Sarcoma cancer curable.

Traducere "de cancer la oase" în engleză

Chemotherapeutic sarcoma cancer curable can be classified based on the following criteria: chemical properties or mechanism of action; source e. Based on the modality sarcoma cancer curable which they are obtained, their mechanism of action and sarcoma cancer curable biochemical structure, chemotherapeutic agents are divided into several classes. Alkylating agents Alkylating agents sarcoma cancer curable a diverse group of chemical compounds capable of forming molecular bonds with nucleic acids, proteins, and many other low weight molecules.

These compounds are electrophilic avid for electrons or generate electrophilic radicals in vivo that form covalent bonds with the molecule regions that have a positive charge. Alkylating agents have the ability of forming compounds attached to DNA DNA adducts by covalent bonds via an alkyl group.

The cytotoxic effect occurs due to the interaction between electrophilic radicals and DNA, by substitution reactions, interstrand bonds or strand breaking, eventually with inhibition or inadequate replication, alteration of information coded in DNA, and cell death.

Sarcomas: A Rare, Serious Cancer

The alkylating agents more frequently used in the present are: cyclophosphamide, ifosphamide, dacarbazine, temozolomide, trabectedin, and others 4,5. Platinum salts platinum analogues Besides the ability to form G-G intrastrand DNA links adducts like classic alkylating agents do, platinum salts also have the ability to form intrastrand crosslinks, affecting replication and transcription.

Recent studies highlighted the repair mechanisms involved in the DNA lesions after chemotherapy with platinum salts. Sarcoma cancer curable the substances of current therapeutic use in this categ­ory we note: cisplatin, carboplatin, and oxaliplatin 3,4,5.

Antimetabolites Antimetabolites are a group of compounds with low molecular weight that perform their function due to their structural or functional similarity with the natural metabolites involved in nucleic acid synthesis.

Sarcoma cancer curable structural analogues sarcoma cancer curable metabolites involved in DNA and RNA synthesis, they act by competition with these for a catalytic site or regulator of certain key enzymes sarcoma cancer curable by their substitution and incorporation in DNA or RNA, in the synthesis S phase of the cell cycle.

By inhibiting critical enzymes involved in nucleic acid synthesis or by becoming incorporated in the nucleic acid, they cause incorrect coding. Both mechanisms cause cell death via inhibition of the DNA synthesis.

Chimioterapia citotoxică – principii şi indicaţii în cancer

sarcoma cancer curable Blocking the DNA synthesis, antimetabolites are very active on cells with a rapid growth, and they are all considered S cell cycle-phase specific. Frequently used antimetabolites are: methotrexate, pemetrexed, 5-fluorouracil, capecitabine oral fluoropyrimidinegemcitabine. Natural derivatives Natural products are grouped together as they are derived from natural sources.

The group includes usual cytostatic agents, products of vegetal extraction, fermentation products of various Streptomyces fungi species, and bacterial products 9. Three subgroups are included: antitumor antibiotics topoisomerase I and II inhibitors cytostatic agents that act on the microtubules of the division spindle.

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Antitumor antibiotics a. Anthracyclines: doxorubicin Adriamicin®epirubicin Farmorubicin®daunorubicin, idarubicin. The mechanism of action of anthracyclines is complex, and it involves: intercalation between the base pairs of the DNA alkylating-like topoisomerase II inhibitors: anthracyclines form a ternary cleavable complex with DNA-topoisomerase II, that grasps the DNA chains generation of free oxygen radicals that damage the macromolecules via REDOX oxidation cycles sarcoma cancer curable peroxidation of membrane lipids, which explains the cardiotoxicity of these compounds.

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Non-anthracyclines: mitomycin C, mitoxantrone Novantrone®actinomycin D dactinomycinbleomycin 4,5. Topoisomerase inhibitors Topoisomerase I is a nuclear enzyme that acts on a single DNA strand, counteracting the additional torsion that sarcoma cancer curable during replication. In a first step it sections a strand, thus allowing the rotation of the other strand and the detensioning of the chain.

Subsequently, the same enzyme is responsible for the reverse process, reconstructing the sectioned area.

She thinks that you might have cancer in your bone.

Topoisomerase II acts on both strands by sectioning them and creating a breach that allows the passing of an intact double-strand fragment, and detensioning of the chain, and then the same enzyme reestablished the continuity. Among the sarcoma cancer curable of topoisomerase I inhibitors sarcoma cancer curable note: irinotecan, topotecan, camptothecin, and lamellarin D, and among those of topoisomerase II inhibitors: etoposide VP16teniposide VM26and, respectively, anthracyclines doxorubicin, epirubicin 4,5.

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Cytostatic agents that act on the division spindle. These include antimitotic agents they act on the division spindle via binding to the microtubule proteins, preventing cell division in the M phase of the cell cycle.

Cytotoxic chemotherapy – principles and indications in cancer

They are classified into Vinca derivatives and taxanes. Vinca rosea alkaloid derivatives are: vincristine vinorelbine vindesine. The cytotoxicity of Vinca alkaloids is mainly related to depolymerization of the microtubules, causing the blockage of the cells in the G and M phases of the cell cycle. Vinca derivatives prevent the forming of microtubules by depolymerization.

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Microtubules are integral components of the mitotic spindle during the metaphase of cell mitosis that contain polymers of tubulin a contractile protein.

Taxanes: paclitaxel, docetaxel, cabazitaxel, nab-pa­cli­ta­xel 3,4,5.

sarcoma cancer curable

Enzymes, retinoids and other sarcoma cancer curable These are represented, for example, by L-asparaginase which decomposes the L-asparagine from the blood, therefore preventing proliferation of lymphoblastsretinoids e.

Table 1.