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Topic Review
Cancer-Derived Exosomes in Carcinogenesis
The exosome-mediated crosstalk between cancer and non-cancer cells within the tumor microenvironment (TME) contributes to the acquisition of all hallmarks of cancer and leads to the formation of cancer stem cells (CSCs), which exhibit resistance to a range of anticancer drugs. 
  • 655
  • 22 Nov 2021
Topic Review
SALL Proteins in Cancer
SALL proteins are a family of four conserved C2H2 zinc finger transcription factors that play critical roles in organogenesis during embryonic development. They regulate cell proliferation, survival, migration, and stemness; consequently, they are involved in various human genetic disorders and cancer. SALL4 is a well-recognized oncogene; however, SALL1–3 play dual roles depending on the cancer context and stage of the disease.
  • 655
  • 11 Jan 2022
Topic Review
Tumor Microenvironment and Metabolism
There is a growing appreciation that the cells of the tumor microenvironment interact via variations in their dynamic regulation of mitochondrial function. The melatonergic pathway is a core aspect of mitochondrial function, with tumors 'domineering' the homeostasis established in the tumor microenvironment by regulating the core functioning of other cells. This is predominantly achieved by regulating the levels of melatonin and its immediate precursor, N-acetylserotonin (NAS). Applying melatonin to any tumor drives tumor death via apoptosis, whilst NAS can activate the trophic receptor, TrkB, to increase the survival and proliferation of tumors. Given such contrasting effects of melatonin and NAS, it is crucial for tumors to regulate the NAS/melatonin ratio within the tumor microenvironment. Two immune cells can readily kill cancer cells, namely natural killer (NK) cells and CD8+ t cells. The tumor inactivates these cells by releasing kynurenine, which activates the aryl hydrocarbon receptor (AhR) on these immune cells, leading to their inactivation ('exhaustion'), with AhR activation also increasing the NAS/melatonin ratio. NAS release enhances the survival and proliferation of cancer stem-like cells, thereby driving tumor maintenance and spread (metastasis). The cells that can readily kill cancer cells are therefore turned into providers of support for tumor survival and spread. This is achieved via the tumor's regulation of the mitochondrial melatonergic pathway. Similar tumor interactions with the mitochondrial melatonergic pathway allows the tumor to regulate other cells in the tumor microenvironment, as well as influencing how these cells interact with each other. This is predominantly achieved by the altered metabolism and mitochondrial function in the tumor shaping the mitochondrial function of other cells in the tumor microenvironment. As mitochondria evolved over evolution from ancient bacteria, these interactions across cell types in the tumor microenvironment may be viewed as evolutionary modified bacteria dynamically interacting with each other within a quest to achieve 'dominance' via the regulation of mitochondrial melatonergic pathway. This is a novel conceptualization of the tumor microenvironment that emphasizes core metabolic processes, and their regulation by the melatonergic pathway. As a frame of reference this allows the incorporation of previously disparate pieces of data on the tumor microenvironment and also provides a clearer pathway to new research, coupled to treatment implications. 
  • 655
  • 05 Jan 2023
Topic Review
Neoadjuvant Chemotherapy of Breast Cancer
Breast cancer has an extremely high incidence in women, and its morbidity and mortality rank first among female tumors. With the increasing development of medicine today, the clinical application of neoadjuvant chemotherapy has brought new hope to the treatment of breast cancer. Based on the relevant research on the existing drug resistance mechanism, the current treatment plan for reversing the resistance of breast cancer to neoadjuvant chemotherapy is explored, and the potential drug targets are analyzed, aiming to provide a new idea and strategy to reverse the resistance of neoadjuvant chemotherapy drugs in breast cancer.
  • 654
  • 18 Sep 2021
Biography
Dr. Kalirajan Rajagopal
R. Kalirajan has 23 years of teaching and research experience. Currently he is working as an Associate professor at JSS College of Pharmacy, Ooty under JSS Academy of Higher Education & Research (Deemed to be University), Mysuru since July, 2006. Before joining this institution, he worked as an professor at Arulmigu Kalasalingam College of Pharmacy, Srivilliputtur, Tamilnadu from June, 2003
  • 654
  • 17 Jan 2023
Topic Review
Human Glioblastoma Multiforme Cells
Glioblastoma multiforme is one of the most deadly neurooncological diseases due to its prominent drug resistance and pronounced potential to reccurence. Both surgical interventions and tumor invasion within brain tissue causes local mechanical disruption of healthy tissues and may be related to enhancement of epidermal growth factor (EGF) secretion by numerous non-neuronal cells (e.g glioma associated microglia and macrophages; GAMs). Thus, in our research we examined the effect of EGF on human glioblastoma T98G cells, especially in the field of the ROS-dependent mechanisms which regulate cytoskeleton architecture rearrangements and their implications for invasive potential enhancement. IMC and DIC contrast microscopy coupled with time-lapse module were applied for visualization of cellular morphology changes and motile activity modulation. Transwell® assay was applied for estimation of cellular transmigration potential. Cell cycle activity was examined with ImageStreamX image flow cytometry (PI/RNAse staining). Moreover, detailed immunocytochemical analysis of cytoskeleton architecture changes (F-actin and vinculin distribution) and determination of ROS production (CellROX probe) were performed with epi-fluorescence and TIRF microscopy coupled with 2D deconvolution. Additional measurements of chosen proteins levels were confirmed with Western blot technique. Finally, estimation of the changes in cellular bioenergetic  status (ATP and lactate levels) which is crucial for effective invasion, was conducted with bioluminescence and spectrophotometric methods. Exposition of GBM cells to EGF resulted in considerable enhancement of cells proliferation accompanied by cell cycle acceleration. Such effect was followed by remarkable augmentation of cellular motility and transmigration potential correlated with noticeable F-actin filaments rearrangements with simultaneous re-distribution of vinculin towards leading edges. Moreover, increase in cellular ROS production and changes in ATP/lactate production were noticeable, pointing the undoubted role of cellular bioenergetic homeostasis modulation in response to EGF. It is worth emphasizing, that erlotinib (EGFR inhibitor) admittedly inhibited cellular invasive potential and cytoskeleton rearrangements during incubation both with or without EGF. Additionally, in our hands, application of antioxidant N-acetyl-L-cysteine prominently endured the EGF-induced up-regulation of cellular motility. Our research indicates strong pro-mitotic and pro-migratory effect of EGF on human GBM cells. Such effect is accompanied by considerable cytoskeleton rearrangements induction and bioenergetic homeostasis modulation. Collectively, we suppose that collaborative EGFR/ROS signaling is one of the key players within EGF-induced invasiveness of GBM cells.
  • 653
  • 27 Oct 2020
Topic Review
Endometrial Cancer Racial Disparity
In contrast to the decline in incidence and mortality of most other cancers, these rates are rising for endometrial cancer. Black women with endometrial cancer have an earlier diagnosis, more aggressive histology, advanced stage, and worse outcomes compared with their White counterparts. Socioeconomic status, a higher incidence of aggressive histology, and comorbid conditions are known factors leading to racial disparity in patients with endometrial cancer; nevertheless, they do not account for the entire racial disparity, which emphasizes the roles of molecular, histopathological and genetic factors. 
  • 652
  • 22 Sep 2021
Topic Review
Lysophosphatidic Acid and Cancer
Lysophosphatidic acid (LPA) is a bioactive lipid mediator primarily derived from membrane phospholipids. LPA initiates cellular effects upon binding to a family of G protein-coupled receptors, termed LPA receptors (LPAR1 to LPAR6). LPA signaling drives cell migration and proliferation, cytokine production, thrombosis, fibrosis, angiogenesis, and lymphangiogenesis.
  • 652
  • 14 Jul 2021
Topic Review
Connexins and Integrins in Exosomes
Connexins and integrins, the two structurally and functionally distinct families of transmembrane proteins, have been shown to be inter-connected by various modes of cross-talk in cells, such as direct physical coupling via lateral contact, indirect physical coupling via actin and actin-binding proteins, and functional coupling via signaling cascades.
  • 652
  • 11 Oct 2021
Topic Review
Promising Biomarkers of RILI
Radiation-induced lung injury (RILI) is one of the main dose-limiting side effects in patients with thoracic cancer during radiotherapy. No reliable predictors or accurate risk models are currently available in clinical practice. Severe radiation pneumonitis (RP) or pulmonary fibrosis (PF) will reduce the quality of life, even when the anti-tumor treatment is effective for patients. Since the clinical symptoms or imaging changes identifying toxicity do not appear in the early stage, ideal biomarkers are crucial for early diagnosis and intervention in order to prevent lung complications.
  • 652
  • 26 Sep 2021
Topic Review
Obesity and Cancer
The obesity is associated with many adverse health effects, including worse cancer outcomes. It has been established that obesity (BMI > 30 kg/m2) is a major risk factor for many types of cancer.
  • 652
  • 13 Apr 2022
Topic Review
Hypoxia
Hypoxia is a condition commonly observed in the core of solid tumors. The hypoxia-inducible factors (HIF) act as hypoxia sensors that orchestrate a coordinated response increasing the pro-survival and pro-invasive phenotype of cancer cells, and determine a broad metabolic rewiring. These events favor tumor progression and chemoresistance. The increase in glucose and amino acid uptake, glycolytic flux, and lactate production; the alterations in glutamine metabolism, tricarboxylic acid cycle, and oxidative phosphorylation; the high levels of mitochondrial reactive oxygen species; the modulation of both fatty acid synthesis and oxidation are hallmarks of the metabolic rewiring induced by hypoxia.
  • 651
  • 18 Dec 2020
Topic Review
Inflammatory Response in Cancer Cachexia
Cancer cachexia (CC) is a multifactorial clinical complication in numerous human malignancies. Its incidence in Europe is highest in patients with lung (83/36% inpatients/outpatients, respectively) and gastrointestinal cancers (62/42%). There are currently no therapeutic agents used for treatment of this paraneoplastic syndrome, caused by impaired/reduced nutritional intake, or metabolic disorders with increased catabolism and chronic inflammation. In the mechanisms of CC pathogenesis, in addition to inflammation, the role of insulin resistance, damage to mitochondrial function, oxidative stress, as well as the activation of lipolysis and proteolysis through the ubiquitin-proteasome system and macro-autophagy are emphasized. The main target in CC is skeletal and cardiac muscle, as well as the adipose tissue (AT).  The most important role in CRC-associated cachexia is played by pro-inflammatory cytokines, including the tumor necrosis factor α (TNFα), originally known as cachectin, Interleukin (IL)-1, IL-6, and certain chemokines (e.g., IL-8). Heterogeneous CRC cells themselves also produce numerous cytokines (including chemokines), as well as novel factors called “cachexokines”. The tumor microenvironment (TME) contributes to systemic inflammation and increased oxidative stress and fibrosis. 
  • 651
  • 20 Apr 2021
Topic Review
Diffuse Intrinsic Pontine Gliomas
Diffuse intrinsic pontine gliomas are malignant brain tumors which arise from the pons in children. These tumors are incurable and nearly all the patients die within a year after diagnosis. 
  • 651
  • 19 Apr 2021
Topic Review
CML-HMGB1 in Gastric Cancer
Advanced glycation end products (AGEs) are produced in response to a high-glucose environment and oxidative stress and exacerbate various diseases. Nε-(Carboxymethyl)lysine (CML) is an AGE that is produced by the glycation of lysine residues of proteins. 
  • 651
  • 12 Oct 2021
Topic Review
Survival in Metastatic Prostate Cancer
The real-world survival trends are largely unexplored in patients with de novo metastatic prostate cancer. A recent population-based analysis provided data about the survival improvements in patients with de novo metastatic prostate cancer diagnosed in USA between 2000 and 2014. Despite the advent of several new drugs, limited improvements in overall and cancer-specific survival were observed in 2011-2014 compared to 2000-2003 and 2004-2010.
  • 650
  • 27 Oct 2020
Topic Review
Malignant Transformation of Postmenopausal Endometriosis
Endometriosis is a disease that affects 6–10% of women of reproductive age. Although it is a benign condition, endometriotic lesions have around a 1% risk of malignant transformation. Since endometriosis is an estrogen-dependent disease, it can be expected to resolve or disappear in menopause. However, the prevalence of menopausal endometriosis is 2–4%. In these cases, the risk of malignant transformation is a rare but possible event. 
  • 650
  • 16 Aug 2021
Topic Review
PARP Inhibitors in Cancer Immunotherapy
Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi) induce cytotoxic effects as single agents in tumors characterized by defective repair of DNA double-strand breaks deriving from BRCA1/2 mutations or other abnormalities in genes associated with homologous recombination. Preclinical studies have shown that PARPi-induced DNA damage may affect the tumor immune microenvironment and immune-mediated anti-tumor response through several mechanisms. In particular, increased DNA damage has been shown to induce the activation of type I interferon pathway and up-regulation of PD-L1 expression in cancer cells, which can both enhance sensitivity to Immune Checkpoint Inhibitors (ICIs).
  • 650
  • 30 Nov 2022
Topic Review
The Adaptor Protein p66Shc
p66Shc is an adaptor protein with anti-mitogenic, anti-chemotactic, pro-apoptotic and pro-oxidant activities.  Neoplastic B cells from chronic lymphocytic leukemia (CLL) patients  have a profound deficiency in the expression of p66Shc which results in leukemic cell resistance to apoptosis and in an altered balance between homing and egress receptors that control B cell homing to and residency into the pro-survival lymphoid niche. Ablation of the gene encoding p66Shc in the Eμ-TCL1 mouse model of human CLL worsens disease presentation  by promoting leukemic cell invasiveness, providing in vivo evidence of the pathogenic role of the p66Shc defect in CLL pathogenesis. Here we briefly summarize the functions of p66Shc in lymphocytes, focalizing on the mechanisms exploited by p66Shc to control B cell trafficking and the abnormalities in this process caused by p66Shc deficiency in CLL. 
  • 648
  • 12 Nov 2020
Topic Review
RAAS in HF and Cancer
Heart failure (HF) and cancer are the main public health issues in industrialized countries and are increasing in prevalence, especially, in the ageing population. These two diseases were thought to be independent; however, new research has revealed that cancer and HF frequently coexist in the same patient. Furthermore, as cancer-specific mortality decreases and the surviving population gets older, the overlap between cardiac disease and cancer patients is growing. As a result, the discipline of cardio-oncology has primarily focused on the adverse effects of anti-cancer therapy. HF is one of the most serious consequences of cardiotoxic cancer therapy.
  • 648
  • 16 Aug 2021
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