scholarly journals Cancer Treatment Based on the Selective Accumulation of a Photosensitiser and Laser Light Irradiation: A Review

2021 ◽  
Vol 46 (3) ◽  
pp. 150-153
Author(s):  
Zahra Al Timimi
Keyword(s):  
Cancer Treatment ◽  
Cancer Cells ◽  
Laser Light ◽  
Active Form ◽  
Acquired Resistance ◽  
Resistance Mechanisms ◽  
Treatment Quality ◽  
Laser Source ◽  
Normal Tissues ◽  
Selective Accumulation

Background: Cancer Photodynamic Therapy (CPDT) is a promising future treatment quality based on the selective accumulation of a photosensitiser in the malignant tissues and the dependent irradiation with laser light. Objective: The aim of this work was to estimate an optimum effect involves the performance of a photosensitizing agent served by irradiation at a wavelength corresponding to an absorbance band of the sensitizer. In the appearance of oxygen, a series of effects lead to direct tumour cell death and damage to the microvasculature and initiation of a local inflammatory reaction. Methods: Photosensitiser is a material that sensitizes an organism, cell, or tissue to the light. It is a deeprooted part of CPDT, which absorbed by cancerous cells and exposed to laser light, gets activated, damaging and killing cancer cells. The direct targeting of laser source on hyper proliferative tissue and its preferential origin absorption at the targeted site gives rise CPDT double selectivity with least damage to adjacent normal tissues. Results: Photosensitiser absorbs the light and then produces an active form of oxygen, which destroys nearby cancer cells. The photosensitiser is able to spoil the blood vessels in the tumour, that way preventing cancer from receiving any necessary nutrients. The light which needed to activate most of the photosensitisers cannot pass through more than about one-third of an inch of tissue, because of that reason, the CPDT is usually used to treat cancer on or just under the skin or on the lining of internal organs. In addition, CPDT may activate the immune system to attack the tumour cells, directly killing cancer cells. Conclusion: This review focuses on the aspects of CPDT as an advanced and original site directed therapy for cancer treatment and the other non-oncogenic diseases. Minimal average of tissue toxicity controlled a long-term morbidity, deficiency of intrinsic or acquired resistance mechanisms. Bangladesh Med Res Counc Bull 2020; 46(3): 150-153

Resveratrol as an Adjuvant for Normal Tissues Protection and Tumor Sensitization

2020 ◽  
Vol 20 (2) ◽  
pp. 130-145 ◽  
Author(s):  
Keywan Mortezaee ◽  
Masoud Najafi ◽  
Bagher Farhood ◽  
Amirhossein Ahmadi ◽  
Dheyauldeen Shabeeb ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Cancer Treatment ◽  
Cancer Cells ◽  
Clinical Studies ◽  
Normal Tissue ◽  
Medical Science ◽  
Treatment Modalities ◽  
Radiation Toxicity ◽  
Normal Tissues ◽  
Normal Tissue Toxicity

Cancer is one of the most complicated diseases in present-day medical science. Yearly, several studies suggest various strategies for preventing carcinogenesis. Furthermore, experiments for the treatment of cancer with low side effects are ongoing. Chemotherapy, targeted therapy, radiotherapy and immunotherapy are the most common non-invasive strategies for cancer treatment. One of the most challenging issues encountered with these modalities is low effectiveness, as well as normal tissue toxicity for chemo-radiation therapy. The use of some agents as adjuvants has been suggested to improve tumor responses and also alleviate normal tissue toxicity. Resveratrol, a natural flavonoid, has attracted a lot of attention for the management of both tumor and normal tissue responses to various modalities of cancer therapy. As an antioxidant and anti-inflammatory agent, in vitro and in vivo studies show that it is able to mitigate chemo-radiation toxicity in normal tissues. However, clinical studies to confirm the usage of resveratrol as a chemo-radioprotector are lacking. In addition, it can sensitize various types of cancer cells to both chemotherapy drugs and radiation. In recent years, some clinical studies suggested that resveratrol may have an effect on inducing cancer cell killing. Yet, clinical translation of resveratrol has not yielded desirable results for the combination of resveratrol with radiotherapy, targeted therapy or immunotherapy. In this paper, we review the potential role of resveratrol for preserving normal tissues and sensitization of cancer cells in combination with different cancer treatment modalities.

scholarly journals Circulating Tumour DNA Sequencing Identifies a Genetic Resistance-Gap in Colorectal Cancers with Acquired Resistance to EGFR-Antibodies and Chemotherapy

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3736
Author(s):  
Franciele H. Knebel ◽  
Louise J. Barber ◽  
Alice Newey ◽  
Dimitrios Kleftogiannis ◽  
Andrew Woolston ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Large Fraction ◽  
Single Agent ◽  
Acquired Resistance ◽  
Genetic Resistance ◽  
Resistance Mutation ◽  
Resistance Mechanisms ◽  
Wild Type ◽  
Primary Resistance ◽  
Clinical Resistance

Epidermal growth factor receptor antibodies (EGFR-Abs) confer a survival benefit in patients with RAS wild-type metastatic colorectal cancer (mCRC), but resistance invariably occurs. Previous data showed that only a minority of cancer cells harboured known genetic resistance drivers when clinical resistance to single-agent EGFR-Abs had evolved, supporting the activity of non-genetic resistance mechanisms. Here, we used error-corrected ctDNA-sequencing (ctDNA-Seq) of 40 cancer genes to identify drivers of resistance and whether a genetic resistance-gap (a lack of detectable genetic resistance mechanisms in a large fraction of the cancer cell population) also occurs in RAS wild-type mCRCs treated with a combination of EGFR-Abs and chemotherapy. We detected one MAP2K1/MEK1 mutation and one ERBB2 amplification in 2/3 patients with primary resistance and KRAS, NRAS, MAP2K1/MEK1 mutations and ERBB2 aberrations in 6/7 patients with acquired resistance. In vitro testing identified MAP2K1/MEK1 P124S as a novel driver of EGFR-Ab resistance. Mutation subclonality analyses confirmed a genetic resistance-gap in mCRCs treated with EGFR-Abs and chemotherapy, with only 13.42% of cancer cells harboring identifiable resistance drivers. Our results support the utility of ctDNA-Seq to guide treatment allocation for patients with resistance and the importance of investigating further non-canonical EGFR-Ab resistance mechanisms, such as microenvironmentally-mediated resistance. The detection of MAP2K1 mutations could inform trials of MEK-inhibitors in these tumours.

Acquired resistance mechanisms to INC280, a MET inhibitor in MET-amplified lung cancer cells

2016 ◽  
Vol 69 ◽  
pp. S135-S136 ◽  
Author(s):  
S. Kim ◽  
T.M. Kim ◽  
D.W. Kim ◽  
S. Kim ◽  
M. Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Acquired Resistance ◽  
Resistance Mechanisms ◽  
Lung Cancer Cells ◽  
Met Inhibitor

Abstract 1832: Acquired resistance mechanisms to afatinib in lung cancer cells harboringHER2alterations

2018 ◽  
Author(s):  
Hidejiro Torigoe ◽  
Kazuhiko Shien ◽  
Tatsuaki Takeda ◽  
Takahiro Yoshioka ◽  
Kei Namba ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Acquired Resistance ◽  
Resistance Mechanisms ◽  
Lung Cancer Cells

scholarly journals Forcing dividing cancer cells to die; low‐dose drug combinations to prevent spindle pole clustering

APOPTOSIS ◽  
2021 ◽  
Author(s):  
Eloise Ducrey ◽  
Cédric Castrogiovanni ◽  
Patrick Meraldi ◽  
Patrycja Nowak-Sliwinska
Keyword(s):  
Cancer Cells ◽  
Single Molecule ◽  
Mitotic Spindle ◽  
Acquired Resistance ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Spindle Pole ◽  
Cancer Treatments ◽  
Mitotic Kinases ◽  
Microtubule Targeting Agents

AbstractMitosis, under the control of the microtubule-based mitotic spindle, is an attractive target for anti-cancer treatments, as cancer cells undergo frequent and uncontrolled cell divisions. Microtubule targeting agents that disrupt mitosis or single molecule inhibitors of mitotic kinases or microtubule motors kill cancer cells with a high efficacy. These treatments have, nevertheless, severe disadvantages: they also target frequently dividing healthy tissues, such as the haematopoietic system, and they often lose their efficacy due to primary or acquired resistance mechanisms. An alternative target that has emerged in dividing cancer cells is their ability to “cluster” the poles of the mitotic spindle into a bipolar configuration. This mechanism is necessary for the specific survival of cancer cells that tend to form multipolar spindles due to the frequent presence of abnormal centrosome numbers or other spindle defects. Here we discuss the recent development of combinatorial treatments targeting spindle pole clustering that specifically target cancer cells bearing aberrant centrosome numbers and that have the potential to avoid resistance mechanism due their combinatorial nature.

Research Progress in Flavonoids as Potential Anticancer Drug Including Synergy with Other Approaches

2020 ◽  
Vol 20 (20) ◽  
pp. 1791-1809 ◽  
Author(s):  
Yusuf Hussain ◽  
Suaib Luqman ◽  
Abha Meena
Keyword(s):  
Multidrug Resistance ◽  
Cancer Treatment ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cell Signalling ◽  
Resistance Mechanisms ◽  
Research Progress ◽  
Potential Candidate ◽  
Proliferating Cells ◽  
Oncology Research

Background: In chemotherapy for cancer, conventional drugs aim to target the rapidly growing and dividing cells at the early stages. However, at an advanced stage, cancer cells become less susceptible because of the multidrug resistance and the recruitment of alternative salvage pathways for their survival. Besides, owing to target non-selectivity, healthy proliferating cells also become vulnerable to the damage. The combination therapies offered using flavonoids to cure cancer not only exert an additive effect against cancer cells by targetting supplementary cell carnage pathways but also hampers the drug resistance mechanisms. Thus, the review aims to discuss the potential and pharmacokinetic limitations of flavonoids in cancer treatment. Further successful synergistic studies reported using flavonoids to treat cancer has been described along with potential drug delivery systems. Methods: A literature search was done by exploring various online databases like Pubmed, Scopus, and Google Scholar with the specific keywords like “Anticancer drugs”, “flavonoids”, “oncology research”, and “pharmacokinetics”. Results: Dietary phytochemicals, mainly flavonoids, hinder cell signalling responsible for multidrug resistance and cancer progression, primarily targeting cancer cells sparing normal cells. Such properties establish flavonoids as a potential candidate for synergistic therapy. However, due to low absorption and high metabolism rates, the bioavailability of flavonoids becomes a challenge. Such challenges may be overcome using novel approaches like derivatization, and single or co-delivery nano-complexes of flavonoids with conventional drugs. These new approaches may improve the pharmacokinetic and pharmacodynamic of flavonoids. Conclusion: This review highlights the application of flavonoids as a potential anticancer phytochemical class in combination with known anti-cancer drugs/nanoparticles. It also discusses flavonoid’s pharmacokinetics and pharmacodynamics issues and ways to overcome such issues. Moreover, it covers successful methodologies employed to establish flavonoids as a safe and effective phytochemical class for cancer treatment.

scholarly journals Acquired resistance mechanisms to afatinib in HER 2 ‐amplified gastric cancer cells

2019 ◽  
Vol 110 (8) ◽  
pp. 2549-2557 ◽  
Author(s):  
Takahiro Yoshioka ◽  
Kazuhiko Shien ◽  
Tatsuaki Takeda ◽  
Yuta Takahashi ◽  
Eisuke Kurihara ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Acquired Resistance ◽  
Resistance Mechanisms ◽  
Gastric Cancer Cells ◽  
Her 2

Cancer Treatment with Liposomes Based Drugs and Genes Co-delivery Systems

2018 ◽  
Vol 25 (28) ◽  
pp. 3319-3332 ◽  
Author(s):  
Chuanmin Zhang ◽  
Shubiao Zhang ◽  
Defu Zhi ◽  
Jingnan Cui
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Synergistic Effects ◽  
Resistance Mechanisms ◽  
Delivery Systems ◽  
Cell Cycle Checkpoints ◽  
Drug Efflux ◽  
Cancer Resistance ◽  
Cancer Models ◽  
Anti Cancer

There are several mechanisms by which cancer cells develop resistance to treatments, including increasing anti-apoptosis, increasing drug efflux, inducing angiogenesis, enhancing DNA repair and altering cell cycle checkpoints. The drugs are hard to reach curative effects due to these resistance mechanisms. It has been suggested that liposomes based co-delivery systems, which can deliver drugs and genes to the same tumor cells and exhibit synergistic anti-cancer effects, could be used to overcome the resistance of cancer cells. As the co-delivery systems could simultaneously block two or more pathways, this might promote the death of cancer cells by sensitizing cells to death stimuli. This article provides a brief review on the liposomes based co-delivery systems to overcome cancer resistance by the synergistic effects of drugs and genes. Particularly, the synergistic effects of combinatorial anticancer drugs and genes in various cancer models employing multifunctional liposomes based co-delivery systems have been discussed. This review also gives new insights into the challenges of liposomes based co-delivery systems in the field of cancer therapy, by which we hope to provide some suggestions on the development of liposomes based co-delivery systems.

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