| Features: treatment category |
| Chemotherapy is a treatment approach that uses drugs to target and kill rapidly dividing cells, primarily cancer cells. However, because many normal cells also divide quickly (such as those in the bone marrow, digestive tract, and hair follicles), chemotherapy can also affect these cells, leading to a range of side effects. Main Classes of Chemotherapy Agents and Examples Alkylating Agents: -work by adding alkyl groups to DNA, which interferes with the DNA’s structure and prevents replication. Examples: Cyclophosphamide, Ifosfamide, Melphalan, Chlorambucil, Busulfan. Anti-metabolites: -interfere with DNA and RNA synthesis by substituting for the normal building blocks of nucleic acids. Examples: Methotrexate, 5-Fluorouracil (5-FU), Cytarabine, Gemcitabine, 6-Mercaptopurine. Anti-microtubule Agents: -interfere with the structures that separate chromosomes during cell division (mitosis). Examples: Paclitaxel, Docetaxel, Vincristine, Vinblastine. Topoisomerase Inhibitors: -target the enzymes topoisomerase I and II, which control the changes in DNA structure required for replication. Examples: Etoposide (topoisomerase II inhibitor), Irinotecan (topoisomerase I inhibitor), Topotecan. Cytotoxic Antibiotics: -intercalate into DNA, inhibiting the replication of cancer cells. Examples: Doxorubicin, Daunorubicin, Bleomycin, Mitoxantrone. Platinum-Based Agents: -contain platinum and cause cross-linking of DNA, which interferes with DNA repair and replication. Examples: Cisplatin, Carboplatin, Oxaliplatin. Many chemotherapy agents exert their effects, at least in part, by inducing oxidative stress in cancer cells. They can increase ROS levels through several mechanisms: -Direct generation of free radicals. -Disruption of mitochondrial function, leading to increased production of ROS. -Interference with the cell’s antioxidant systems. -May want to avoid antioxidants 7 days bef ore and 7 days after chemo. Examples: NAC, Glutathione, Alpha Lipoic Acid, Vitamin E -anti-oxidants known to have pro-oxidant effects (like Quercetin, Curcumin, etc.) should not be taken 2-3 days before and after chemo -pro-oxidants known to bring good benefit to chemo can be continued during chemo. Examples are: Omega 3, Aremisia Annua, Silver NanoParticles. |
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| Cytochrome c ** The term "release of cytochrome c" ** an increase in level for the cytosol. Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis. The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis. In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death. Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation. Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol. The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death. On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer. On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells. Overexpressed in Breast, Lung, Colon, and Prostrate. Underexpressed in Ovarian, and Pancreatic. |
| 2732- | BetA, | Chemo, | Betulinic acid chemosensitizes breast cancer by triggering ER stress-mediated apoptosis by directly targeting GRP78 |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Nor, | MCF10 |
| - | Review, | Var, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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