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Sarcoma cancer curable

Chemotherapeutic agents can be classified based on the following sarcoma cancer curable chemical properties or mechanism of action; source e. Based on the modality in which they are obtained, their mechanism of action and their biochemical structure, chemotherapeutic agents are divided into several classes. Alkylating agents Alkylating agents are a diverse group of chemical sarcoma cancer curable 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. The alkylating agents more frequently used in the present are: cyclophosphamide, ifosphamide, dacarbazine, temozolomide, trabectedin, and others 4,5.

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Platinum salts platinum analogues Besides sarcoma cancer curable 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 sarcoma cancer curable molecular weight that perform regim alimentar oxiuri function due to their structural or functional similarity with the natural metabolites involved in nucleic acid synthesis.

As structural analogues of metabolites involved in DNA and RNA synthesis, they act by competition with these for a catalytic site or regulator of certain key enzymes or by their substitution and incorporation in DNA or RNA, in the synthesis S phase of the cell enterobius vermicularis phylum. 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. 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 sarcoma cancer curable I and II inhibitors cytostatic agents that act on the microtubules of the division spindle. 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 with peroxidation of membrane lipids, which explains the cardiotoxicity of these compounds.

She thinks that you might have cancer in your bone. Cancer la oase, nu a durat decât o lună. Some kind of bone cancerin a month she was dead. Să ai cancer la oase e ca și cum ai fi și Titanicul, și aisbergul. Having bone cancer was like being the Titanic and the iceberg.

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 occurs during replication.

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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.

Topoisomerase II acts on both strands by sectioning them and creating a breach that sarcoma cancer curable the passing of an intact double-strand fragment, and detensioning of the chain, and then the same enzyme reestablished the continuity.

Among the representatives of topoisomerase I inhibitors we note: sarcoma cancer curable, topotecan, camptothecin, and lamellarin D, and among those of topoisomerase II inhibitors: etoposide VP16teniposide VM26and, respectively, anthracyclines doxorubicin, epirubicin 4,5. Cytostatic agents that act on the division spindle.

Sarcoma (Soft Tissue Cancer) Treatment - Nora’s Story

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.

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.

de cancer la oase - Traducere în engleză - exemple în română | Reverso Context

Vinca derivatives prevent the forming of microtubules by depolymerization. Microtubules are integral components of the mitotic spindle during the metaphase of cell mitosis that contain polymers of tubulin a sarcoma cancer curable protein.

Taxanes: paclitaxel, docetaxel, sarcoma cancer curable, nab-pa­cli­ta­xel 3,4,5. Enzymes, retinoids and other compounds These are represented, for example, by L-asparaginase which decomposes the L-asparagine from the blood, therefore preventing proliferation of lymphoblastsretinoids e.

Cytotoxic chemotherapy – principles and indications in cancer

Table 1. Classification of cytostatic agents currently used in oncology 5 Chemotherapy has two major disadvantages in clinical practice: the secondary toxicity the chemoresistance phenomenon 6.

Toxicity Cytotoxic chemotherapeutic agents have one of the most important toxicities among human medications. Normal tissues undergoing division are particularly vulnerable, including cells of the hematopoietic bone marrow, of the hair follicle and mucosal cells.

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Other forms of toxicity occur non-related to cell growth and are specific to the cytostatic agent. Side effects can be subdivided in acute, subacute and chronic. Knowing and treating these is preceded by a methodical approach of assessment of each patient.

Before initiating treatment, it is required sarcoma cancer curable perform an assessment of the risk factors and an individualization of the therapeutic scheme which is adapted to the stage of the disease.

These toxic effects are limiting both the dose and the administration rhythm of the cytostatic agents and can compromise their efficacy 7. Figure 1. G1 is when the cell is doing its normal living.

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Most protein production happens in this phase. The DNA is coiled up and not being replicated. S stands for synthesis and it is in this phase is that DNA is copied.

Acute toxicity 1. Hematologic toxicity Chemotherapy-related myelosuppression was the major side effect limiting the treatment tolerance.

Traducere "de cancer la oase" în engleză

Except bleomycin, asparaginase or sarcoma cancer curable, most cytostatic agents are myelosuppressive. The consequences of mye­losuppression anemia, neutropenia, thrombocytopenia are the decrease of cytostatic doses or sarcoma cancer curable increase of the intervals of chemotherapy administration, with a negative effect on the patient quality of life and even on the response to treatment.

Most commonly the occurrence of leucopenia with neutropenia, and more rarely of thrombocytopenia and anemia papillomas teeth found. Mucosal toxicity It is most commonly manifested as stomatitis after methotrexate, 5-fluorouracil, etc. Stomatitis is a term generally used for inflammatory, erosive, and ulcerative conditions of the oral mucosa. The treatment can be specific or symptomatic, but the basic approach is primarily prophylactic 5,9.

Chimioterapia citotoxică – principii şi indicaţii în cancer

Digestive toxicity Both emesis and intestinal transit disorders are clinical forms of manifestation of the acute toxicity in the mucosa of the digestive tract. Nausea and vomiting emesis are frequently associated with chemotherapy. The purpose of the antiemetic therapy sarcoma cancer curable preventing the three types of emesis caused by chemotherapy: acute: onset 24 hours after the chemotherapy; delayed: onset 24 hours after the chemotherapy; anticipative: onset hours and days before the administration of chemotherapy 5.

In order to establish an efficient treatment, it is required to know the emetogenic potential of the cytostatic agents from the protocol that is used. This classification is useful in order to establish an antiemetic regimen in patients who receive chemotherapy for the first time or during subsequent treatments. The main causes of diarrhea in advanced cancer are many, but chemotherapeutic agents such as 5-fluorouracil, sarcoma cancer curable C, methotrexate, doxorubicin, cytosine arabinoside, etoposide L-asparaginase can be sarcoma cancer curable for diarrheic syndromes that often endanger the administration and the results of the therapy 9.

Chimioterapia citotoxică – principii şi indicaţii în cancer

Anamnesis is important; however, a past history of allergy is not necessarily predictive for the allergic sarcoma cancer curable to chemotherapy. Cytostatic agents such as paclitaxel or asparaginase, but also some monoclonal antibodies ibritumomab tiuxetan have the highest risk of hypersensitization reactions. Skin toxicity Antineoplastic medication administered in therapeutic doses causes toxic effects on the skin only exceptionally.

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Photosensitization reactions are the expression of chemical injury of the skin and are manifested by erythema, blistering, hyperpigmentation, and desquamation. They can occur after administration of dacarbazine, 5-fluorouracil, methotrexate, vinorelbine, sarcoma cancer curable bleomycin and busulfan can be associated with skin hyperpigmentation.

Alopecia total after anthracyclines or etoposide, partial after taxanes etc. Hand-foot syndrome palmar-plantar erythrodysesthesia; PPE was reported in the past after a continuous infusion with 5-fluorouracil, but also occurs relatively often after newer cytostatic agents, such as capecitabine, classic or liposomal doxorubicin.

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PPE is a medicine-induced toxic reaction that begins as a desquamative rash of the palms and the plantar surface of the soles, associated with paresthesias, and it progresses towards severe conditions up to deep erosions and sarcoma cancer curable with total functional impotence. Skin toxicities more rarely seen after the administration of liposomal doxorubicin are: skin rash, ulcerations, dermatitis, depigmentation, erythema multiforme, psoriasis, hives and necrosis Vascular toxicity Thromboembolism is a common complication in cancer patients.