Chemotherapy

Chemotherapy (often abbreviated to chemo and sometimes CTX or CTx) is a type of cancer treatment that uses one or more anti-cancer drugs (chemotherapeutic agents or alkylating agents) as part of a standardized chemotherapy regimen. Chemotherapy may be given with a curative intent (which almost always involves combinations of drugs) or it may aim to prolong life or to reduce symptoms (palliative chemotherapy). Chemotherapy is one of the major categories of the medical discipline specifically devoted to pharmacotherapy for cancer, which is called medical oncology. The term chemotherapy has come to connote non-specific usage of intracellular poisons to inhibit mitosis (cell division) or induce DNA damage, which is why inhibition of DNA repair can augment chemotherapy. The connotation of the word chemotherapy excludes more selective agents that block extracellular signals (signal transduction). The development of therapies with specific molecular or genetic targets, which inhibit growth-p

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This course provides a comprehensive overview of the biology of cancer, illustrating the mechanisms that cancer cells use to grow and disseminate at the expense of normal tissues and organs.

This course introduces the student to the fudamentals of pharmacology, pharmacokinetics and drug-receptor interactions. It discusses also pharmacogenetics and chronopharmacology, to exemplify the challenges of personalized medicine.

The course covers in detail molecular mechanisms of cancer development with emphasis on cell cycle control, genome stability, oncogenes and tumor suppressor genes.

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Cancer

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spr

Leukemia

Leukemia (also spelled leukaemia and pronounced luːˈkiːmiːə ) is a group of blood cancers that usually begin in the bone marrow and result in high numbers of abnormal blood ce

Radiation therapy

Radiation therapy or radiotherapy, often abbreviated RT, RTx, or XRT, is a therapy using ionizing radiation, generally provided as part of cancer treatment to control or kill malignant cells and norma

DNA-Liposome Hybrid Carriers for Triggered Cargo Release

Diana Kornelia Morzy

The design of simple and versatile synthetic routes to accomplish triggered-release properties in carriers is of particular interest for drug delivery purposes. In this context, the programmability and adaptability of DNA nanoarchitectures in combination with liposomes have great potential to render biocompatible hybrid carriers for triggered cargo release. We present an approach to form a DNA mesh on large unilamellar liposomes incorporating a stimuli-responsive DNA building block. Upon incubation with a single-stranded DNA trigger sequence, a hairpin closes, and the DNA building block is allowed to self-contract. We demonstrate the actuation of this building block by single-molecule Forster resonance energy transfer (FRET), fluorescence recovery after photobleaching, and fluorescence quenching measurements. By triggering this process, we demonstrate the elevated release of the dye calcein from the DNA- liposome hybrid carriers. Interestingly, the incubation of the doxorubicin-laden active hybrid carrier with HEK293T cells suggests increased cytotoxicity relative to a control carrier without the triggered-release mechanism. In the future, the trigger could be provided by peritumoral nucleic acid sequences and lead to site-selective release of encapsulated chemotherapeutics.

AMER CHEMICAL SOC2022

Development of mass spectrometric methods to understand the mechanism of action of transition metal-based anticancer compounds

Fook Seng Ronald Lee

Metal based anti-cancer drugs (metallodrugs) such as cisplatin are a cornerstone of cancer chemotherapy. However, development of this class of compound has been hindered by our lack of understanding of how they function. This is mainly because existing method to study the mechanism of action of metallodrugs are lacking as they were either directly adapted from methods to study organic drugs which have very different chemical properties or current limits in technology and knowledge were a bottleneck to the development of suitable methods. Mass spectrometry (MS) has emerged as a powerful tool which can be applied to study the mechanism of action of metallodrugs. Many different MS methods exist which can be adapted to study different aspects of drug action while accounting for the unique chemical nature of metallodrugs. In this dissertation, we develop MS strategies to study how platinum and ruthenium metallodrugs work and study a few important aspects of their function. Firstly, the in vitro distribution of and ligand state of metallodrugs were studied by imaging mass spectrometry. Next, we attempted to find novel protein targets of metallodrugs using a novel protein expression profiling approach. Promising metallodrug protein targets obtained from this study were then validated via biochemical methods. To facilitate the application of MS based protein-metallodrug fragmentation experiments for finding binding sites of metallodrugs on proteins, we developed and optimized web-based tools for automatic processing of complex spectra from these experiment. We then applied these tools to study the interaction of metallodrugs on relevant proteins, which provided insight into the specific binding properties of metallodrugs on proteins.

EPFL2016

Type I interferon/IRF7 axis instigates chemotherapy-induced immunological dormancy in breast cancer

Mauro Delorenzi, Yu-Ting Huang

Neoadjuvant and adjuvant chemotherapies provide survival benefits to breast cancer patients, in particular in estrogen receptor negative (ER-) cancers, by reducing rates of recurrences. It is assumed that the benefits of (neo)adjuvant chemotherapy are due to the killing of disseminated, residual cancer cells, however, there is no formal evidence for it. Here, we provide experimental evidence that ER- breast cancer cells that survived high-dose Doxorubicin and Methotrexate based chemotherapies elicit a state of immunological dormancy. Hallmark of this dormant phenotype is the sustained activation of the IRF7/IFN-beta/IFNAR axis subsisting beyond chemotherapy treatment. Upregulation of IRF7 in treated cancer cells promoted resistance to chemotherapy, reduced cell growth and induced switching of the response from a myeloid derived suppressor cell-dominated immune response to a CD4(+)/CD8(+) T cell-dependent anti-tumor response. IRF7 silencing in tumor cells or systemic blocking of IFNAR reversed the state of dormancy, while spontaneous escape from dormancy was associated with loss of IFN-beta production. Presence of IFN-beta in the circulation of ER- breast cancer patients treated with neoadjuvant Epirubicin chemotherapy correlated with a significantly longer distant metastasis-free survival. These findings establish chemotherapy-induced immunological dormancy in ER- breast cancer as a novel concept for (neo)adjuvant chemotherapy activity, and implicate sustained activation of the IRF7/IFN-beta/IFNAR pathway in this effect. Further, IFN-beta emerges as a potential predictive biomarker and therapeutic molecule to improve outcome of ER- breast cancer patients treated with (neo)adjuvant chemotherapy.

Springer2019

This course provides a comprehensive overview of the biology of cancer, illustrating the mechanisms that cancer cells use to grow and disseminate at the expense of normal tissues and organs.

The course covers in detail molecular mechanisms of cancer development with emphasis on cell cycle control, genome stability, oncogenes and tumor suppressor genes.