Crosslinked DNA is repaired in cells by a combination of enzymes and other factors from the nucleotide excision repair (NER) pathway, homologous recombination, and the base excision repair (BER) pathway. To repair interstrand crosslinks in eukaryotes, a 3' flap endonuclease from the NER, XPF-ERCC1, is recruited to the crosslinked DNA, where it assists in 'unhooking' the DNA by cleaving the 3' strand at the crosslink site. The 5' strand is then cleaved, either by XPF-ERCC1 or another endonuclease, forming a double-strand break (DSB), which can then be repaired by the homologous recombination pathway.[17] DNA crosslinks generally cause loss of overlapping sequence information from the two strands of DNA. Therefore, accurate repair of the damage depends on retrieving the lost information from an undamaged homologous chromosome in the same cell. Retrieval can occur by pairing with a sister chromosome produced during a preceding round of replication. In a diploid cell retrieval may also occur by ...
... (NVB), sold under the brand name Navelbine among others, is a chemotherapy medication used to treat a number of types of cancer.[3] This includes breast cancer and non-small cell lung cancer.[3] It is given by injection into a vein or by mouth.[3][1] Common side effects include bone marrow suppression, pain at the site of injection, vomiting, feeling tired, numbness, and diarrhea.[3] Other serious side effects include shortness of breath.[3] Use during pregnancy may harm the baby.[3] Vinorelbine is in the vinca alkaloid family of medications.[1] It is believed to work by disrupting the normal function of microtubules and thereby stopping cell division.[3] Vinorelbine was approved for medical use in the United States in 1994.[3] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[4] The wholesale price in the developing world as of 2014 is between 18.10 and 42.82 USD per 50 mg vial.[5] This amount in ...
Clinical symptoms include diarrhea, fever, fatigue, nausea, cough, pneumonia, abdominal pain, chills and rash. Laboratory abnormalities may include: neutropenia, hypertriglyceridemia, hyperglycemia and elevated levels of liver enzymes. Idelalisib's safety and effectiveness to treat relapsed FL and relapsed SLL were established in a clinical trial with 123 participants with slow-growing (indolent) non-Hodgkin lymphomas. All participants were treated with idelalisib and were evaluated for complete or partial disappearance of their cancer after treatment (objective response rate, or ORR). Results showed 54% of participants with relapsed FL and 58% of participants with SLL experienced ORR.[7] The U.S. label for idelalisib has a boxed warning describing toxicities that can be serious and fatal, including liver toxicity, severe diarrhea, colon inflammation, lung tissue inflammation (pneumonitis) and intestinal perforation, and the manufacturer was required to put in place a Risk Evaluation and ...
... can lower the body's ability to fight off infection. Those taking it should get permission from a doctor to receive immunizations and vaccinations. It is also recommended that, while on the drug, one should avoid those having recently received oral polio vaccine. This drug was formerly not recommended during pregnancy and early evidence indicated pregnant women on the drug (or the related azathioprine) showed a seven-fold incidence of fetal abnormalities as well as a 20-fold increase in miscarriage.[12] There were also anecdotal reports linking mercaptopurine with spontaneous abortion, leading to the US FDA rating both AZA and mercaptopurine as category D drugs. However, Davis et al. 1999 found mercaptopurine, compared to methotrexate, was ineffective as a single-agent abortifacient; every woman in the mercaptopurine arm of the study had fetal cardiac activity at follow-up (two weeks later) and was given a suction abortion.[13] A more recent, larger study, however, performed by ...
After and/or before[11] the curative resection of colorectal cancer, chemotherapy based on 5-fluorouracil and folinic acid reduces the risk of relapse. The benefit is clinically relevant when cancer has spread to locoregional lymph nodes or penetrated through the wall of the rectum or colon (stage III, Dukes C). The addition of oxaliplatin improves relapse-free survival, but data on overall survival have not yet been published in extenso. When cancer has not spread to the locoregional lymph nodes, nor penetrated through the wall of the rectum or colon (stage II, Dukes B) the benefit of chemotherapy is marginal[citation needed] and the decision on whether to give adjuvant chemotherapy should be carefully evaluated by discussing with the patient the realistic benefits and the possible toxic side effects of treatment. This is even more relevant when the oncologist proposes treatment with oxaliplatin.[why?] ...
... (DTIC), also known as imidazole carboxamide, is a chemotherapy medication used in the treatment of melanoma and Hodgkin's lymphoma.[1] For Hodgkin's it is often used together with vinblastine, bleomycin, and doxorubicin.[1] It is given by injection into a vein.[1] Common side effects include loss of appetite, vomiting, low white blood cell count, and low platelets.[1] Other serious side effects include liver problems and allergic reactions.[1] It is unclear if use in pregnancy is safe for the baby.[1] Dacarbazine is in the alkylating agent and purine analog families of medication.[1] Dacarbazine was approved for medical use in the United States in 1975.[1] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[2] The wholesale cost in the developing world is about US$7.45-18.24 per 200 mg vial.[3] In the United Kingdom this dose costs the NHS about 7.50 pounds.[4] ...
The second generation of mTOR inhibitors is known as ATP-competitive mTOR kinase inhibitors.[7] mTORC1/mTORC2 dual inhibitors are designed to compete with ATP in the catalytic site of mTOR. They inhibit all of the kinase-dependent functions of mTORC1 and mTORC2 and therefore, block the feedback activation of PI3K/AKT signaling, unlike rapalogs that only target mTORC1.[7][18] These types of inhibitors have been developed and several of them are being tested in clinical trials. Like rapalogs, they decrease protein translation, attenuate cell cycle progression, and inhibit angiogenesis in many cancer cell lines and also in human cancer. In fact they have been proven to be more potent than rapalogs.[7] Theoretically, the most important advantages of these mTOR inhibitors is the considerable decrease of AKT phosphorylation on mTORC2 blockade and in addition to a better inhibition on mTORC1.[15] However, some drawbacks exist. Even though these compounds have been effective in rapamycin-insensitive ...
അരിവാൾ കോശ വിളർച്ച, ക്രോണിക് മൈലോജീനസ് ലുക്കീമിയ, ഗർഭാശയ ക്യാൻസർ, പോളിസിത്തീമിയ വെറ എന്നിവയ്ക്കതിരെ ഉപയോഗിക്കുന്ന ഒരു മരുന്നാണ് 'ഹൈഡ്രോക്സി യൂറിയ എന്നും അറിയപ്പെടുന്ന ഹൈഡ്രോക്സി കാർബാമൈഡ്. [1][2]സിക്കിൾ സെൽ ഡിസീസിൽ ഹീമോഗ്ലോബിൻ വർദ്ധിപ്പിക്കുകയും സെൽ ആക്രമണങ്ങളുടെ എണ്ണം കുറയ്ക്കുകയും ചെയ്യുന്നു. ...