المؤلفون: Sharma, Tarang, Gupta, Ashna, Chauhan, Ravi, Bhat, Ajaz A., Nisar, Sabah, Hashem, Sheema, Akhtar, Sabah, Ahmad, Aamir, Haris, Mohammad, Singh, Mayank, Uddin, Shahab

المساهمون: Hamad Medical Corporation, All-India Institute of Medical Sciences, Sidra Medicine Precision Program

المصدر: Cancer and Metastasis Reviews ; volume 41, issue 2, page 281-299 ; ISSN 0167-7659 1573-7233

مصطلحات موضوعية: Cancer Research, Oncology

الوصف: Esophageal cancer (EC) is frequently considered a lethal malignancy and is often identified at a later stage. It is one of the major causes of cancer-related deaths globally. The conventional treatment methods like chemotherapy, radiotherapy, and surgery offer limited efficacy and poor clinical outcome with a less than 25% 5-year survival rate. The poor prognosis of EC persists despite the growth in the development of diagnostic and therapeutic modalities to treat EC. This underlines the need to elucidate the complex molecular mechanisms that drive esophageal oncogenesis. Apart from the role of the tumor microenvironment and its structural and cellular components in tumorigenesis, mounting evidence points towards the involvement of the esophageal microbiome, inflammation, and their cross-talk in promoting esophageal cancer. The current review summarizes recent research that delineates the underlying molecular mechanisms by which the microbiota and inflammation promote the pathophysiology of esophageal cancer, thus unraveling targets for potential therapeutic intervention.

الإتاحة: https://doi.org/10.1007/s10555-022-10026-6Test

المؤلفون: Kuttikrishnan, Shilpa, Masoodi, Tariq, Sher, Gulab, Bhat, Ajaz A., Patil, Kalyani, El-Elimat, Tamam, Oberlies, Nicholas H., Pearce, Cedric J., Haris, Mohmmad, Ahmad, Aamir, Alali, Feras Q., Uddin, Shahab

المصدر: Frontiers in Oncology ; volume 12 ; ISSN 2234-943X

مصطلحات موضوعية: Cancer Research, Oncology

الوصف: Abnormal expression of Forkhead box protein M1 (FOXM1) and serine/threonine kinase Budding uninhibited by benzimidazoles 1 (BUB1B) contributes to the development and progression of several cancers, including chronic myelogenous leukemia (CML). However, the molecular mechanism of the FOXM1/BUB1B regulatory network and the role of Neosetophomone-B (NSP-B) in leukemia remains unclear. NSP-B, a meroterpenoid fungal secondary metabolite, possesses anticancer potential in human leukemic cells lines; however, the underlying mechanism has not been elucidated. The present study aimed to explore the role of NSP-B on FOXM1/BUB1B signaling and the underlying molecular mechanism of apoptosis induction in leukemic cells. We performed gene expression profiling of NSP-B-treated and untreated leukemic cells to search for differentially expressed genes (DEGs). Interestingly BUB1B was found to be significantly downregulated (logFC -2.60, adjusted p = 0.001) in the treated cell line with the highest connectivity score among cancer genes. Analysis of TCGA data revealed overexpression of BUB1B compared to normal in most cancers and overexpression was associated with poor prognosis. BUB1B also showed a highly significant positive correlation with FOXM1 in all the TCGA cancer types. We used human leukemic cell lines (K562 and U937) as an in vitro study model to validate our findings. We found that NSP-B treatment of leukemic cells suppressed the expression of FOXM1 and BUB1B in a dose-dependent manner. In addition, NSP-B also resulted in the downregulation of FOXM1-regulated genes such as Aurora kinase A, Aurora kinase B, CDK4, and CDK6. Suppression of FOXM1 either by siRNA or NSP-B reduced BUB1B expression and enhanced cell survival inhibition and induction of apoptosis. Interestingly combination treatment of thiostrepton and NSP-B suppressed of cell viability and inducted apoptosis in leukemic cells via enhancing the activation of caspase-3 and caspase-8 compared with single-agent treatment. These results demonstrate the important ...

الإتاحة: https://doi.org/10.3389/fonc.2022.929996Test

المؤلفون: Patil, Kalyani, Khan, Farheen B., Akhtar, Sabah, Ahmad, Aamir, Uddin, Shahab

المساهمون: Hamad Medical Corporation

المصدر: Cancer and Metastasis Reviews ; volume 40, issue 3, page 691-720 ; ISSN 0167-7659 1573-7233

مصطلحات موضوعية: Cancer Research, Oncology

الوصف: The ever-growing perception of cancer stem cells (CSCs) as a plastic state rather than a hardwired defined entity has evolved our understanding of the functional and biological plasticity of these elusive components in malignancies. Pancreatic cancer (PC), based on its biological features and clinical evolution, is a prototypical example of a CSC-driven disease. Since the discovery of pancreatic CSCs (PCSCs) in 2007, evidence has unraveled their control over many facets of the natural history of PC, including primary tumor growth, metastatic progression, disease recurrence, and acquired drug resistance. Consequently, the current near-ubiquitous treatment regimens for PC using aggressive cytotoxic agents, aimed at ‘‘tumor debulking’’ rather than eradication of CSCs, have proven ineffective in providing clinically convincing improvements in patients with this dreadful disease. Herein, we review the key hallmarks as well as the intrinsic and extrinsic resistance mechanisms of CSCs that mediate treatment failure in PC and enlist the potential CSC-targeting ‘natural agents’ that are gaining popularity in recent years. A better understanding of the molecular and functional landscape of PCSC-intrinsic evasion of chemotherapeutic drugs offers a facile opportunity for treating PC, an intractable cancer with a grim prognosis and in dire need of effective therapeutic advances.

الإتاحة: https://doi.org/10.1007/s10555-021-09979-xTest

المؤلفون: Ahmad, Aamir, Poltronieri, Palmiro, Uddin, Shahab

المصدر: Frontiers in Oncology ; volume 11 ; ISSN 2234-943X

مصطلحات موضوعية: Cancer Research, Oncology

الإتاحة: https://doi.org/10.3389/fonc.2021.813274Test

المؤلفون: Ahmad, Aamir

المصدر: Current Cancer Drug Targets ; volume 19, issue 7, page 513-514 ; ISSN 1568-0096

مصطلحات موضوعية: Cancer Research, Drug Discovery, Pharmacology, Oncology

الإتاحة: https://doi.org/10.2174/156800961907190802112321Test
http://eurekaselect.com/article/download/174051Test

المؤلفون: Khan, Mohammad Imran, Ahmad, Aamir

المصدر: Frontiers in oncology. 12

مصطلحات موضوعية: Cancer Research, Oncology

الوصف: Acquired resistance is a major clinical challenge for tamoxifen-based therapy. In this study, we focused on lncRNA SNHG6 which plays a role in chemoresistance of cancer cells, but has never been investigated in the context of tamoxifen resistance. We found elevated levels of SNHG6 in tamoxifen-resistant estrogen receptor (ER)-positive MCF-7 cells (MCF7TR), relative to naïve MCF-7 cells, as well as in tamoxifen-resistant T47D cells (T47DTR), relative to naïve T47D cells, which correlated with induced vimentin, ZEB1/2 and decreased e-cadherin, thus implicating a role of EMT in SNHG6-mediated tamoxifen resistance. Downregulation of SNHG6, using specific siRNA, sensitized MCF7TR as well as T47DTR cells to tamoxifen along with markedly reduced proliferation, invasion and anchorage-independent clonogenicity. Further, SNHG6 was found to sponge and inhibit miR-101 as the endogenous expression levels of SNHG6 and miR-101 inversely correlated in paired parental and tamoxifen-resistant cells and, moreover, silencing of SNHG6 in tamoxifen-resistant cells resulted in de-repression of miR-101, along with reversal of EMT. SNHG6 expression also directly correlated with increased stem cells markers Sox2, Oct4 and EZH2. miR-101 levels, manipulated by transfections with pre/anti-miR-101 oligos, directly affected tamoxifen sensitivity of ER-positive cells with pre-miR-101 sensitizing MCF7TR and T47DTR cells to tamoxifen whereas anti-miR-101 inducing resistance of parental MCF-7 and T47D cells to tamoxifen. Further, miR-101 was found to attenuate SNHG6-mediated effects on tamoxifen resistance, EMT as well as stem cell markers, thereby making a case for SNHG6-miR-101 axis in tamoxifen resistance of ER-positive breast cancer cells. Thus, lncRNA SNHG6 is a novel modulator of tamoxifen resistance through its sponging of miR-101 and the resulting effects on EMT.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5eeb5e62680f306fcb3cc76cfb057322Test
https://pubmed.ncbi.nlm.nih.gov/36212408Test

المؤلفون: Bao, Bin, Wang, Zhiwei, Ali, Shadan, Kong, Dejuan, Li, Yiwei, Ahmad, Aamir, Banerjee, Sanjeev, Azmi, Asfar S., Miele, Lucio, Sarkar, Fazlul H.

المصدر: Cancer Letters ; volume 423, page 153 ; ISSN 0304-3835

مصطلحات موضوعية: Cancer Research, Oncology

الإتاحة: https://doi.org/10.1016/j.canlet.2018.03.020Test
https://api.elsevier.com/content/article/PII:S0304383518302118?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0304383518302118?httpAccept=text/plainTest

المؤلفون: Srivastava, Sanjeev K., Ahmad, Aamir, Miree, Orlandric, Patel, Girijesh Kumar, Singh, Seema, Rocconi, Rodney P., Singh, Ajay P.

المساهمون: National Cancer Institute

المصدر: Journal of Ovarian Research ; volume 10, issue 1 ; ISSN 1757-2215

مصطلحات موضوعية: Obstetrics and Gynecology, Oncology

الإتاحة: https://doi.org/10.1186/s13048-017-0355-yTest

المؤلفون: Ahmad, Aamir, Wang, Zhiwei, Kong, Dejuan, Ali, Shadan, Li, Yiwei, Banerjee, Sanjeev, Ali, Raza, Sarkar, Fazlul H.

المصدر: Breast Cancer Research and Treatment ; volume 158, issue 3, page 607-607 ; ISSN 0167-6806 1573-7217

مصطلحات موضوعية: Cancer Research, Oncology

الإتاحة: https://doi.org/10.1007/s10549-016-3904-yTest

المؤلفون: Ahmad, Aamir, Wang, Zhiwei, Kong, Dejuan, Ali, Raza, Ali, Shadan, Banerjee, Sanjeev, Sarkar, Fazlul H.

المصدر: Breast Cancer Research and Treatment ; volume 158, issue 3, page 605-605 ; ISSN 0167-6806 1573-7217

مصطلحات موضوعية: Cancer Research, Oncology

الإتاحة: https://doi.org/10.1007/s10549-016-3905-xTest