Publications by authors named "Mohan Adithi"

Article Synopsis
  • FGFR2 and FGFR3 are proteins that can become cancer-causing (oncogenic) through changes, and they are important in certain types of cancers like bile duct cancer and bladder cancer.
  • A new drug called KIN-3248 was tested and showed it can still work against some common mutations that make other drugs ineffective.
  • KIN-3248 might be a promising treatment for these cancers, especially when used with other drugs that target different cancer pathways.
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Background: Menopausal transition phase is a difficult time in a woman's life. Many factors such as age, socioeconomic status, education, ethnic cultural, and body physique determine the presence of menopausal symptoms. This study helps us to understand the severity and perseverance of menopausal symptoms in women of this locality.

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Fibroblast growth factor receptor (FGFR) alterations are present as oncogenic drivers and bypass mechanisms in many forms of cancer. These alterations can include fusions, amplifications, rearrangements, and mutations. Acquired drug resistance to current FGFR inhibitors often results in disease progression and unfavorable outcomes for patients.

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Contact with the extracellular matrix is essential for maintenance of epithelial cells in many tissues, while in its absence epithelial cells can detach and undergo anoikis. Here, we show that anoikis of luminal cells in the prostate epithelium is followed by a program of tissue repair that is mediated in part by differentiation of basal epithelial cells to luminal cells. We describe a mouse model in which inducible deletion of E-cadherin in prostate luminal cells results in their apoptotic cell death by anoikis, in the absence of phenotypic effects in the surrounding stroma.

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In the 1970s, several human retinoblastoma cell lines were developed from cultures of primary tumors. As the human retinoblastoma cell lines were established in culture, growth properties and changes in cell adhesion were described. Those changes correlated with the ability of the human retinoblastoma cell lines to invade the optic nerve and metastasize in orthotopic xenograft studies.

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Recent studies have shown the presence of human papillomavirus (HPV) genome in retinoblastoma (RB) tumor samples. There is no information on the HPV status in the RB tumors of Indian patients. We studied the presence of HPV genome in RB tumor samples from patients with unilateral tumor.

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The aim of the study was to explore the expression profile of p63, p73 and their delta isoforms in the retinoblastoma tumor samples and to correlate with clinicopathological parameters. Immunohistochemistry was performed for p63, delta p63, p73 and delta p73 on the archival paraffin sections of retinoblastoma and correlated with clinicopathological features. Western blotting was performed to confirm immunoreactivity results.

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Tumor invasion is the critical step that could lead to metastasis in retinoblastoma (RB), a common childhood cancer. Matrix metalloproteinases (MMPs) degrade extracellular matrix, which is a crucial step involved in various stages of tumor progression, including tumor angiogenesis, tumor growth, and also local invasion and subsequent distant metastasis. We investigated the role of extracellular MMP inducer (EMMPRIN), MMP-2, MMP-9 and tissue inhibitor of metalloproteinases (TIMPs): TIMP-1, TIMP-2 in RB and correlated clinicopathologically.

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In our earlier study we showed that invasive retinoblastoma (RB) had down regulated tetraspanin protein KAI1/CD82, a family of cell surface glycoprotein. KAI1 may link to the cell surface molecules, such as integrins, E-cadherin, and other TM4SF members, and loss of KAI1 function may have a significant role in the progression of retinoblastoma. We also showed that epithelial cell adhesion molecule (EpCAM) is overexpressed in invasive RB.

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Chemotherapy is an essential modality in the treatment of retinoblastoma (RB). Mammalian serine/arginine-rich protein-specific kinase 1 (SRPK1) is a cisplatin-sensitivity-related protein and its downregulation is known to be associated with decreased response to cisplatin and carboplatin. We investigated the expression of SRPK1 in 63 archival RB and correlated its expression with pathologic staging and exposure to chemotherapy.

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Most human tumours have genetic mutations in their Rb and p53 pathways, but retinoblastoma is thought to be an exception. Studies suggest that retinoblastomas, which initiate with mutations in the gene retinoblastoma 1 (RB1), bypass the p53 pathway because they arise from intrinsically death-resistant cells during retinal development. In contrast to this prevailing theory, here we show that the tumour surveillance pathway mediated by Arf, MDM2, MDMX and p53 is activated after loss of RB1 during retinogenesis.

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The Rho GTPases are the molecular regulators of the cell motility processes and are involved in cell cycle progression and gene transcription. We studied the expression of Rho-like GTPases molecules, particularly Rac, Tiam1 and cdc42, in retinoblastoma and correlated these with clinicopathological parameters of the tumors. Sixty-seven tumors were included which were divided in to two groups; group A: tumors with optic nerve/choroidal/orbital invasion (n=35) and group B: tumors with no invasion (n=32).

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Purpose: Human leukocyte antigen (HLA) mediates interactions of tumor cells with cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. Retinoblastoma (RB) is the most common intraocular malignant tumor in childhood and is characterized by direct spread to the optic nerve and orbit as well as hematogenous and lymphatic spread. Earlier, we observed that invasive RB showed reduced HLA, which could contribute to its escape from the immune system.

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We examine the immunoreactivity of the non-receptor tyrosine kinase, c-Src kinase and its downstream molecule, signal transducer and activator of transcription 3 (pStat3) in retinoblastoma (RB), and correlation with invasiveness and differentiation. Tumor samples from 40 patients with RB were available for the study. There were 18 tumors in group 1 (non-invasive) and 22 tumors in group 2 (invasive).

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Background: To investigate the potential involvement of the nitric oxide (NO) pathway in retinoblastoma, the authors correlated immunoreactivity for endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and nitrotyrosine (NT) with the degree of tumor invasiveness in retinoblastoma.

Methods: eNOS, iNOS, and NT reactivity was evaluated by immunohistochemistry in 34 archival retinoblastoma specimens and in a human Y79 retinoblastoma cell line. The tumors were divided into 2 groups: Group A tumors (n = 17 tumors) with no invasion and Group B tumors (n = 17 tumors) with invasion of the choroid, optic nerve, and/or orbit.

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Purpose: This study was conducted to investigate the potential of targeting epithelial cell adhesion molecules (EpCAMs) in the treatment of retinoblastoma. It was first determined whether EpCAM is expressed in retinoblastoma and then whether EpCAM reactivity correlates with tumor aggressiveness.

Methods: EpCAM reactivity was evaluated by immunohistochemistry in 43 retinoblastoma specimens from 43 patients, by using the monoclonal antibody GA733.

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Background: The importance of the Fas-Fas ligand (FasL) mechanism for the immune evasion by tumors provided a strong rationale for the examination of FasL expression in retinoblastoma. In an earlier publication, the authors reported that invasive retinoblastomas decreased Fas expression. Because to the authors' knowledge there is not much information regarding the effect of FasL expression on retinoblastoma, the authors studied the expression of FasL in retinoblastoma and correlated it with invasiveness.

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