Browsing by Author "Vasudeva, Kanika"
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Item Analysis of pro‐ and anti‐inflammatory cytokine gene variants and serum cytokine levels as prognostic markers in breast cancer(Wiley, 2018) Kaur, Raman Preet; Vasudeva, Kanika; Singla, Heena; Benipal, Raja Paramjeet Singh; Khetarpal, Preeti; Munshi, AnjanaThe aim of current study was to evaluate the genetic variation in all the genes encoding pro‐ and anti‐inflammatory cytokines in association with breast cancer development in patients from Malwa region of Punjab. The importance of the levels of interleukin (IL)‐17, tumor necrosis factor, interferon γ, IL‐10, IL‐6, IL‐4, and IL‐2 with respect to clinicopathological data, prognosis, and disease‐free survival was also determined in these patients. Two hundred and fifty female breast cancer patients and 250 age‐matched controls were screened for variations in cytokine‐encoding genes using global screening array microchip and PCR‐RFLP. The level of cytokines was estimated in 150 patients and 60 age‐matched controls using BD™ Cytometric Bead Array (CBA) Human Th1/Th2/Th17 cytokine kit by BD Accuri flow cytometer. The difference in cytokine levels was evaluated by Mann–Whitney test. No significant variation in the genes encoding various cytokines was found between patients and controls. Out of the seven cytokines evaluated, the levels of IL‐6 and IL‐17a were found to be significantly high in patients in comparison with controls ( p = 0.001 and 0.02, respectively). The elevated levels of these cytokines are also associated significantly with poor outcome. We did not find any specific variation in the genes encoding various cytokines between patients and controls. However, there was a significant difference in the serum levels of IL‐6 and IL‐17a between patients and controls, and the elevated levels of these two cytokines associated significantly with poor outcome in breast cancer patients and, therefore, can be used as prognostic markers.Item Genetic signatures in ischemic stroke: Focus on aspirin resistance(Bentham Science Publishers B.V., 2017) Vasudeva, Kanika; Chaurasia, Pratibha; Singh, Sulena; Munshi, AnjanaBackground and Objective: Stroke is one of the leading causes of death. There has been compelling evidence that stroke has a genetic component. Genetic variants not only influence susceptibility to stroke but have also been found to alter the response to pharmacological agents and influence the clinical outcome of the disease. Stroke patients are treated with antiplatelet drugs like aspirin and clopidogrel to prevent a secondary stroke. In spite of the fact that many new antiplatelet drugs have been developed, aspirin is still considered as a golden standard for the antiplatelet therapy. Aspirin achieves its action by inhibiting platelet cyclooxygenase (COX) system involved in the formation of thromboxane A2 (TXA2). TXA2 triggers reactions leading to platelet activation and aggregation. This Non-steroidal anti-inflammatory drug (NSAID) acts by inhibiting this mediator. Despite the demonstrated benefits of aspirin, many patients develop secondary stroke or other vascular events, an observation that has led to the concept of aspirin resistance. Studies have demonstrated that adequate antiplatelet effects are not achieved in 5-45% patients suggesting that many individuals are aspirin resistant. Aspirin resistance is multifactorial in origin. A genetic component has also been suggested, and variants in more than a dozen genes involved in absorption, distribution, metabolism, excretion (ADME) and pharmacodynamics of aspirin have been shown to be responsible for aspirin resistance. In addition, the patients on aspirin treatment also face adverse drug reactions on account of genetic variation. Conclusion: The present review has been compiled with an aim to revisit all the studies related to genetic variation contributing to aspirin resistance as well as adverse drug reactions. The output of high throughput genomic technology like genome wide association studies and others has also been discussed. ? 2017 Bentham Science Publishers.Item High-throughput sequencing technologies in metagenomics(Elsevier, 2022-09-30T00:00:00) Vasudeva, Kanika; Kaur, Prabhsimran; Munshi, AnjanaMicrobes are a distinct and dynamic group of organisms that require a diverse set of nutritional requirements and environmental conditions to thrive. To culture the desired microorganism a chemically defined media can be prepared based on the nutritional requirements of the specific species. However, all microbes cannot be cultured under similar laboratory conditions since specific microorganisms require unique growing conditions and therefore, the existence of the significant members (nearly 99.99%) of microbiota remains undiscovered. This cultivation constraint has limited our understanding of microbial diversity and restricted our appreciation for the microbial world and thereby suggests the need for a detailed metagenomic analysis. Metagenomics is the study of the genome sequences of a community of organisms sharing a common environment. In contrast, genomics involves the complete decoding of the genetic material of an organism by high-throughput sequencing. Metagenomics has the potential to highlight the community structure and functional potential of a microbial community in an unprejudiced manner. Any species can be subjected to metagenomic analysis bearing either DNA or RNA as the genetic material. Metagenomic techniques have been used to define a wide range of niches, from coastal environments to hazardous soils to vectors causing arthropod diseases as well as microbiome of humans. These methods are also being used to detect infections in the anthropological remains and uncover new pathogenic viruses and characterize the human microbiome in disease and health conditions as well as for forensic purposes. Metagenomic studies have been revolutionized since 2005 when the NGS technologies were developed. The introduction of next-generation sequencing (NGS) technologies in 2005 sparked the metagenomics revolution. A variety of novel sequencing technologies and platforms like Roche 454 sequencing, sanger sequencing, Illumina sequencing, and ion torrent Personal Genome Machine (PGM) have emerged in recent years, increasing the practicality of metagenomic research. The current chapter aims to explore the potential high throughput sequencing technologies for metagenomic analysis of species from diverse environmental backgrounds. In addition, the challenges faced and future perspectives will also be discussed. � 2023 Elsevier Inc. All rights reserved.Item Natural Compound-Based Nanoparticles to Target Free Radicals in Cancer(Springer Singapore, 2022-09-28T00:00:00) Yadav, Umesh Prasad; Rhuthuparna, M.; Vasudeva, Kanika; Suman, Prabhat; Munshi, Anjana; Kumar, Santosh; Singh, SandeepCell proliferation and malignant transformation are enabled by genetic and epigenetic changes. During the malignancy process, malignant cells acquire distinguishing characteristics. Cancer cells have acquired the ability to generate more reactive oxygen species (ROS), resulting in high oxidative stress. ROS-mediated signaling is needed for cancer cell physiology, and high levels of ROS cause oxidative stress-induced cytotoxicity in cancer cells. To avoid ROS-mediated cytotoxicity, cancer cells modulate their redox state through various antioxidant mechanisms and keep their ROS levels below the threshold. Cancer treatment that targets oxidative stress is an appealing option. Many natural oxidative stress modulators and bioactive compounds have been used in the treatment of cancer. Conventional uptake of bioactive molecule is associated with lower bioavailability, solubility, unlikely biodistribution, and side effects. Traditional drug uptake is improved by nanoformulation, making it easier to overcome side effects, improve biodistribution, and extend drug duration time. Natural prooxidant-loaded nanoparticles efficiently carry prooxidant to the tumor site and selectively and efficiently induce oxidative stress-mediated cell death in cancer cells. � Springer Nature Singapore Pte Ltd. 2022.Item Oncogenic metabolic reprogramming in breast cancer: focus on signaling pathways and mitochondrial genes(Springer, 2023-05-11T00:00:00) Malayil, Rhuthuparna; Chhichholiya, Yogita; Vasudeva, Kanika; Singh, Harsh Vikram; Singh, Tashvinder; Singh, Sandeep; Munshi, AnjanaOncogenic metabolic reprogramming impacts the abundance of key metabolites that regulate signaling and epigenetics. Metabolic vulnerability in the cancer cell is evident from the Warburg effect. The research on metabolism in the progression and survival of breast cancer (BC) is under focus. Oncogenic signal activation and loss of�tumor suppressor are important regulators of tumor cell metabolism. Several intrinsic and extrinsic factors contribute to metabolic reprogramming. The molecular mechanisms underpinning metabolic reprogramming in BC are extensive and only partially defined. Various signaling pathways involved in the metabolism play a significant role in the modulation of BC. Notably, PI3K/AKT/mTOR pathway, lactate-ERK/STAT3 signaling, loss of the tumor suppressor Ras, Myc, oxidative stress, activation of the cellular hypoxic response and acidosis contribute to different metabolic reprogramming phenotypes linked to enhanced glycolysis. The alterations in mitochondrial genes have also been elaborated upon along with their functional implications. The outcome of these active research areas might contribute to the development of novel therapeutic interventions and the remodeling of known�drugs. � 2023, This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.Item Role of lncRNAs in the Development of Ischemic Stroke and Their Therapeutic Potential(Springer, 2021-04-05T00:00:00) Vasudeva, Kanika; Dutta, Anyeasha; Munshi, AnjanaStroke is a major cause of premature mortality and disability around the world. Therefore, identification of cellular and molecular processes implicated in the pathogenesis and progression of ischemic stroke has become a priority. Long non-coding RNAs (lncRNAs) are emerging as significant players in the pathophysiology of cerebral ischemia. They are involved in different signalling pathways of cellular processes like cell apoptosis, autophagy, angiogenesis, inflammation, and cell death, impacting the progression of cerebral damage. Exploring the functions of these lncRNAs and their mechanism of action may help in the development of promising treatment strategies. In this review, the current knowledge of lncRNAs in ischemic stroke, focusing on the mechanism by which they cause cellular apoptosis, inflammation, and microglial activation, has been summarized. Very few lncRNAs have been functionally annotated. Therefore, the therapies based on lncRNAs still face many hurdles since the potential targets are likely to increase with the identification of new ones. Majority of experiments involving the identification and function of lncRNAs have been carried out in animal models, and the role of lncRNAs in human stroke presents a challenge. However, mitigating these issues through more rational experimental design might lead to the development of lncRNA-based stroke therapies to treat ischemic stroke. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item Role of p53 gene in breast cancer: Focus on mutation spectrum and therapeutic strategies(Bentham Science Publishers B.V., 2018) Kaur, Raman Preet; Vasudeva, Kanika; Kumar, Roshan; Munshi, AnjanaTP53 is a tumor suppressor gene which is commonly mutated in various cancers including breast cancer. Alterations in the gene lead to an altered expression of various genes that are directly or indirectly under the transcriptional control of p53. This results in malfunctioning of DNA damage repair pathways, cell-cycle arrest, chromatin remodeling and apoptosis. Different mutations in TP53 gene have been reported in different ethnic groups and exon 4 and intron 3 are reported to be frequently mutated in breast cancer patients especially triple-negative breast cancer. Increased global burden of TP53 mutated breast tumors has paved the path for various therapies targeting p53/TP53. Numerous molecules including nutilins, MI series, RO5693, PRIMA-1, RITA, etc. have been developed. Majority of these restore p53/TP53 function by targeting negative regulators of p53/TP53, wtp53/TP53 (wild-type) and mtp53/TP53 (mutant). Most of these molecules are in the preclinical phase except for two APR-246 and COTI-2 that have progressed to clinical trials. The current review has been compiled with an aim to give an overview of mutations in p53 across various ethnic groups, the effect of these alterations on TP53 function and the therapeutic strategies developed till date targeting p53/TP53 especially in breast cancer.Item Targeting Redox Homeostasis of Tumor Cells by Therapeutic Compounds in Cancer: An Indian Perspective(Springer Singapore, 2022-09-28T00:00:00) Vasudeva, Kanika; Chaturvedi, Pragya; Khan, Rahul; Sahu, Prachi; Munshi, AnjanaCancer is one of the significant causes of morbidity and mortality in the world. The role of oxidative stress in tumor progression and metastasis has been under focus since the last two decades, suggesting the importance of redox balance upon which cancer cells thrive to promote oncogenic phenotype. Therefore, it is highly warranted to develop therapies that can disrupt the fine-tuned intracellular reactive oxygen species (ROS) balance of tumor cells. Even though classical chemotherapy, radiotherapy, and many FDA-approved chemotherapeutic drugs modulate ROS levels, the associated side effects make it worthwhile to explore alternative options. Various compounds of natural origin have high efficacy and minimum side effects and pose a low risk of recurrence. This chapter has been compiled to give a thorough account of medicinal plants of Indian origin that have been implicated in ROS modulation and their potential applications in clinical settings. � Springer Nature Singapore Pte Ltd. 2022.