scholarly journals Numerical Analysis of Human Cancer Therapy Using Microwave Ablation

2019 ◽  
Vol 10 (1) ◽  
pp. 211 ◽  
Author(s):  
Marwa Selmi ◽  
Abdul Aziz Bin Dukhyil ◽  
Hafedh Belmabrouk
Keyword(s):  
Temperature Distribution ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Microwave Power ◽  
Microwave Ablation ◽  
Human Cancer ◽  
Surrounding Tissue ◽  
Hyperthermia Treatment ◽  
Distribution Profile ◽  
Wave Effects

Microwave ablation is one type of hyperthermia treatment of cancer that involves heating tumor cells. This technique uses electromagnetic wave effects to kill cancer cells. A micro-coaxial antenna is introduced into the biological tissue. The radiation emitted by the antenna is absorbed by the tissue and leads to the heating of cancer cells. The diffuse increase in temperature should reach a certain value to achieve the treatment of cancer cells but it should be less than a certain other value to avoid damaging normal cells. This is why hyperthermia treatment should be carefully monitored. A numerical simulation is useful and may provide valuable information. The bio-heat equation and Maxwell’s equations are solved using the finite element method. Electro-thermal effects, temperature distribution profile, specific absorption rate (SAR), and fraction of necrotic tissue within cancer cells are analyzed. The results show that SAR and temperature distribution are strongly affected by input microwave power. High microwave power causes a high SAR value and raises the temperature above 50 °C, which may destroy healthy cells. It is revealed that with a power of 10 W, the tumor cells will be killed without damaging the surrounding tissue.

scholarly journals Finite Element Analysis of the Microwave Ablation Method for Enhanced Lung Cancer Treatment

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3500
Author(s):  
Marija Radmilović-Radjenović ◽  
Martin Sabo ◽  
Marta Prnova ◽  
Lukaš Šoltes ◽  
Branislav Radjenović
Keyword(s):  
Dielectric Properties ◽  
Cancer Cells ◽  
Microwave Ablation ◽  
Absorption Rate ◽  
Specific Absorption Rate ◽  
Surrounding Tissue ◽  
Physical Parameters ◽  
Medical Procedure ◽  
Ablation Zone ◽  
Specific Absorption

Knowledge of the frequency dependence of the dielectric properties of the lung tissues and temperature profiles are essential characteristics associated with the effective performance of microwave ablation. In microwave ablation, the electromagnetic wave propagates into the biological tissue, resulting in energy absorption and providing the destruction of cancer cells without damaging the healthy tissue. As a consequence of the respiratory movement of the lungs, however, the accurate prediction of the microwave ablation zone has become an exceptionally demanding task. For that purpose, numerical modeling remains a primordial tool for carrying out a parametric study, evaluating the importance of the inherent phenomena, and leading to better optimization of the medical procedure. This paper reports on simulation studies on the effect of the breathing process on power dissipation, temperature distribution, the fraction of damage, and the specific absorption rate during microwave ablation. The simulation results obtained from the relative permittivity and conductivity for inflated and deflated lungs are compared with those obtained regardless of respiration. It is shown that differences in the dielectric properties of inflated and deflated lungs significantly affect the time evolution of the temperature and its maximum value, the time, the fraction of damage, and the specific absorption rate. The fraction of damage determined from the degree of tissue injury reveals that the microwave ablation zone is significantly larger under dynamic physical parameters. At the end of expiration, the ablation lesion area is more concentrated around the tip and slot of the antenna, and the backward heating effect is smaller. The diffuse increase in temperature should reach a certain level to destroy cancer cells without damaging the surrounding tissue. The obtained results can be used as a guideline for determining the optimal conditions to improve the overall success of microwave ablation.

The Effects of Large Blood Vessels on Three-Dimensional Tissue Temperature Distributions During Electromagnetic Induced Nano-Hyperthermia: Numerical Simulation

2008 ◽  
Author(s):  
Zhong-Shan Deng ◽  
Jing Liu
Keyword(s):  
Blood Vessels ◽  
Tumor Cells ◽  
Three Dimensional ◽  
The Body ◽  
Thermal Therapy ◽  
Tissue Temperature ◽  
Surrounding Tissue ◽  
Temperature Profiles ◽  
Hyperthermia Treatment ◽  
Tumor Hyperthermia

As is well known, the blood flowing through large blood vessels acts as a heat sink and plays an important role in affecting temperature profiles of heated tissues [1]. In hyperthermia, heating is usually limited to the tumor and a small margin of the surrounding tissue. Since the temperatures in the rest of the body remain normal, the blood that supplies the tumor will be relatively cold. Consequently, the blood flow inside a large vessel will represent a sink which cools the nearby heated tissues and then limits heating lesion during tumor hyperthermia. Under this adverse condition, a part of vital tumor cells may remain in the thermally lethal area and lead to recurrence of tumors after hyperthermia treatment. More specifically, tumor cell survival in the vicinity of large blood vessels is often correlated with tumor recurrence after thermal therapy. Therefore, it is difficult to implement an effective hyperthermia treatment when a tumor is contiguous to a large blood vessel or such vessel transits the tumor. How to totally destroy tumor cells in the vicinity of large blood vessels has been a major challenge in hyperthermia [2].

scholarly journals Repression of LKB1 by miR-17∼92 sensitizes MYC-dependent lymphoma to biguanide treatment

2019 ◽  
Author(s):  
Said Izreig ◽  
Alexandra Gariepy ◽  
Ariel O. Donayo ◽  
Gaëlle Bridon ◽  
Daina Avizonis ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Tumor Cells ◽  
Human Cancer ◽  
Tca Cycle ◽  
Mirna Cluster ◽  
Lymphoma Cells ◽  
Ampk Signaling ◽  
Potential Biomarker

AbstractCancer cells display metabolic plasticity to survive metabolic and energetic stresses in the tumor microenvironment, prompting the need for tools to target tumor metabolism. Cellular adaptation to energetic stress is coordinated in part by signaling through the Liver Kinase B1 (LKB1)-AMP-activated protein kinase (AMPK) pathway. Reducing LKB1-AMPK signaling exposes metabolic vulnerabilities in tumor cells with potential for therapeutic targeting. Here we describe that miRNA-mediated silencing of LKB1 (mediated by the oncogenic miRNA cluster miR-17∼92) confers sensitivity of lymphoma cells to mitochondrial inhibition by biguanides. Using both classic (phenformin) and novel (IM156) biguanides, we demonstrate that Myc+ lymphoma cells with elevated miR-17∼92 expression display increased sensitivity to biguanide treatment both in cell viability assays in vitro and tumor growth assays in vivo. This increased biguanide sensitivity is driven by miR-17-dependent silencing of LKB1, which results in reduced AMPK activation in response to bioenergetic stress. Mechanistically, biguanide treatment inhibits TCA cycle metabolism and mitochondrial respiration in miR-17∼92-expressing tumor cells, targeting their metabolic vulnerability. Finally, we demonstrate a direct correlation between miR-17∼92 expression and biguanide sensitivity in human cancer cells. Our results identify miR-17∼92 expression as a potential biomarker for biguanide sensitivity in hematological malignancies and solid tumors.One Sentence SummarymiR-17∼92 expression in Myc+ tumors sensitizes cancer cells to biguanide treatment by disrupting bioenergetic stability in lymphoma cells.

scholarly journals Biochemical Basis of Anti-Cancer-Effects of Phloretin—A Natural Dihydrochalcone

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 278 ◽  
Author(s):  
Bu Choi
Keyword(s):  
Cancer Cells ◽  
Tumor Cells ◽  
Human Cancer ◽  
Cancer Drug ◽  
Biochemical Basis ◽  
Human Cancer Cells ◽  
Anti Cancer ◽  
Anti Inflammatory ◽  
Natural Agent ◽  
Growth Of Tumor

Apple is a rich source of bioactive phytochemicals that help improve health by preventing and/or curing many disease processes, including cancer. One of the apple polyphenols is phloretin [2′,4′,6′-Trihydroxy-3-(4-hydroxyphenyl)-propiophenone], which has been widely investigated for its antioxidant, anti-inflammatory and anti-cancer activities in a wide array of preclinical studies. The efficacy of phloretin in suppressing xenograft tumor growth in athymic nude mice implanted with a variety of human cancer cells, and the ability of the compound to interfere with cancer cells signaling, have made it a promising candidate for anti-cancer drug development. Mechanistically, phloretin has been reported to arrest the growth of tumor cells by blocking cyclins and cyclin-dependent kinases and induce apoptosis by activating mitochondria-mediated cell death. The blockade of the glycolytic pathway via downregulation of GLUT2 mRNA and proteins, and the inhibition of tumor cells migration, also corroborates the anti-cancer effects of phloretin. This review sheds light on the molecular targets of phloretin as a potential anti-cancer and anti-inflammatory natural agent.

scholarly journals Adaptation of the Newcastle Disease Virus to Cell Cultures for Enhancing Its Oncolytic Properties

Acta Naturae ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 66-73
Author(s):  
K. S. Yurchenko ◽  
Yi. Jing ◽  
A. M. Shestopalov
Keyword(s):  
Newcastle Disease Virus ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Disease Virus ◽  
Cell Cultures ◽  
Newcastle Disease ◽  
Human Cancer ◽  
Genetic Material ◽  
Human Tumor ◽  
Natural Strains

This study focuses on the adaptation of natural Newcastle disease virus (NDV) strains isolated from wild birds to human tumor cells. Many candidates for virotherapy are viruses pathogenic for human. During recombination of genetic material, there always exists a risk of getting a virus with an unstable genome. This problem can be solved by using natural apathogenic viruses as oncolytic agents. The Newcastle disease virus is the causative agent of contagious avian diseases. Its natural strains exhibit an antitumor effect and are considered safe for humans. As shown in earlier studies, the oncolytic properties of natural strains can be enhanced during adaptation to cell cultures, without interference in the virus genome. This study demonstrates that serial passaging increases the viral infectious titer in cancer cells. Moreover, the viability of tumor cells decreases post-infection when Newcastle disease virus strains are adapted to these cell cultures. The findings of this study complement the well-known data on the adaptation of the Newcastle disease virus to human cancer cells. Hence, it is possible to obtain a NDV strain with a more pronounced oncolytic potential during adaptation. This should be taken into account when choosing a strategy for designing anticancer drugs based on this virus.

scholarly journals Numerical Analysis of Breast Cancer Cell with Gold Nanoparticles Necrosis by Laser Hyperthermia

2020 ◽  
Vol 10 (2) ◽  
pp. 138-144
Author(s):  
Shna A. Karim ◽  
Yousif M. Hassan
Keyword(s):  
Breast Cancer ◽  
Heat Transfer ◽  
Gold Nanoparticles ◽  
Cancer Cells ◽  
Biological Tissues ◽  
Surrounding Tissue ◽  
Threshold Temperature ◽  
Cancer Tissue ◽  
Hyperthermia Treatment ◽  
Laser Hyperthermia

Laser hyperthermia treatment of cancer tissue is widely used in cancer treatment to destroy cancer cells. This study focus on the mechanisms of heat transfer in biological tissues to minimize damage to the tissues resulting from extra heat applied. The important feature of this method is heating of specific region to raise its temperature to a threshold temperature and destroying cancer cells without to destroy surrounding tissue. In this study, we have used the combinations of laser light and gold nanoparticles to investigate the influence of nanoparticles on the spatial distribution of temperature in the tumor and healthy tissues. Accurate simulations and solving Penne’s bio-heat transfer equation were used to solve and model the thermal tumor breast cancer in the presence of gold. Nanoparticles of some particular sizes and concentrations were selected. We would like here to stress that our attempt was a theoretical and computer model with some real and hypothesized parameters and homogeneous target. The results of this study help the doctors in the study for results of hyperthermia treatment before using it on the vivo by known the properties of the laser used and the properties of the breast tumor trying to reduce the damage of the treatment.

Novel HIF-1α inhibitor CDMP-TQZ for cancer therapy

2021 ◽  
Author(s):  
Po-Chen Chu ◽  
Yu-Chieh Wu ◽  
Chien-Yu Chen ◽  
Yu-Syuan Hung ◽  
Chih-Shiang Chang
Keyword(s):  
Transcription Factor ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Human Cancer ◽  
Proteasomal Degradation ◽  
Low Oxygen ◽  
Therapeutic Targeting ◽  
Human Cancer Cells ◽  
Unique Ability

Aim: Tumor cells adapt to hypoxic microenvironments by releasing the key transcription factor HIF-1α, which promotes angiogenesis, glycolytic phenotype, metastasis and erythropoiesis, allowing proliferation amid low oxygen levels. Therefore, therapeutic targeting of HIF-1α represents a viable strategy for cancer therapy. Methods & Results: The authors synthesized a series of novel tetrahydroquinazoline derivatives in six steps and demonstrated that their development had a unique ability to suppress HIF-1α expression through proteasomal degradation. Conclusion: Among these compounds, CDMP-TQZ (8bf) exhibited the highest antiproliferative potency in human cancer cells, in part through downregulation of HIF-1α.

Expression and signaling of Toll-like receptor 4 (TLR4) and MyD88 in ovarian carcinoma cells

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e16508-e16508 ◽  
Author(s):  
M. E. Szajnik ◽  
M. J. Szczepanski ◽  
M. Czystowska ◽  
E. Elishaev ◽  
M. Mandapathil ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Growth ◽  
Ovarian Carcinoma ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Ex Vivo ◽  
Human Cancer ◽  
Progression Free Survival

e16508 Background: TLR4, expressed by the cells of the immune system play a role in the protection of the host against pathogens. TLRs are also expressed on human cancer cells, but their role in tumor growth is unknown. The aim of this study was to correlate the presence of TLR4 and MyD88 expression with clinicopathologic outcome in patients with ovarian cancer and to analyze the consequences of signaling via the TLR4/MyD88 pathway in ovarian cancer cell lines. Methods: Tumor specimens from 41 patients with ovarian carcinoma were evaluated for TLR4 and MyD88 by immunohistochemistry and correlated with clinical and pathologic disease features. TLR4/MyD88 expression in OVCAR3, SKOV3, and A2780 was determined using RT-PCR, WB, and immunohistochemistry. NF-kB translocation to nucleus was measured by confocal microscopy. Culture supernatants were tested for levels of cytokines in Luminex-based assays. Proliferation of cancer cells was measured in the CFSE assays. Their sensitivity to paclitaxel (PLX) was measured by Annexin V binding. Western Blot analysis was used to measure activation of the PI3K/Akt, IRAK 1, IRAK 4, and TRIF. Results: In ovarian cancer patients TLR4 and MyD88 expression by the tumor was observed in 100% and 83% of tissues, respectively. The expression of MyD88 was associated with shorter progression-free survival (42 vs 31 months, p < 0.05). Ex vivo studies showed that TLR4 was expressed on OVCAR3, SKOV3, and A2780 cell lines, while A2780 did not expressed MyD88. In MyD88+ tumor cells, LPS increased proliferation (PI 17 vs 8, p < 0.05), activated NF-kB pathway and promoted cytokine production (IL-8, IL-6, RANTES, VEGF and MCP-1). LPS and PLX binding to TLR4 on MyD88+ cells induced activation of PI3K/Akt, IRAK4, and IRAK1, but decreased expression of pro-apoptotic TRIF. In contrast, in MyD88(-) cells LPS did not induce proliferation and neither LPS nor PLX induced secretion of pro-inflammatory cytokines. Further, no changes were noted in IRAK1 expression, but strong signal was observed for TRIF. TLR4+/MyD88+ tumor cells showed grater resistance to PLX. Conclusions: Our ex vivo studies elucidate the molecular mechanisms involved in TLR4/MyD88 signaling. Ligation via TLR4 leads to tumor growth, release of proinflammatory cytokines and induction of resistance to PLX-induced apoptosis. No significant financial relationships to disclose.

Ceramide Glycanase Activities in Human Cancer Cells

1999 ◽  
Vol 19 (5) ◽  
pp. 449-460 ◽  
Author(s):  
Manju Basu ◽  
Patrick Kelly ◽  
Peter O'Donnell ◽  
Maria Miguel ◽  
Mathew Bradley ◽  
...  
Keyword(s):  
Double Bond ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Copper Ions ◽  
Human Cancer ◽  
Human Tumor ◽  
Supernatant Fraction ◽  
Enzyme Preparations ◽  
Human Cancer Cells ◽  
Ceramide Glycanase

Ceramide glycanase (CGase) activities have been detected in different human tumor cells (colon, carcinoma Colo-205; neuroblastoma, IMR-32; breast cancer lines, SKBr3 and MCF7). However, the level of enzymatic activity is lower in these cells compared to that present in other mammalian tissues reported before (Basu, M., Kelly, P., Girzadas, M. A., Li, Z., and Basu, S. Methods Enzymol. (in press)). The majority of CGase activity was found in the 100,000g soluble supernatant fraction isolated from all these cell lines and tissues. Using the soluble enzyme, the requirement for optimum CGase activity was found to be consistent with previous observations found for rat and rabbit tissues (Basu, M., Dastgheib, S., Girzadas, M. A., O'Donnell, P. H., Westervelt, C. W., Li, Z., Inokuchi, J. I., and Basu, S. (1998) Acta Pol. Biochim. 42:327). The CGase activities from both Colo-205 and IMR-32 cells are optimum at a protein to detergent ratio of one. All the mammalian CGases, including human cancer cells, show an optimum pH between 5.5 and 5.8 in sodium acetate buffer. The CGase activities from cancer cells are found to be cation-independent; however, mercury, zinc, and copper ions seem to inhibit the enzyme activity substantially in both tumor cells lines. The mercury ion inhibition of CGase activities from all different sources indicates a possible structural homology in the CGase proteins. Radiolabeled substrates, labeled at the sphingosine double bond or at the 3-position of sphingosine without modifying double bond of sphingosine were used in this investigation. Both were active substrates with all enzyme preparations isolated from different cancer cells (apparent Km, 500 μM for nLcOse5[3H-DT]Cer and 350 μM for GgOse4[sph-3-3H]Cer with Colo-205 enzyme). Structural analogues of ceramide and sphingosine (L-PPMP, L-PDMP, alkylamines, and Tamoxifen) inhibited cancer cell CGase activities in vitro.

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