Suchandrima Ghosh's research while affiliated with Biomedical Informatics Centre and other places

... NEAT1 has been found to be highly expressed in various types of solid tumors, such as non-small cell lung cancer, ovarian cancer, cervical cancer, hepatocellular carcinoma, colorectal cancer, gastric cancer, HNSCC and etc [18,[41][42][43][44][45][46][47][48][49][50][51]. This evidence suggests a strong association between NEAT1 overexpression and the presence of these tumors. ...

... The complement activation plays a crucial role in the pathogenesis of IgAN. 21,22 Although the precise interplay between chronic HBV infection and complement remains largely unknown, several studies have documented reduced levels of complement components (including C3, C4, C7, and C9) in individuals suffering from chronic HBV infection, 23,24 thus indicative of a possible activation of the complement system. Notably, the extent to which the involvement of the complement pathway contributes to the pathogenesis of IgAN in the setting of HBV infection remains to be elucidated and requires comprehensive investigation and rigorous evaluation. ...

... Crohn's disease (CD) and intestinal TB have similar features and insensitive diagnostic tools, which makes their identification extremely difficult, but the use of miRNAs as biomarkers can solve this problem. The plasma miR-375-3p concentration is higher in patients with ITB than in patients with CD, whereas higher miR-375-3p expression is observed in the tissues of patients with CD (232). The clinical treatment and prognosis of tuberculosis pleural effusion (TPE) and malignant FIGURE 3 Differential expression of miRNAs after Mtb infection. ...

... Host and viral factors; coinfection with other viruses such as hepatitis C virus (HCV), hepatitis D virus (HDV) or human immunodeficiency virus (HIV); family history; and other comorbidities, including obesity, can affect the natural course of HBV infection [1][2][3][4][5][6][7][8][9][10][11][12]. Another important thing to mention is that the covalently closed circular HBV-DNA (cccDNA) persists indefinitely in hepatocytes, and low-level viral replication or re-activation in some circumstances is possible; at the same time, the HBV genome may integrate in the host genome, generating risk for hepatocarcinoma (HCC) [13][14][15]. Routes of transmission include vertical (mother Life 2024, 14, 348 3 of 15 97% of newborns have received TBD vaccination and 85% of children younger than 1 year old were immunized with all doses [36]. Prenatal screening for HBV is not routinely used in Romania. ...

... Site directed mutagenesis kit (Agilent, #200523) was used to incorporate mutation in 3′ UTR sequences following manufacturer's protocol. A non-specific Pre-miRNA sequence (miR-c12) cloned in pRNAU6.1 [29] and mutated at the seed sequence was considered as pScramble pre-miRNA. ...

... FCA of BSE-gated plasma EVs with scattering and fluorescent signals distinct from background noise (Figure 5a,c) revealed that IP of SEC-isolated plasma EVs targeting the L1CAM ectodomain with the antibody clone 5G3 results in a ∼24-fold enrichment of L1CAM+ EVs over plasma EVs and EVs immunoprecipitated with an isotype control antibody (Figure 5b vs. d, f and g; Figure S12a). A high percentage of immunocaptured L1CAM+ EVs carried tetraspanins and VAMP2, whilst being negative for ASGR2, a membrane marker of hepatocytes considered a main source of peripheral L1CAM (Ghosh et al., 2020) (Figure 5h-k), thus confirming the EV identity and neuronal origin of a sizable sub-population of L1CAM+ EVs recovered via L1CAM IP. Following L1CAM IP, the percentages of L1CAM+ EVs double-positive for all the markers evaluated as part of the experiment shown in Figure 5, out of all BSE events, were as follows (mean ± standard deviation): L1CAM/pan-tetraspanin++ EVs, 50.09 ± 13.51%; L1CAM/VAMP2++ EVs, 37.47 ± 10.11%; L1CAM/ASGR2++ EVs, 0.30 ± 0.05%. ...

... Studies have also analyzed HBV sub-genotypes and its association with HCC. Recent reports suggest that HBV sub-genotype D1 may have higher potential to cause HCC than D3 [44]. ...

... Hence, it is of great importance to discover immune bio-markers to forecast the prognosis of HCC patients, which may be helpful in immunotherapy. [18][19][20] In our study, we built an exosome-related gene prognostic model to forecast the prognosis of HCC patient based on TCGA database, and validated the prediction ability in external database successfully. We con rmed that the prognostic model can divide HCC patients into low-risk and high-risk subtypes, and showed that the oncology outcome of low-risk subtypes is better than that of high-risk groups. ...

... As previously discussed, several factors are being studied concerning their possible role in development of HCC chemoresistance, a typical and highly troublesome characteristic of this cancer. Ghosh et al., reported that HBV HBx-E2F1-ATAD5 axis is recruited in hepatocellular carcinoma cell lines to promote ATAD5 expression, and HCC chemoresistance thereof [179]. The result of this study indicated for a positive regulatory feedback loop between ATAD5 and HBV, in which HBV adds to ATAD5 expression levels and ATAD5 enhance HBV replication rate. ...