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1  mitigating cellular DNA damage formation by platinum compounds.
2 eived adjuvant chemotherapy with taxanes and platinum compounds.
3 stance of cancer cells to therapy, including platinum compounds.
4 ppressor BRCA2 are particularly sensitive to platinum compounds.
5  to bifunctional DNA-damaging agents such as platinum compounds.
6 d affect the ability of cells to internalize platinum compounds.
7  to enhance the sensitivity of SCLC cells to platinum compounds.
8                  The trifunctional dinuclear platinum compounds 1,2/c,c [[cis-PtCl(NH(3))(2)]mu-H(2)N
9           Similar results were obtained with platinum compounds' 5-fluorouracil and irinotecan.
10 maximal cytoreduction, dose-intensity of the platinum compound administered, proportion of patients w
11 he formation of covalent adducts between the platinum compound and certain bases in DNA.
12 and fast ultracentrifuge method here for two platinum compounds and a taxane that otherwise bound irr
13 tro transcription of RNA is inhibited by the platinum compounds and indicate G residues as primary bi
14        Prior treatment with camptothecins or platinum compounds and prior pelvic irradiation were not
15   It also enhances the anticancer effects of platinum compounds and taxanes in non-small-cell lung ca
16 year of diagnosis, exposure to radiation and platinum compounds, and length of follow-up) showed a si
17    Several molecules, including multinuclear platinum compounds, belong to the family of platinum dru
18                                          The platinum compound bound G4 includes multiple complexes f
19  from therapy with PARP inhibitor (PARPi) or platinum compounds, but acquired resistance limits clini
20  cell death ligand 1 (PD-L1) status; type of platinum-compound chemotherapy; number of cycles of neoa
21             The mechanisms of action for the platinum compounds cisplatin and oxaliplatin have yet to
22 has included surgery and chemotherapy with a platinum compound (cisplatin or carboplatin).
23 he hypothesis that activation of the JNKs by platinum compounds controls c-Jun-dependent transcriptio
24 ion of the pharmacological factors affecting platinum compound cytotoxicity such as cellular accumula
25                                              Platinum compounds display clinical activity against a w
26 ioavailability and toxicity of anthropogenic platinum compounds emitted into the environment from sou
27                                              Platinum compounds form electrophilic intermediates that
28                                              Platinum compounds have activity in triple-negative brea
29 utes to cell death by these two broadly used platinum compounds have not yet been carefully explored.
30 s effect was not related to the abundance of platinum compounds in the cochlea, rather cisplatin had
31                                    Cytotoxic platinum compounds including cisplatin are standard canc
32 ated ovarian cancers previously treated with platinum compounds, including five with acquired platinu
33    PARP-1 also binds to DNA damaged by other platinum compounds, including oxaliplatin and pyriplatin
34                                              Platinum compounds induce apoptosis in malignant cells a
35 high risk populations and the integration of platinum compounds into treatment regimens will most lik
36                    The carrier ligand of the platinum compound is likely to affect the conformation o
37          The combination of paclitaxel and a platinum compound is the most active first-line regimen
38          Resistance to alkylating agents and platinum compounds is associated with elevated levels of
39 elting temperature of CT DNA adducted by the platinum compounds is observed at low salt concentration
40 with colorectal cancer, oxaliplatin, a novel platinum compound, is an active agent.
41                BBR3464, a charged trinuclear platinum compound, is the first representative of a new
42     Treatment with genotoxic agents, such as platinum compounds, is still the mainstay therapeutical
43 dination of the stannylenes to palladium and platinum compounds led to unusual silastannene complexes
44  agents with promising activity, such as new platinum compounds, new taxanes, and other cytotoxic age
45 f supramolecular aggregates of a luminescent platinum compound (Pt(AC)).
46   We show that the anticancer 'rule breaker' platinum compound [Pt[N(p-HC6F4)CH2]2py2] preferentially
47  lesions formed by therapeutically effective platinum compounds [Pt(en)Cl2] and [Pt(dach)Cl2], in add
48 the optical properties of the phosphorescent platinum compounds: Pt(II) (2-(4',6'-difluorophenyl)pyri
49 e with representative bifunctional dinuclear platinum compounds [[PtCl(NH(3))(2)](2)mu-H(2)N(CH(2))(n
50               In non-small-cell lung cancer, platinum compounds represent the cornerstone of systemic
51              Understanding the mechanisms of platinum compound resistance, including cisplatin resist
52 e interplay with the solubility of different platinum compounds revealed potassium tetrachloroplatina
53 with mutated BRCA1 or BRCA2 are sensitive to platinum compounds, such carcinomas eventually develop p
54 effective chemotherapeutic agents, including platinum compounds, taxanes, and vinca alkaloids.
55  In particular, most reactions are caused by platinum compounds, taxanes, epipodophyllotoxins and asp
56 cidence or severity of neuropathy related to platinum compounds, taxanes, or thalidomide.
57 e, vinorelbine, the taxanes, anthracyclines, platinum compounds, topoisomerase I and II inhibitors, a
58          Isocyanide-supported cyclometalated platinum compounds undergo nucleophilic addition with di
59 Jun, significantly protected SCLC cells from platinum compounds, whereas expression of a c-Jun mutant
60 actice, metal-based drugs are represented by platinum compounds, which are constituents of a wide var
61 eous mouse mammary tumor model, we show that platinum compounds, which generate DNA breaks during the
62                       Oxaliplatin is a novel platinum compound with clinical activity in several mali
63 le-targeting agents, the effect of combining platinum compounds with programmed cell death 1 (PD-1)/P
64 (4-Me-Py)Cl]+, the interactions of these two platinum compounds with the DNA heptamer CCTG*TCC:GGACAG