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    • In this precancerous condition though cancer develops

    2022-08-09

    In this precancerous condition, though cancer develops from the epithelium, the subepithelial connective tissue also play crucial biological role in pathogenesis and progression to malignancy. In this context it may be noted that some recent reports addressed the problem of the mechanical interaction of the matrix with the embedded tumor and claims that stiffer tissues promote malignant behavior. It is also proposed that reducing matrix stiffness minimizes the number of invasive cells and their invasion rate (Postovit et al., 2006, Paszek et al., 2005). Therefore, logical correlated quantitative analysis of different histological features of both these tissue compartments may help us to characterize the disease tissue in a more meaningful way. Computerized digital image analysis gives us some suitable options in this regard (Paul et al., 2005, Landini and Rippin, 1996, Mukherjee et al., 2006). Gutathione-S-transferase (GSTs) constitutes a superfamily of ubiquitous multifunctional enzymes involved in the metabolism of both endogenous and xenobiotic compounds thus facilitating cellular detoxification (Strange and Fryer, 1999). GSTs catalyze the conjugation of reduced glutathione (GSH) to electrophilic centers on a wide variety of substrates and thereby play a significant role in the inactivation or occasional activation of many electrophilic substances (Ketterer et al., 1990). It is represented by several isozymes and many of them are polymorphic in humans (Hayes et al., 2005). GSTM1 bears a common polymorphism (the null allele) that is present in about 40% of Caucasians in a homozygous form and causes the lack of enzymatic activity (Garte et al., 2001). About 60% of Asians, 40% of Africans and 20% of Caucasians do not express GSTT1 (Strange and Fryer, 1999). Genetic variants of GST, alone or in combination with other genetic variations and environmental factors, were associated with a number of multifactorial diseases and conditions, such as N1-Methyl-ATP cancer, colorectal cancer; esophageal cancer, myelodysplastic syndrome and leukemia, cutaneous malignant melanoma and other diseases like systemic lupus erythematosus, chronic obstructive pulmonary disease, bronchial asthma, hypertension, arsenic related skin lesions and solar keratosis (Engel et al., 2002, Cotton et al., 2000, Lu et al., 2005, Kelsey et al., 1997, McCarty et al., 2007, Karlson et al., 2007, Marinho et al., 2007). No such information is, however, available for OSF. With this knowledge base, the present study analyses the NOM and OSF tissues in respect to some important histological features and null gene frequencies of GSTM1 and GSTT1 to have an integrated idea regarding this disease at the level of tissue architecture and genetic predisposition.
    Materials and methods
    Results and discussions
    Conclusion
    Acknowledgement
    Introduction Polycomb repressive complex 2 (PRC2) promotes the establishment of a repressed chromatin state through trimethylation of lysine 27 of histone H3 (H3K27me3; Margueron and Reinberg, 2011) and regulates differentiation of mouse embryonic stem cells (ESCs) (Chamberlain et al., 2008, Shen et al., 2008, Leeb et al., 2010, Montgomery et al., 2005, Pasini et al., 2007, Cruz-Molina et al., 2017). PRC2 is also required to maintain transcriptional repression of developmental regulators and for self-renewal of human ESCs (Collinson et al., 2016). Even though the individual core PRC2 subunits Ezh2, Suz12, and Eed are highly expressed (Shen et al., 2008), the chromatin of ESCs is partially refractory to H3K27me3. The low percentage of the ESC genome occupied by H3K27me3 (Zhu et al., 2013a) coincides with an hyperdynamic chromatin-protein-binding pattern in which a fraction of histones and other chromatin-associated proteins with a short residence time generate a permissive “breathing” chromatin state (Meshorer et al., 2006). PRC2 engagement and H3K27me3 deposition are avoided at ESC regulatory regions of actively transcribed genes, including those for the core pluripotency transcription factors (TFs) Pou5f1 (Oct4), Sox2, and Nanog (henceforth collectively referred to as OSN) (Ng and Surani, 2011, Young, 2011, Orkin and Hochedlinger, 2011). OSN bind a set of active enhancers, including their own, implicated in controlling ESC pluripotency (Boyer et al., 2005, Whyte et al., 2013). However, OSN are also engaged with PRC2 at regulatory regions of repressed or lowly expressed bivalent genes (Azuara et al., 2006, Bernstein et al., 2006, Marson et al., 2008, Young, 2011). Artificial inhibition of transcription or transcriptional elongation results in PRC2 recruitment and H3K27me3 deposition and, conversely, active transcription is mutually exclusive with PRC2 binding (Riising et al., 2014). While active chromatin marks inhibit PRC2 activity (Schmitges et al., 2011), the mechanisms repelling PRC2 binding at transcribed regions remain poorly understood.