Solid/solid interfacial reactions between Sn–0.7 wt% Cu and Ni–7 wt% V

Chen, Chih-Chi; Chen, Sinn-wen; Chang, Chih‐Ming

doi:10.1557/jmr.2008.0235

Cited by 11 publications

(6 citation statements)

References 39 publications

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“…The importance of Top2␣ in VP-16 cytotoxicity is consistent with results from previous studies that the TOP2␣ gene is mutated in cell lines selected for lower levels of resistance to Top2 drugs, and the TOP2␤ gene is mutated only in top2␣ mutant cells selected for higher levels of resistance to Top2 drugs (45,46). It has been suggested that the collision between the replication forks and Top2 cleavage complexes plays a major role in VP-16 cytotoxicity (47); consequently, the predominant role of Top2␣ in DNA replication may lead to more frequent collisions between this isozyme and the replication fork, and hence its higher cytotoxicity.…”

Section: Discussionsupporting

confidence: 89%

Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies

Azarova¹,

Lyu²,

Lin³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

262

222

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Drugs that target DNA topoisomerase II (Top2), including etoposide (VP-16), doxorubicin, and mitoxantrone, are among the most effective anticancer drugs in clinical use. However, Top2-based chemotherapy has been associated with higher incidences of secondary malignancies, notably the development of acute myeloid leukemia in VP-16-treated patients. This association is suggestive of a link between carcinogenesis and Top2-mediated DNA damage. We show here that VP-16-induced carcinogenesis involves mainly the ␤ rather than the ␣ isozyme of Top2. In a mouse skin carcinogenesis model, the incidence of VP-16-induced melanomas in the skin of 7,12-dimethylbenz[a]anthracene-treated mice is found to be significantly higher in TOP2␤ ؉ than in skin-specific top2␤-knockout mice. Furthermore, VP-16-induced DNA sequence rearrangements and double-strand breaks (DSBs) are found to be Top2␤-dependent and preventable by cotreatment with a proteasome inhibitor, suggesting the importance of proteasomal degradation of the Top2␤-DNA cleavage complexes in VP-16-induced DNA sequence rearrangements. VP-16 cytotoxicity in transformed cells expressing both Top2 isozymes is, however, found to be primarily Top2␣-dependent. These results point to the importance of developing Top2␣-specific anticancer drugs for effective chemotherapy without the development of treatment-related secondary malignancies.DNA rearrangements ͉ melanoma ͉ skin-specific topoisomerase II␤-knockout ͉ tumor cell killing ͉ carcinogenesis A nticancer drugs that target DNA topoisomerase II (Top2), including etoposide (VP-16), doxorubicin, and mitoxantrone, are often referred to as Top2 poisons and are among the most effective and widely used anticancer drugs in the clinic. However, life-threatening toxic side effects, including drug-induced secondary malignancies, have been noted in patients receiving Top2-based chemotherapy. An association between infant leukemia and in utero exposure to Top2 poisons has also been reported (reviewed in refs. 1-3). In all cases, the molecular basis underlying carcinogenesis in Top2-based chemotherapy is unclear.Clinical evidence for a direct link between VP-16 treatment and treatment-related acute myeloid leukemia (t-AML) is particularly strong (1-3). VP-16-induced t-AML is frequently associated with balanced translocations between the mixed lineage leukemia (MLL) gene on chromosome 11q23 and Ͼ50 partner genes (the MLL gene is also known as ALL-1, hTRX, or HRX) (4-7). These rearrangements, as well as those found in infant leukemia, cluster within a well characterized 8.3-kb breakpoint cluster region (bcr) (8-16). The bcr of MLL is AT-rich and contains Alu sequences, putative recognition sites of Top2-mediated DNA cleavage, and chromosome scaffold/matrix attachment regions (SAR/MAR) (5,(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). There is substantial evidence that chromosome 11q23 translocations in t-AML and infant leukemia are a consequence of drug-induced formation of double-strand breaks (DSBs) (6-9). VP-16 is known to induce DSBs by the format...

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Section: Discussionsupporting

confidence: 89%

Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies

Azarova¹,

Lyu²,

Lin³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

262

222

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“…Although topoisomerase IIα is essential for the survival of proliferating cells, topoisomerase IIβ is dispensable at the cellular level 52–54. Furthermore, levels of topoisomerase IIα protein rise dramatically during periods of cell growth,55–58 while expression of the β isoform is independent of proliferative status 34, 59–60.…”

Section: Topoisomerase IImentioning

confidence: 99%

The use of divalent metal ions by type II topoisomerases

Deweese

Osheroff

2010

Metallomics

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Type II topoisomerases are essential enzymes that regulate DNA under- and overwinding and remove knots and tangles from the genetic material. In order to carry out their critical physiological functions, these enzymes utilize a double-stranded DNA passage mechanism that requires them to generate a transient double-stranded break. Consequently, while necessary for cell survival, type II topoisomerases also have the capacity to fragment the genome. This feature of the prokaryotic and eukaryotic enzymes, respectively, is exploited to treat a variety of bacterial infections and cancers in humans. All type II topoisomerases require divalent metal ions for catalytic function. These metal ions function in two separate active sites and are necessary for the ATPase and DNA cleavage/ligation activities of the enzymes. ATPase activity is required for the strand passage process and utilizes the metal-dependent binding and hydrolysis of ATP to drive structural rearrangements in the protein. Both the DNA cleavage and ligation activities of type II topoisomerases require divalent metal ions and appear to utilize a novel variant of the canonical two-metal-ion phosphotransferase/hydrolase mechanism to facilitate these reactions. This article will focus primarily on eukaryotic type II topoisomerases and the roles of metal ions in the catalytic functions of these enzymes.

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“…24 The VSn 2 phase was named V 2 Sn 3 in previous studies. 20,25 However, the nomenclature VSn 2 was used in more recent studies. 21,26 …”

Section: Sadp Resultsmentioning

confidence: 99%

“…The observation that V was immobile and Ni diffused out from Ni-V alloys has been reported in the literature. [9][10][11][12][13][15][16][17][18][19][20][21] …”

Section: Stem Line Scan Analysesmentioning

confidence: 99%

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Transmission Electron Microscopy Characterization of Ni(V) Metallization Stressed Under High Current Density in Flip Chip Solder Joints

Tsai

Lin

et al. 2010

Journal of Elec Materi

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The Ni(V) under bump metallization (UBM) in flip chip solder joints is known to be consumed in a two-stage process during current stressing. The Ni(V) UBM transforms first to the ''consumed Ni(V)'' state. Then, this consumed Ni(V) transforms to a so-called porous structure. In this study, the details of the consumed Ni(V) and the porous structure were analyzed by transmission electron microscopy. Bright-field images showed that the consumed Ni(V) was a continuous layer without columnar structures and that the porous structure had many voids in the matrix. The compositional analyses showed that V atoms were immobile and trapped in the original Ni(V) layer. Cu and Sn atoms diffused into the original Ni(V) layer, and Ni atoms diffused outward. Selected-area diffraction patterns and high-resolution transmission electron microscopy of the porous structure showed that it was composed of an amorphous matrix with fine crystalline Cu 6 Sn 5 and VSn 2 phases.

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Solid/solid interfacial reactions between Sn–0.7 wt% Cu and Ni–7 wt% V

Cited by 11 publications

References 39 publications

Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies

Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies

The use of divalent metal ions by type II topoisomerases

Transmission Electron Microscopy Characterization of Ni(V) Metallization Stressed Under High Current Density in Flip Chip Solder Joints

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