Overcoming drug resistance in multi-drug resistant cancers and microorganisms

Avner, Benjamin S.; Fialho, Arsénio M.; Chakrabarty, Ananda M.

doi:10.4161/bioe.21130

Cited by 43 publications

(53 citation statements)

References 38 publications

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“…Molecules-Drug resistance can be induced by various mechanisms, such as pumping out of drug, change of target molecule, interruption of drug influx, or increase in proliferation, including aberrant programmed cell death in response to anticancer drugs (32). In response to proapoptotic 5-FU, cleavage of poly(ADP-ribose) polymerase 1 (PARP-1), PARP1/2 and p53 induction was assessed as the representative pro-apoptosis readouts.…”

Section: Ris-induced Chemoresistance To Anticancer Drugs Is Due To Atmentioning

confidence: 99%

Acquisition of Chemoresistance and Other Malignancy-related Features of Colorectal Cancer Cells Are Incremented by Ribosome-inactivating Stress

Oh¹,

Lee²,

Park

et al. 2016

Journal of Biological Chemistry

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Colorectal cancer (CRC) as an environmental disease is largely influenced by accumulated epithelial stress from diverse environmental causes. We are exposed to ribosome-related insults, including ribosome-inactivating stress ( Colorectal cancer (CRC)3 is one of most commonly diagnosed cancers in developed countries, with a high morbidity and mortality rate because of metastasis via hepatic venous drainage from the original tumor mass (1, 2). This enables latestage tumors to endow a very high metastatic potential to other organs, which is one of the important reasons for early treatment with surgical resection, chemotherapy, and radiotherapy for CRC patients. Although chemotherapy is the most general and effective strategy of treatment for metastatic colon cancer, occasional chemoresistance to anticancer drugs is a serious bottleneck for a successful cure. Fluorouracil (5-FU) and cisplatin are the first-choice chemotherapy drugs for metastatic colon cancer. 5-FU is a pyrimidine analog that causes DNA damage, ultimately inducing apoptosis. It is a representative chemical that induces tumor suppressor p53 (3,4

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Section: Ris-induced Chemoresistance To Anticancer Drugs Is Due To Atmentioning

confidence: 99%

Acquisition of Chemoresistance and Other Malignancy-related Features of Colorectal Cancer Cells Are Incremented by Ribosome-inactivating Stress

Oh¹,

Lee²,

Park

et al. 2016

Journal of Biological Chemistry

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“…The coevolutionary activities may also lead to multiple drug resistance in the treatments of infectious diseases and cancers [4]. Such issues can be tackled using different therapeutic protocols under different conditions to avoid the adaptation.…”

mentioning

confidence: 99%

Toward Dynamical Systems Medicine: Personalized and Preventive Strategies

Yan¹

2017

Per. Med.

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“…Examples will be imatinib, sorafenib, and sunitinib which block several kinases, and therefore exhibit a range of activities against multiple cancers, as opposed to a single or limited number, targeting drug such as erlotinib or gefitinib. Because the target for these kinase inhibitors is often the ATP-binding pocket, the cancer cells can quickly change the target or switch to a different one, thereby developing resistance 9 . For small molecule drugs, an active efflux system also plays a major role 9 .…”

Section: Small Molecule Anticancer Drugsmentioning

confidence: 99%

Bacterial proteins and peptides in cancer therapy

2014

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Cancer is one of the most deadly diseases worldwide. In the last three decades many efforts have been made focused on understanding how cancer grows and responds to drugs. The dominant drug-development paradigm has been the “one drug, one target.” Based on that, the two main targeted therapies developed to combat cancer include the use of tyrosine kinase inhibitors and monoclonal antibodies. Development of drug resistance and side effects represent the major limiting factors for their use in cancer treatment. Nowadays, a new paradigm for cancer drug discovery is emerging wherein multi-targeted approaches gain ground in cancer therapy. Therefore, to overcome resistance to therapy, it is clear that a new generation of drugs is urgently needed. Here, regarding the concept of multi-targeted therapy, we discuss the challenges of using bacterial proteins and peptides as a new generation of effective anti-cancer drugs.

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Overcoming drug resistance in multi-drug resistant cancers and microorganisms

Cited by 43 publications

References 38 publications

Acquisition of Chemoresistance and Other Malignancy-related Features of Colorectal Cancer Cells Are Incremented by Ribosome-inactivating Stress

Acquisition of Chemoresistance and Other Malignancy-related Features of Colorectal Cancer Cells Are Incremented by Ribosome-inactivating Stress

Toward Dynamical Systems Medicine: Personalized and Preventive Strategies

Bacterial proteins and peptides in cancer therapy

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