Molecular and Clinical Approach to Intra-abdominal Adverse Effects of Targeted Cancer Therapies

Though modern available cancer therapies are effective, they possess major adverse effects, causing non-compliance to patients. Furthermore, the majority of the polymeric-based medication platforms are certainly not universally acceptable, due to their several restrictions. With this juxtaposition, lipid-based medication delivery systems have appeared as promising drug nanocarriers to replace the majority of the polymer-based products because they are in a position to reverse polymer as well as, drug-associated restrictions. Furthermore, the amalgamation of the basic principle of nanotechnology in designing lipid nanocarriers, which are the latest form of lipid carriers, has tremendous chemotherapeutic possibilities as tumor-targeted drug-delivery pertaining to tumor therapy. Apart from this, it is reported that nearly 40% of the modern medication entities are lipophilic. Moreover, research continues to be efficient in attaining a significant understanding of the absorption and bioavailability of the developed lipids systems.

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91 Retinopathy Secondary to Targeted Cancer Therapies

The Retina Illustrated ◽

10.1055/b-0040-174276 ◽

2020 ◽

Keyword(s):

Cancer Therapies ◽

Targeted Cancer Therapies

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AB0080 A SYSTEM-LEVEL APPROACH IDENTIFIES A CRITICAL REGULATOR OF CHONDROSARCOMA PROGRESSION

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2020-eular.5305 ◽

2020 ◽

Vol 79 (Suppl 1) ◽

pp. 1340.3-1340

Author(s):

H. Kim ◽

Y. Cho ◽

J. H. Kim

Keyword(s):

Histological Grade ◽

System Level ◽

Clinical Approach ◽

Cancer Therapies ◽

Functional Roles ◽

Network Analyses ◽

Molecular Events ◽

Anti Cancer ◽

Tumor Growth And Metastasis ◽

Chemotherapy Agents

Background:Chondrosarcomas are cartilaginous tumors that constitute one-third of skeletal system cancers. Chondrosarcomas are capable of transitioning to highly metastatic and treatment-refractory states, resulting in significant patient mortality. However, the molecular events accompanying this behavior remain unknown.Objectives:We aimed to uncover the molecular pathway underlying such tumor progression that confers a higher malignancy to chondrosarcoma.Methods:We conducted unsupervised gene co-expression network analyses using transcriptomes of patients with chondrosarcoma and extracted a characteristic transcription network underlying chondrosarcoma malignancy. By implementing a system-level upstream analysis of this gene network, we identified the transcriptional factor as a key regulator governing chondrosarcoma progression. We unraveled the functional roles of the identified factor in promoting tumor growth and metastasis of chondrosarcomas in the context of their unique microenvironments.Results:By conducting system-level upstream analysis, we identified a factor as a transcriptional regulator that governs the malignancy gene module. The identified factor was upregulated in chondrosarcoma biopsies associated with a high histological grade and conferred chondrosarcoma cells invasiveness and tumor-initiating capacity. In an orthotopic xenograft mouse model, the identified factor modulated local outgrowth and pulmonary metastasis of chondrosarcoma. Pharmacological inhibition of the identified factor in conjunction with the chemotherapy agents such as cisplatin or doxorubicin synergistically enhanced chondrosarcoma cell apoptosis and abolished malignant phenotypes of chondrosarcoma in mice.Conclusion:Our study provides a proof of concept evidence that inhibiting the identified factor suppresses progression of chondrosarcoma and improves the efficacy of chemotherapy in cellular and pre-clinical levels. Taken together, we believe that our findings provide novel molecular insights for the development of new anti-cancer therapies to target chondrosarcomas.References:[1]Gelderblom H, et al. The clinical approach towards chondrosarcoma. Oncologist 13, 320-329 (2008)Disclosure of Interests:None declared

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Senolytics for Cancer Therapy: Is All that Glitters Really Gold?

Cancers ◽

10.3390/cancers13040723 ◽

2021 ◽

Vol 13 (4) ◽

pp. 723

Author(s):

Valerie J. Carpenter ◽

Tareq Saleh ◽

David A. Gewirtz

Keyword(s):

Cancer Therapy ◽

Tumor Cell ◽

Cancer Therapies ◽

Cell Models ◽

Future Directions ◽

Targeted Cancer Therapies

Senolytics represent a group of mechanistically diverse drugs that can eliminate senescent cells, both in tumors and in several aging-related pathologies. Consequently, senolytic use has been proposed as a potential adjuvant approach to improve the response to senescence-inducing conventional and targeted cancer therapies. Despite the unequivocal promise of senolytics, issues of universality, selectivity, resistance, and toxicity remain to be further clarified. In this review, we attempt to summarize and analyze the current preclinical literature involving the use of senolytics in senescent tumor cell models, and to propose tenable solutions and future directions to improve the understanding and use of this novel class of drugs.

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