Nanotechnology-based cancer chemoprevention in glioblastoma.

Brain tumours are heterogeneous and are classified comprehensively into molecular subtypes based on genetic alterations. Glioblastoma rapid progression, drug resistance, and recurrence have been scientifically linked to several factors, including its rapid growth rate, loss of apoptosis, pro-survival signalling, molecular heterogeneities and hallmark features to infiltrate vital brain structures. Because of the growing demand for design and development of delivery systems to overcome the existing limitations with the current therapeutic strategies, researchers are exploiting multifaceted aspects of nanotechnology to improve delivery of the drug payload.

Molecular basis of acute coronary syndrome.

Cardiovascular diseases (CVD) comprise of various heart and blood vessels-related diseases. Acute coronary syndrome (ACS) is one of them. Basic researchers and cardiologists have witnessed landmark developments related to ACS and despite rapid refinement in our understanding; scientists are seeking answers for more questions.

Underlying causes of cerebral palsy: public health perspectives.

Cerebral palsy (CP) is a neurological pathology that is characterized by a combination of signs and symptoms that occur in neurodegenerative or metabolic disorder during the first few years of life. It is a complex pathology orchestrated by a plethora of different causes. The current diagnostic regimen for CP involves brain magnetic resonance imaging (MRI), and antenatal and perinatal insult.

Regulation of RUNX proteins by long non-coding RNAs and circular RNAs in different cancers.

RUNX proteins have been shown to behave as "double-edge sword" in wide variety of cancers. Discovery of non-coding RNAs has played linchpin role in improving our understanding about the post-transcriptional regulation of different cell signaling pathways. Several new mechanistic insights and distinct modes of cross-regulation of RUNX proteins and non-coding RNAs have been highlighted by recent research.

Regulation of TGFβ/SMAD signaling by long non-coding RNAs in different cancers: Dark Knight in the Castle of molecular oncology.

One of the complex themes in recent years has been the multi-layered regulation of TGFβ signaling in cancer cells. TGFβ/SMAD signaling pathway is a highly complicated web of proteins which work spatio-temporally to regulate multiple steps of carcinogenesis. TGFβ/SMAD has been shown to dualistically regulate cancer progression.

Vitamin C as an Anticancer Agent: Regulation of Signaling Pathways.

Treatment options for effective treatment of cancer with minimum off-target effects and maximum clinical outcomes have remained overarching goals in the clinical oncology. Vitamin C has remained in the shadows of controversy since the past few decades; burgeoning evidence has started to shed light on wide-ranging anticancer effects exerted by Vitamin C to induce apoptosis in drug-resistant cancer cells, inhibit uncontrolled proliferation of the cancer cells and metastatic spread. Landmark achievements in molecular oncology have ushered in a new era, and researchers have focused on the identification of oncogenic pathways regulated by Vitamin C in different cancers.

Realizing the Potential of Blueberry as Natural Inhibitor of Metastasis and Powerful Apoptosis Inducer: Tapping the Treasure Trove for Effective Regulation of Cell Signaling Pathways.

Blueberries belong to the genus Vaccinium of the family Ericaceae. Rapidly accumulating experimentally verified data is uncovering the tremendous pharmacological properties of biologically active constituents of blueberries against different diseases. Our rapidly evolving knowledge about the multifaceted nature of cancer has opened new horizons to search for different strategies to target multiple effectors of oncogenic networks to effectively inhibit cancer onset and progression.

Focusing on the brighter side of Sevoflurane: Realizing true potential of an anesthetic agent as a regulator of cell signaling pathways and microRNAs in different cancers.

Reconceptualization of different anesthetics as anticancer agents has opened new horizons for a better and sharper analysis of true potential of Sevoflurane as a promising and frontline candidate in the pipeline of anticancer agents. Sevoflurane mediated regulation of cell signaling pathways and non-coding RNAs has leveraged our understanding to another level. There have been remarkable advancements in unraveling mechanistic insights related to the ability of sevoflurane to modulate microRNAs in different cancers.

Recent updates on true potential of an anesthetic agent as a regulator of cell signaling pathways and non-coding RNAs in different cancers: Focusing on the brighter side of propofol.

There has always been a quest to search for synthetic and natural compounds having premium pharmacological properties and minimum off-target and/or side effects. Therefore, in accordance with this approach, scientists have given special attention to the molecules having remarkable ability to target oncogenic protein network, restore drug sensitivity and induce apoptosis in cancer cells. The mechanisms through which general anesthetics modulated wide-ranging deregulated cell signaling pathways and non-coding RNAs remained unclear.

Regulation of signaling pathways by Ampelopsin (Dihydromyricetin) in different cancers: exploring the highways and byways less travelled.

Ampelopsin or Dihydromyricetin is gradually emerging as a high-quality natural product because of its ability to modulate wide-ranging signaling pathways. Ampelopsin (Dihydromyricetin) has been reported to effectively modulate growth factor receptor (VEGFR2 and PDGFRβ) mediated signaling,  TRAIL/TRAIL-R pathway, JAK/STAT and mTOR-driven signaling in different cancers. Ampelopsin (Dihydromyricetin) has also been shown to exert inhibitory effects on the versatile regulators which trigger EMT (Epithelial-to-Mesenchymal Transition).

[The effect of thyroid hormones and 5-azacytidine on the gene transcription of malic enzyme and 6-phosphogluconate dehydrogenase].

The effect of thyroid hormones and the methylation inhibitor 5-azacytidine on the level of expression of thyroid hormone-responsive genes (malic enzyme and 6-phosphogluconate dehydrogenase genes) has been studied. DNA-RNA hybridization has shown there is an inverse correlation between the level of DNA methylation and gene expression of malic enzyme and 6-phosphogluconate dehydrogenase. Thus it suggests that the regulation of thyroid hormone gene expression can take place via DNA methylation blocking and that DNA demethylation is part of structural changes essential to the binding of thyroid hormones with DNA elements recognized by thyroid hormone receptors and to further induction of synthesis of specific mRNA.

[Human thyroid gland DNA methylase in nodular and diffuse goiter].

The heterogeneity and some properties of DNA-methylases isolated from nonmalignant human thyroid formations--nodular and diffuse goiters--have been studied. Isoelectrofocusing of methylase preparations produced 6-7 distinct activity peaks distinguished by pI, activity towards Ca2+ and Mg2+, sensitivity towards dithiothreitol and capacity to methylase cytosine into mono-, di- and tripyrimidine blocks in vitro. The degree of DNA methylation in vivo depended on the origin of of the goiter.

[Liver nuclear phospholipids of rats with varying thyroid status].

Thin-layer chromatography was used for fractionation of rat liver nuclear phospholipids after in vivo administration of 14C-sodium acetate. The administration of T3 to thyroidectomized rats caused a sharp increase in the incorporation of the label in all phospholipids of the nuclear fraction. The action of sphingomyelin and sphingomyelase on RNA-polymerase of nuclei isolated from the liver of thyroidectomized rats was tested.

[Multiple forms of DNA methylases in hepatic cell nuclei of animals in the normal state and in pathology].

Using hydrophobic chromatography multiple nature of DNA-methylating enzymes have been revealed. It was established that the most active enzymatic fraction of rats' liver and that of chicken are completely identical.

[The effect of thyroid hormones on DNA methylation in rat liver in vivo and in vitro].

Methylation of rat liver DNA was studied in vivo and in vitro in presence of various content of thyroid hormones. Both administration of triiodothyronine into intact rats and thyroidectomy led to considerable alterations in activity of endogenous DNA-methylases and in content of m5C in DNA although distinct correlation between these two factors was not detected. Alterations in the acceptor activity of endogenous DNA towards bacterial DNA-methylases of thy Mbu type demonstrated the processes occurring in vivo.

[Interaction of hormone-receptor complexes of triiodothyronine with DNA and RNA].

Some parameters of triiodothyronine hormone-receptor complexes (HRC) interactions with DNA-cellulose were studied. The competition between DNA and polyribonucleotides for HRC was demonstrated. It was found that in a model system of RNA transport HRC stimulate the 3H-RNA liberation from the nuclei.

[Use of bacterial DNA-methylases for structuro-functional analysis of the eukaryotic genome].

Bacterial DNA-methylases with known recognition sites (RS) were used as probes for structural-and-functional analysis of eukaryotic genome. Adenine and cytosine DNA-methylases recognizing 4 to 6-member unique and degenerative nucleotide sequences having a symmetrical and asymmetrical structure were used for probing. The use of a set of methylases enabled the selection of a probe that was the most sensitive for the given pathology.

[Stimulation with triiodothyronine of the synthesis of DNA, total proteins, nuclear proteins and nuclear matrix proteins in cultured cells of hepatoma Morris 7777].

Intensity of DNA and protein biosynthesis was decreased in Morris hepatoma 7777 cultivated cells in absence of thyroid hormones. Physiological concentrations of triiodothyronine increased synthesis of DNA and total proteins after lag phase within 12-48 hrs, while synthesis of nuclear and nuclear matrix proteins was stimulated already within 2 hrs. This suggests that stimulation of nuclear proteins biosynthesis occurred prior to the hormone effect on proliferation and cell metabolism.

[The effect of thyroid hormones on structural-functional relations in rat liver chromatin].

The effects of thyroid hormones on chromatin structure at different levels of its functional activity were investigated. No differences in the sensitivity of hepatocyte nuclei to DNAase I were found, presumably due to the restriction of acceptor sites for thyroid hormones on DNA.

[Cytoplasmic thyroxine-binding protein: the role of RNA in the interactions between thyroxine receptor and cell nuclei].

The presence of 3H-orotic acid in the cytoplasmic receptor fraction isolated in our laboratory, the sensitivity of this fraction to treatment with RNAases accompanied by a shift of the absorption peak of the receptor preparation towards the long-wave region as well as the use of the absorption filter technique point to the existence of ternary thyroxine-thyroxine-binding protein-RNA complex in the cytoplasm. It was found that the cytoplasmic hormone-receptor complex of thyroxine is a genetically active form which can interact with the nuclei and modify the activity of chromatin. The role of RNA in these interactions is discussed.

[Interaction of hormone-receptor complexes from normal and tumorous tissues with DNA and their effect on the RNA polymerase activity of isolated nuclei].

A study was made of the interaction of the thyroxine hormone-receptor complexes (HRC) from hepatocytes and sarcoma M1 cells with DNA and the involvement of these complexes in the regulation of the RNA-polymerase activity of isolated hepatic cell nuclei. Unlike sarcoma HRC, rat liver HRC showed a weak interaction with DNA. Against a background of considerable stimulation of the incorporation of precursors in RNA under the influence of rat liver HRC (2.