lesions are considered a cause of cancer recurrence. A study showed that premalignant lesions surrounding the primary tumor drove a high local cancer recurrence rate after surgery in head and neck cancer. Based on the multistage theory of carcinogenesis, cells harboring an intermediate number of mutations are not cancer cells yet but have a higher risk of becoming cancer than normal cells. This study constructed a mathematical model for cancer initiation and recurrence by combining the Moran and branching processes in which cells require two specific mutations to become malignant. There are three populations in this model: (i) normal cells with no mutation, (ii) premalignant cells with one mutation, and (iii) cancer cells with two mutations. The total number of healthy tissue is kept constant to represent homeostasis, and there is a rare chance of mutation every time a cell divides. If a cancer cell with two mutations arises, the cancer population proliferates, violating the homeostatic balance of the tissue. Once the number of cancer cells reaches a certain size, we conduct computational resection and remove the cancer cell population, keeping the ratio of normal and premalignant cells in the tissue unchanged. After surgery, we considered tissue dynamics and eventually observed the second appearance of cancer cells as recurrence. Consequently, we computationally revealed the conditions where the time to recurrence became short by parameter sensitivity analysis. Particularly, when the premalignant cells’ fitness is higher than normal cells, the proportion of premalignant cells becomes large after the surgical resection. Moreover, the mathematical model was fitted to clinical data on disease-free survival of 1,087 patients in 23 cancer types from the TCGA database. Finally, parameter values of tissue dynamics are estimated for each cancer type, where the likelihood of recurrence can be elucidated. Thus, our approach provides insights into the concept to identify the patients likely to experience recurrence as early as possible.

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