Publications by authors named "Anbalagan Muralidharan"

Background: It is generally accepted that the greater palatine nerve and artery supply the palatal mucosa, gingiva, and glands, but not the bone or tooth adjacent to those tissues. When the bony palate is observed closely, multiple small foramina are seen on the palatal surface of the alveolar process. The authors hypothesized that the greater palatine nerve and artery might supply the maxillary teeth via the foramina on the palatal surface of the alveolar process and the superior alveolar nerve and artery.

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Legumes are a predominant source of isoflavones, termed phytoestrogens, that mimic 17β-estradiol (E2). Phytoalexins are inducible isoflavones produced in plants subjected to environmental stressors (e.g.

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Article Synopsis
  • Endometrial cancer (EC) is the most common gynecological cancer in the U.S., with obesity contributing to 57% of cases, emphasizing the need to study its molecular mechanisms in relation to obesity.
  • The research found that obese EC patients had higher levels of extracellular vesicles (EVs) carrying oncogenic proteins, which are linked to increased cancer growth, inflammation, and changes in protein expression in both adipose and uterine tissues.
  • Treatments with small molecule inhibitors like HO-3867 and Metformin were effective in reducing EV secretion, slowing cancer cell proliferation, and inhibiting the early stages of cancer development in high-fat diet-induced models.
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The novel coronavirus disease 2019 (COVID-19) pandemic outbreak caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has garnered unprecedented global attention. It caused over 2.47 million deaths through various syndromes such as acute respiratory distress, hypercoagulability, and multiple organ failure.

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Background: Astrocyte elevated gene-1 (AEG-1) is overexpressed in various malignancies. Exostosin-1 (EXT-1), a tumor suppressor, is an intermediate for malignant tumors. Understanding the mechanism behind the interaction between AEG-1 and EXT-1 may provide insights into colon cancer metastasis.

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Article Synopsis
  • - Histological observation under light microscopy is commonly used in studies of human cadavers, but can lead to incorrect interpretations if not done properly.
  • - This article aims to establish guidelines for using histology in cadaveric research, developed through discussions with experts across various medical fields.
  • - The consensus reached emphasizes the SQIP principle (structure, quantification, interaction, position) for accurate histological interpretation, making this the first comprehensive guide for such studies.
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The embryological origin of the trapezius and sternocleidomastoid muscles has been debated for over a century. To shed light on this issue, the present anatomical study was performed. Five fresh frozen human cadavers, three males and two females, were used for this study.

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Colorectal cancer is one of the most common cancer types worldwide. Since colorectal cancer takes time to develop, its incidence and mortality can be treated effectively if it is detected in its early stages. As a result, non-invasive or invasive biomarkers play an essential role in the early diagnosis of colorectal cancer.

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Introduction: Ceramides are known to show anti-cancer activity. A novel ceramide analog, (S,E)-3-hydroxy-2-(2-hydroxybenzylidene)amino-N-tetradecylpropanamide (analog 315) was developed as part of a larger study focused on finding more effective breast cancer treatments.

Objective: To assess whether analog 315 shows any or a combination of the following effects in breast cancer cells in vitro: inhibiting proliferation, inducing apoptosis, and altering protein expression.

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The cancer stem cell (CSC) hypothesis is an evolving oncogenesis concept. CSCs have a distinct ability to self-renew themselves and also give rise to a phenotypically diverse population of cells. Targeting CSCs represents a promising strategy for cancer treatment.

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We have previously reported that treating triple-negative tumor bearing nude mice with intraperitoneal (ip) 10 mg/kg body weight of (S,E)-3-hydroxy-2-(2-hydroxybenzylidene)aminotetradecylpropanamide, a ceramide analog, 5 days per week for 3 weeks, was shown not only to suppress tumor growth but also to reduce metastasis. Studies reported here focus on determining the toxicity of this drug in the nude mice. During the first study, treated animals (single intraperitoneal (ip) injection, 0, 40, 80 and 120 mg/kg body weight) were closely monitored for 14 days for any signs of illness or death.

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Patients with advanced breast cancer often develop bone metastases. Treatment is limited to palliative care. Parathyroid hormone (PTH)/parathyroid hormone-related peptide (PTHrP) antagonists for bone metastases failed clinically due to short half-life and inadequate concentration in bone.

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Background: To understand the mechanism underlying tamoxifen-induced multidrug resistance (MDR) and stem-like phenotypes in breast cancer cells, we treated the MCF-7 cells with 4-hydroxy-tamoxifen (TAM) for 6 months continuously and established MCF-7 tamoxifen resistance (TR) phenotypes.

Methods: In the present study, the following methods were used: cell viability assay, colony formation, cell cycle analysis, ALDEFLUOR assay, mammosphere formation assay, chromatin immunoprecipitation (ChIP) assay, PCR array, western blot analysis and quantitative reverse transcription polymerase chain reaction (QRT-PCR).

Results: The expression of ERα was significantly higher in MCF7-TR cells when compared with parental MCF-7 cells.

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Conventional mitogen-activated protein kinase (MAPK) family members regulate diverse cellular processes involved in tumor initiation and progression, yet the role of ERK5 in cancer biology is not fully understood. Triple-negative breast cancer (TNBC) presents a clinical challenge due to the aggressive nature of the disease and a lack of targeted therapies. ERK5 signaling contributes to drug resistance and metastatic progression through distinct mechanisms, including activation of epithelial-to-mesenchymal transition (EMT).

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Most hereditary tumors show aberrations in DNA repair genes or their regulators. In contrast, only a minority of sporadic tumors show alterations in these genes. As a result, genomic instability is currently considered an enhancer of tumorigenesis rather than an obligatory event in this process.

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Background: Triple-negative breast cancer (TNBC) represents an aggressive subtype with limited therapeutic options. Experimental preclinical models that recapitulate their tumors of origin can accelerate target identification, thereby potentially improving therapeutic efficacy. Patient-derived xenografts (PDXs), due to their genomic and transcriptomic fidelity to the tumors from which they are derived, are poised to improve the preclinical testing of drug-target combinations in translational models.

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Breast cancer is a heterogeneous disease that accounts for 30% of all cancers diagnosed in women and over half a million deaths per year. Cancer stem cells (CSCs) make up a small subpopulation of cells within a tumor, are capable of self-renewal and, are responsible for tumor initiation, formation, and recurrence. Breast CSCs (BCSCs) have been the subject of concentrated research as potential targets for breast cancer therapies.

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Liver cancer is the second leading cause of cancer death worldwide. Metabolic pathways within the liver and liver cancers are highly regulated by the central circadian clock in the suprachiasmatic nuclei (SCN). Daily light and dark cycles regulate the SCN-driven pineal production of the circadian anticancer hormone melatonin and temporally coordinate circadian rhythms of metabolism and physiology in mammals.

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Unlike breast cancer that is positive for estrogen receptor-α (ERα), there are no targeted therapies for triple-negative breast cancer (TNBC). ERα is silenced in TNBC through epigenetic changes including DNA methylation and histone acetylation. Restoring ERα expression in TNBC may sensitize patients to endocrine therapy.

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Estrogen receptor alpha (ERα) signaling pathways are frequently disrupted in breast cancer and contribute to disease progression. ERα signaling is multifaceted and many ERα regulators have been identified including transcription factors and growth factor pathways. More recently, microRNAs (miRNAs) are shown to deregulate ERα activity in breast carcinomas, with alterations in both ERα and miRNA expression correlating to cancer progression.

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Background: Fat grafting has become popular for repair of postsurgical/postradiation defects after head/neck cancers resection. Fat graft supplementation with adipose tissue-derived stromal/stem cells (ASCs) is proposed to improve graft viability/efficacy, although the impact of ASCs on head/neck cancer cells is unknown.

Objectives: To determine whether ASCs affect growth, migration, and metastasis of human head/neck cancer.

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DNA polymerase kappa is a Y-family polymerase that participates to bypass the damaged DNA known as translesion synthesis (TLS) polymerase. Higher frequency of mutations in DNA polymerase kappa (POLK) recently been reported in prostate cancer. We sequenced entire exons of the POLK gene on genomic DNA from 40 prostate cancers and matched normal samples.

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Estrogen receptor α (ERα) is a member of the nuclear receptor superfamily of transcription factors that regulates cell proliferation, differentiation and homeostasis in various tissues. Sustained exposure to estrogen/estradiol (E2) increases the risk of breast, endometrial and ovarian cancers. ERα function is also regulated by phosphorylation through various kinase signaling pathways that will impact various ERα functions including chromatin interaction, coregulator recruitment and gene expression, as well impact breast tumor growth/morphology and breast cancer patient response to endocrine therapy.

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Resistance to endocrine therapy is a major impediment to successful treatment of breast cancer. Preclinical and clinical evidence links resistance to antiestrogen drugs in breast cancer cells with the overexpression and/or activation of various pro-oncogenic tyrosine kinases. Disruption of circadian rhythms by night shift work or disturbed sleep-wake cycles may lead to an increased risk of breast cancer and other diseases.

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Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype that lacks effective targeted therapies. The epithelial-to-mesenchymal transition (EMT) is a key contributor in the metastatic process. We previously showed the pan-deacetylase inhibitor LBH589 induces CDH1 expression in TNBC cells, suggesting regulation of EMT.

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