Human brain glioblastoma cells do not induce but do respond to the bleomycin-induced bystander response from lung adenocarcinoma cells

Basheerudeen, Safa Abdul Syed; Chinnadurai, Mani; Kulkarni, Megha Anil Kumar; Pillai, K. M. R.; Rajan, Anila; Prakash, Venkatachalam

doi:10.1016/j.mrgentox.2013.07.005

Cited by 14 publications

(5 citation statements)

References 20 publications

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“…Breast cancer (BC) is most frequently diagnosed cancer and remains one of leading cause of cancer-related death in women worldwide [1] , [2] . Altered signaling pathways [3] , [4] , [5] , [6] , [7] , mutation in genes [8] , activation of oncogenic pathways [9] , [10] , [11] , DNA damage [12] , [13] and non-targeted effects of chemotherapeutic agents [14] , [15] , [16] , [17] significantly contributes in cancer progression. Therapeutic strategies including chemotherapy [18] , application of toxins obtained from pathogen [19] , [20] , [21] , [22] , [23] , [24] have shown limited clinical efficacy against cancer.…”

Section: Introductionmentioning

confidence: 99%

Role of let-7 family microRNA in breast cancer

Thammaiah

Jayaram

2016

Non-coding RNA Research

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Metastasis and resistance to therapy significantly contribute to cancer-related deaths. Growing body of evidence suggest that altered expression of microRNAs (miRNAs) is one of the root cause of adverse clinical outcome. miRNAs such as let-7 are the new fine tuners of signaling cascade and cellular processes which regulates the genes in post-transcriptional manner. In this review, we described the regulation of let-7 expression and the involvement of molecular factors in this process. We discussed the mechanism by which let-7 alter the expression of genes involved in the process of tumorigenesis. Further, we listed the pathways targeted by let-7 to reduce the burden of the tumor. In addition, we described the role of let-7 in breast cancer metastasis and stemness properties. This article will provide the in-depth insight into the biology of let-7 miRNA and its role in the breast cancer progression.

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Section: Introductionmentioning

confidence: 99%

Role of let-7 family microRNA in breast cancer

Thammaiah

Jayaram

2016

Non-coding RNA Research

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“…Bystander responses were observed in many cell types, but there are reports suggesting not all cells can generate bystander response. For example, in the case of glioblastoma, cells do not induce a bystander effect if treated with bleomycin but do respond to bleomycin-induced bystander effect from lung adenocarcinoma cells, if incubated together [ 51 ].…”

Section: General Adc Structurementioning

confidence: 99%

Antibody-Drug Conjugates in Solid Tumor Oncology: An Effectiveness Payday with a Targeted Payload

Kondrashov,

Sapkota,

Sharma

et al. 2023

Pharmaceutics

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Antibody–drug conjugates (ADCs) are at the forefront of the drug development revolution occurring in oncology. Formed from three main components—an antibody, a linker molecule, and a cytotoxic agent (“payload”), ADCs have the unique ability to deliver cytotoxic agents to cells expressing a specific antigen, a great leap forward from traditional chemotherapeutic approaches that cause widespread effects without specificity. A variety of payloads can be used, including most frequently microtubular inhibitors (auristatins and maytansinoids), as well as topoisomerase inhibitors and alkylating agents. Finally, linkers play a critical role in the ADCs’ effect, as cleavable moieties that serve as linkers impact site-specific activation as well as bystander killing effects, an upshot that is especially important in solid tumors that often express a variety of antigens. While ADCs were initially used in hematologic malignancies, their utility has been demonstrated in multiple solid tumor malignancies, including breast, gastrointestinal, lung, cervical, ovarian, and urothelial cancers. Currently, six ADCs are FDA-approved for the treatment of solid tumors: ado-trastuzumab emtansine and trastuzumab deruxtecan, both anti-HER2; enfortumab-vedotin, targeting nectin-4; sacituzuzmab govitecan, targeting Trop2; tisotumab vedotin, targeting tissue factor; and mirvetuximab soravtansine, targeting folate receptor-alpha. Although they demonstrate utility and tolerable safety profiles, ADCs may become ineffective as tumor cells undergo evolution to avoid expressing the specific antigen being targeted. Furthermore, the current cost of ADCs can be limiting their reach. Here, we review the structure and functions of ADCs, as well as ongoing clinical investigations into novel ADCs and their potential as treatments of solid malignancies.

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“…Bystander cells are the normal cells that are surrounding the tumor or infected cells. Bystander effects have been studied extensively to both radiation and chemotherapeutic treatment [30][31][32][33]. In present scenario, human intestine infection with Enterococcus faecalis activates macrophages that secretes increased TNF-α, that acts upon the bystander epithelial cells and induces a pro-proliferation and anti-apoptotic pathways [34].…”

Section: Tumor Growthmentioning

confidence: 99%

Cancer Progression Related with Tumor-associated Macrophages

Ethiraj¹,

Loganathan²,

Arul³

2016

cor

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Tumor-associated macrophages are one of the main populations of inflammatory cells in cancers that favor tumor cell growth and survival. Tumor-derived factors such as VEGF-A and CSF-1 recruit the macrophages in tumor micro environment and alter their phenotype in M1 to M2 or tumor-associated macrophages by secretion of several cytokines including IL-4, IL-13 and VEGF-A. In return tumor-associated macrophages released growth factors and cytokine that helps in cancer cell proliferation and metastasis. Tumor-associated macrophage secreted cytokines promotes the angiogenesis and lymphangiogenesis that assist tumor cell to metastasize in distant organs. Importantly, tumor-associated macrophages promote an immunosuppressive environment with the help of other immune cells in the tumor-bearing host that helps tumor to grow unchecked and unchallenged. In addition, tumor-associated macrophages induce resistance against cancer therapy and boost tumor regrowth after therapy. In this review, we discuss the role of tumor-associated macrophages in the pathobiology of cancer. Understanding of the crucial role of tumor-associated macrophages in cancer progression may help to assess potential therapeutic strategies.

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Human brain glioblastoma cells do not induce but do respond to the bleomycin-induced bystander response from lung adenocarcinoma cells

Cited by 14 publications

References 20 publications

Role of let-7 family microRNA in breast cancer

Role of let-7 family microRNA in breast cancer

Antibody-Drug Conjugates in Solid Tumor Oncology: An Effectiveness Payday with a Targeted Payload

Cancer Progression Related with Tumor-associated Macrophages

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