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Journal articles on the topic 'Anti-Ramsey number'

Author: Grafiati
Published: 6 September 2023
Last updated: 25 May 2024

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1

Gorgol, Izolda, and Anna Lechowska. "Anti-Ramsey number of Hanoi graphs." Discussiones Mathematicae Graph Theory 39, no. 1 (2019): 285. http://dx.doi.org/10.7151/dmgt.2078.

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2

Haas, Ruth, and Michael Young. "The anti-Ramsey number of perfect matching." Discrete Mathematics 312, no. 5 (March 2012): 933–37. http://dx.doi.org/10.1016/j.disc.2011.10.017.

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3

Özkahya, Lale, and Michael Young. "Anti-Ramsey number of matchings in hypergraphs." Discrete Mathematics 313, no. 20 (October 2013): 2359–64. http://dx.doi.org/10.1016/j.disc.2013.06.015.

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4

Fang, Chunqiu, Ervin Győri, Mei Lu, and Jimeng Xiao. "On the anti-Ramsey number of forests." Discrete Applied Mathematics 291 (March 2021): 129–42. http://dx.doi.org/10.1016/j.dam.2020.08.027.

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5

余, 婷. "Anti-Ramsey Number of 4-Cycle in Complete Multipartite Graphs." Advances in Applied Mathematics 10, no. 07 (2021): 2378–84. http://dx.doi.org/10.12677/aam.2021.107249.

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6

Axenovich, Maria, Tao Jiang, and Z. Tuza. "Local Anti-Ramsey Numbers of Graphs." Combinatorics, Probability and Computing 12, no. 5-6 (November 2003): 495–511. http://dx.doi.org/10.1017/s0963548303005868.

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A subgraph H in an edge-colouring is properly coloured if incident edges of H are assigned different colours, and H is rainbow if no two edges of H are assigned the same colour. We study properly coloured subgraphs and rainbow subgraphs forced in edge-colourings of complete graphs in which each vertex is incident to a large number of colours.
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7

周, 韦佳. "The Anti-Ramsey Number of Trees in Maximal Out-Planar Graph." Advances in Applied Mathematics 13, no. 01 (2024): 169–75. http://dx.doi.org/10.12677/aam.2024.131020.

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8

Xiang, Changyuan, Yongxin Lan, Qinghua Yan, and Changqing Xu. "The Outer-Planar Anti-Ramsey Number of Matchings." Symmetry 14, no. 6 (June 16, 2022): 1252. http://dx.doi.org/10.3390/sym14061252.

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A subgraph H of an edge-colored graph G is called rainbow if all of its edges have different colors. Let ar(G,H) denote the maximum positive integer t, such that there is a t-edge-colored graph G without any rainbow subgraph H. We denote by kK2 a matching of size k and On the class of all maximal outer-planar graphs on n vertices, respectively. The outer-planar anti-Ramsey number of graph H, denoted by ar(On,H), is defined as max{ar(On,H)|On∈On}. It seems nontrivial to determine the exact values for ar(On,H) because most maximal outer-planar graphs are asymmetry. In this paper, we obtain that ar(On,kK2)≤n+3k−8 for all n≥2k and k≥6, which improves the existing upper bound for ar(On,kK2), and prove that ar(On,kK2)=n+2k−5 for n=2k and k≥5. We also obtain that ar(On,6K2)=n+6 for all n≥29.
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9

Jin, Zemin, Rui Yu, and Yuefang Sun. "Anti-Ramsey number of matchings in outerplanar graphs." Discrete Applied Mathematics 345 (March 2024): 125–35. http://dx.doi.org/10.1016/j.dam.2023.11.049.

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10

Jin, Zemin, Oothan Nweit, Kaijun Wang, and Yuling Wang. "Anti-Ramsey numbers for matchings in regular bipartite graphs." Discrete Mathematics, Algorithms and Applications 09, no. 02 (April 2017): 1750019. http://dx.doi.org/10.1142/s1793830917500197.

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Let [Formula: see text] be a family of graphs. The anti-Ramsey number [Formula: see text] for [Formula: see text] in the graph [Formula: see text] is the maximum number of colors in an edge coloring of [Formula: see text] that does not have any rainbow copy of any graph in [Formula: see text]. In this paper, we consider the anti-Ramsey number for matchings in regular bipartite graphs and determine its value under several conditions.
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11

Ding, Jili, Hong Bian, and Haizheng Yu. "Anti-Ramsey Numbers in Complete k-Partite Graphs." Mathematical Problems in Engineering 2020 (September 7, 2020): 1–5. http://dx.doi.org/10.1155/2020/5136104.

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The anti-Ramsey number ARG,H is the maximum number of colors in an edge-coloring of G such that G contains no rainbow subgraphs isomorphic to H. In this paper, we discuss the anti-Ramsey numbers ARKp1,p2,…,pk,Tn, ARKp1,p2,…,pk,ℳ, and ARKp1,p2,…,pk,C of Kp1,p2,…,pk, where Tn,ℳ, and C denote the family of all spanning trees, the family of all perfect matchings, and the family of all Hamilton cycles in Kp1,p2,…,pk, respectively.
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12

Gorgol, Izolda. "Avoiding rainbow 2-connected subgraphs." Open Mathematics 15, no. 1 (April 17, 2017): 393–97. http://dx.doi.org/10.1515/math-2017-0035.

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Abstract While defining the anti-Ramsey number Erdős, Simonovits and Sós mentioned that the extremal colorings may not be unique. In the paper we discuss the uniqueness of the colorings, generalize the idea of their construction and show how to use it to construct the colorings of the edges of complete split graphs avoiding rainbow 2-connected subgraphs. These colorings give the lower bounds for adequate anti-Ramsey numbers.
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13

Jin, Zemin, Kangyun Zhong, and Yuefang Sun. "Anti-Ramsey Number of Triangles in Complete Multipartite Graphs." Graphs and Combinatorics 37, no. 3 (March 26, 2021): 1025–44. http://dx.doi.org/10.1007/s00373-021-02302-z.

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14

Lu, Linyuan, and Zhiyu Wang. "Anti-Ramsey Number of Edge-Disjoint Rainbow Spanning Trees." SIAM Journal on Discrete Mathematics 34, no. 4 (January 2020): 2346–62. http://dx.doi.org/10.1137/19m1299876.

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15

Guo, Mingyang, Hongliang Lu, and Xing Peng. "Anti-Ramsey Number of Matchings in 3-Uniform Hypergraphs." SIAM Journal on Discrete Mathematics 37, no. 3 (August 31, 2023): 1970–87. http://dx.doi.org/10.1137/22m1503178.

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16

Yousifi, Noorya. "A short proof of anti-Ramsey number for cycles." International Journal of Multidisciplinary Research and Growth Evaluation 2, no. 3 (2021): 108–9. http://dx.doi.org/10.54660/.ijmrge.2021.2.3.108-109.

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Ramsey's theorem states that there exists a least positive integer R(r, s) for which every blue-red edge colouring of the complete graph on R(r, s) vertices contains a blue clique on r vertices or a red clique on s vertices. This work contains a simplified proof of Anti-Ramsey theorem for cycles. If there is an edge e between H and H0, incident to, say, some v ∈ H of color from NEWc(v), then we can make H and H0 connected by adding the edge e and deleting some edge incident to v of the same color as e in H, so the resulting graph G˜ has a connected component of order ≥ 2( k+1/2 ), which contradicts that every connected component is of order ≤ k − 1. Since each component is Hamiltonian and of order ≥ k+1/ 2 , to avoid a rainbow Ck, by the same type of argument as in Claim 1, we must have that |c(H, H0 )| = 1.
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17

罗, 冬连. "The Anti-Ramsey Number of Unconnected Graphs in Plane Triangulation Graphs." Advances in Applied Mathematics 12, no. 06 (2023): 3030–38. http://dx.doi.org/10.12677/aam.2023.126304.

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18

Tang, Yucong, Tong Li, and Guiying Yan. "Anti-Ramsey number of disjoint union of star-like hypergraphs." Discrete Mathematics 347, no. 4 (April 2024): 113748. http://dx.doi.org/10.1016/j.disc.2023.113748.

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19

Xue, Yisai, Erfang Shan, and Liying Kang. "Anti-Ramsey number of matchings in r-partite r-uniform hypergraphs." Discrete Mathematics 345, no. 4 (April 2022): 112782. http://dx.doi.org/10.1016/j.disc.2021.112782.

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20

Jin, Zemin, Yite Wang, Huawei Ma, and Huaping Wang. "Computing the anti-Ramsey number for trees in complete tripartite graph." Applied Mathematics and Computation 456 (November 2023): 128151. http://dx.doi.org/10.1016/j.amc.2023.128151.

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21

Jin, Zemin, Weijia Zhou, Ting Yu, and Yuefang Sun. "Anti-Ramsey number for perfect matchings in 3-regular bipartite graphs." Discrete Mathematics 347, no. 7 (July 2024): 114011. http://dx.doi.org/10.1016/j.disc.2024.114011.

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22

Lu, Linyuan, Andrew Meier, and Zhiyu Wang. "Anti-Ramsey Number of Edge-Disjoint Rainbow Spanning Trees in All Graphs." SIAM Journal on Discrete Mathematics 37, no. 2 (June 20, 2023): 1162–72. http://dx.doi.org/10.1137/21m1428121.

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23

Jiang, T., and D. West. "On the Erdős–Simonovits–Sós Conjecture about the Anti-Ramsey Number of a Cycle." Combinatorics, Probability and Computing 12, no. 5-6 (November 2003): 585–98. http://dx.doi.org/10.1017/s096354830300590x.

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Given a positive integer n and a family of graphs, let denote the maximum number of colours in an edge-colouring of such that no subgraph of belonging to has distinct colours on its edges. Erdös, Simonovits and Sós [6] conjectured for fixed k with that . This has been proved for . For general k, in this paper we improve the previous bound of to . For even k, we further improve it to . We also prove that , which is sharp.
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24

Budden, Mark, and William Stiles. "Anti-Ramsey Hypergraph Numbers." Electronic Journal of Graph Theory and Applications 9, no. 2 (October 16, 2021): 397. http://dx.doi.org/10.5614/ejgta.2021.9.2.12.

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25

Gilboa, Shoni, and Dan Hefetz. "On degree anti-Ramsey numbers." European Journal of Combinatorics 60 (February 2017): 31–41. http://dx.doi.org/10.1016/j.ejc.2016.09.002.

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26

Alon, Noga. "Size and Degree Anti-Ramsey Numbers." Graphs and Combinatorics 31, no. 6 (June 3, 2015): 1833–39. http://dx.doi.org/10.1007/s00373-015-1583-9.

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27

Chen, Gang, Yongxin Lan, and Zi-Xia Song. "Planar anti-Ramsey numbers of matchings." Discrete Mathematics 342, no. 7 (July 2019): 2106–11. http://dx.doi.org/10.1016/j.disc.2019.04.005.

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28

Axenovich, Maria, Kolja Knauer, Judith Stumpp, and Torsten Ueckerdt. "Online and size anti-Ramsey numbers." Journal of Combinatorics 5, no. 1 (2014): 87–114. http://dx.doi.org/10.4310/joc.2014.v5.n1.a4.

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29

Jiang, Tao. "Anti-Ramsey Numbers of Subdivided Graphs." Journal of Combinatorial Theory, Series B 85, no. 2 (July 2002): 361–66. http://dx.doi.org/10.1006/jctb.2001.2105.

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30

Axenovich, Maria, Tao Jiang, and André Kündgen. "Bipartite anti-Ramsey numbers of cycles." Journal of Graph Theory 47, no. 1 (May 25, 2004): 9–28. http://dx.doi.org/10.1002/jgt.20012.

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31

Wu, Fangfang, Shenggui Zhang, Binlong Li, and Jimeng Xiao. "Anti-Ramsey numbers for vertex-disjoint triangles." Discrete Mathematics 346, no. 1 (January 2023): 113123. http://dx.doi.org/10.1016/j.disc.2022.113123.

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32

Gorgol, Izolda. "Anti-Ramsey numbers in complete split graphs." Discrete Mathematics 339, no. 7 (July 2016): 1944–49. http://dx.doi.org/10.1016/j.disc.2015.10.038.

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33

Li, Yibo, Huiqing Liu, and Xiaolan Hu. "Anti-Ramsey numbers for cycles in n-prisms." Discrete Applied Mathematics 322 (December 2022): 1–8. http://dx.doi.org/10.1016/j.dam.2022.07.029.

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34

Xie, Tian-Ying, and Long-Tu Yuan. "On the anti-Ramsey numbers of linear forests." Discrete Mathematics 343, no. 12 (December 2020): 112130. http://dx.doi.org/10.1016/j.disc.2020.112130.

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35

Lan, Yongxin, Yongtang Shi, and Zi-Xia Song. "Planar anti-Ramsey numbers of paths and cycles." Discrete Mathematics 342, no. 11 (November 2019): 3216–24. http://dx.doi.org/10.1016/j.disc.2019.06.034.

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36

Gorgol, Izolda, and Agnieszka Görlich. "Anti-Ramsey numbers for disjoint copies of graphs." Opuscula Mathematica 37, no. 4 (2017): 567. http://dx.doi.org/10.7494/opmath.2017.37.4.567.

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37

Jiang, Tao, and Oleg Pikhurko. "Anti-Ramsey numbers of doubly edge-critical graphs." Journal of Graph Theory 61, no. 3 (July 2009): 210–18. http://dx.doi.org/10.1002/jgt.20380.

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38

Gilboa, Shoni, and Yehuda Roditty. "Anti-Ramsey Numbers of Graphs with Small Connected Components." Graphs and Combinatorics 32, no. 2 (June 3, 2015): 649–62. http://dx.doi.org/10.1007/s00373-015-1581-y.

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39

Gu, Ran, Jiaao Li, and Yongtang Shi. "Anti-Ramsey Numbers of Paths and Cycles in Hypergraphs." SIAM Journal on Discrete Mathematics 34, no. 1 (January 2020): 271–307. http://dx.doi.org/10.1137/19m1244950.

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40

Ryder, Alex B., Jeanne E. Hendrickson, and Christopher A. Tormey. "Chronic Inflammatory Autoimmune Disorders Are a Risk Factor for Blood Group Alloimmunization in Transfused Patients." Blood 124, no. 21 (December 6, 2014): 4294. http://dx.doi.org/10.1182/blood.v124.21.4294.4294.

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Abstract Background: Alloimmunization to red blood cell (RBC) antigens is a clinically-significant problem, but the mechanisms underlying antibody induction remain poorly understood. Data from murine models has suggested that inflammation can promote blood group alloimmunization. To our knowledge, only one group (Ramsey & Smietana, Transfusion 1995;35:582) has examined the influence of inflammation on RBC alloimmunization; however, study subjects were predominantly female, making it difficult to determine the contribution of inflammation towards transfusion-related alloimmunization. Thus, the aim of our study was to examine whether inflammation associated with chronic autoimmune disorders increases the risk for development of transfusion-related RBC alloantibodies in a primarily male patient cohort. Methods: The transfusion records of alloimmunized patients at a Veterans’ Affairs facility were extracted from a large database of individuals who underwent type and screen testing from 1961 through May, 2014. For alloimmunized patients, the following information was retrospectively collected: 1) demographic data including gender, 2) the number and specificity of alloantibodies reactive at 37°C and/or antihuman globulin phase, and 3) the presence of an underlying chronic inflammatory autoimmune disorder (and the specific diagnosis, as applicable). In addition, the records of 250 randomly-selected patients undergoing RBC administration were reviewed to establish the transfusion rate among individuals with chronic inflammatory autoimmune disorders. Results: Among all patients undergoing type and screen testing at our facility, 220 had one or more detectable alloantibodies. Patients with a chronic inflammatory autoimmune disorder constituted nearly 16% (35/220) of total alloimmunized individuals. These patients formed 50 total alloantibodies (1.4 antibodies per alloimmunized patient). Anti-D (n=10) and anti-K (n=10) were the two most common alloantibodies detected in this group, followed by anti-E (n=8) and anti-C (n=6). Men represented about 86% (30/35) of alloimmunized patients with an autoimmune disorder, indicating that the vast majority of detected antibodies resulted from transfusion rather than pregnancy. The most common autoimmune disorder among alloimmunized patients was psoriasis (9/33; 27%), followed by rheumatoid arthritis (6/33; 18%). Examination of the charts of randomly-selected patients who underwent RBC transfusion showed that 8.4% (21/250) had an underlying chronic inflammatory disorder. The ratio of alloimmunized patients with an autoimmune disease to those without one was significantly different than the ratio of transfused patients with an autoimmune disease to those without one (P=0.012, chi square test; P=0.018, chi square test with Yates’ correction for continuity). Conclusions: Patients with autoimmune diseases represented a substantial portion of individuals with transfusion-associated alloantibodies. Patients with chronic inflammatory disorders formed alloantibodies at nearly double the rate at which they were transfused. As such, precautionary interventions (e.g., extended phenotypic matching for K, E, and C antigens) may be warranted for patients with chronic inflammatory disorders. Disclosures No relevant conflicts of interest to declare.
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41

Zhang, Meiqiao, and Fengming Dong. "Anti-Ramsey numbers for trees in complete multi-partite graphs." Discrete Mathematics 345, no. 12 (December 2022): 113100. http://dx.doi.org/10.1016/j.disc.2022.113100.

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42

Liu, Huiqing, Mei Lu, and Shunzhe Zhang. "Anti-Ramsey numbers for cycles in the generalized Petersen graphs." Applied Mathematics and Computation 430 (October 2022): 127277. http://dx.doi.org/10.1016/j.amc.2022.127277.

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43

Jin, Zemin. "Anti-Ramsey numbers for matchings in 3-regular bipartite graphs." Applied Mathematics and Computation 292 (January 2017): 114–19. http://dx.doi.org/10.1016/j.amc.2016.07.037.

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44

Jungic, V., J. Licht, M. Mahdian, J. Nesetril, and R. Radoicic. "Rainbow Arithmetic Progressions and Anti-Ramsey Results." Combinatorics, Probability and Computing 12, no. 5-6 (November 2003): 599–620. http://dx.doi.org/10.1017/s096354830300587x.

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The van der Waerden theorem in Ramsey theory states that, for every k and t and sufficiently large N, every k-colouring of [N] contains a monochromatic arithmetic progression of length t. Motivated by this result, Radoičić conjectured that every equinumerous 3-colouring of [3n] contains a 3-term rainbow arithmetic progression, i.e., an arithmetic progression whose terms are coloured with distinct colours. In this paper, we prove that every 3-colouring of the set of natural numbers for which each colour class has density more than 1/6, contains a 3-term rainbow arithmetic progression. We also prove similar results for colourings of . Finally, we give a general perspective on other anti-Ramsey-type problems that can be considered.
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45

Pei, Yifan, Yongxin Lan, and Hua He. "Improved bounds for anti-Ramsey numbers of matchings in outer-planar graphs." Applied Mathematics and Computation 418 (April 2022): 126843. http://dx.doi.org/10.1016/j.amc.2021.126843.

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46

Fang, Chunqiu, Ervin Győri, Binlong Li, and Jimeng Xiao. "The anti-Ramsey numbers of C3 and C4 in complete r-partite graphs." Discrete Mathematics 344, no. 11 (November 2021): 112540. http://dx.doi.org/10.1016/j.disc.2021.112540.

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47

Chandran, L. Sunil, Talha Hashim, Dalu Jacob, Rogers Mathew, Deepak Rajendraprasad, and Nitin Singh. "New bounds on the anti-Ramsey numbers of star graphs via maximum edge q-coloring." Discrete Mathematics 347, no. 4 (April 2024): 113894. http://dx.doi.org/10.1016/j.disc.2024.113894.

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48

Fischer, Melissa A., Maria Arrate, Merrida A. Childress, Brianna N. Smith, Yuanbin Song, Rana Gbyli, Thomas Stricker, Stephanie Halene, and Michael R. Savona. "Variable Response to BCL2 Inhibition in MDS Is Enhanced across MDS Subtypes with Synergistic Combination of BCL2+MCL1 Inhibition." Blood 134, Supplement_1 (November 13, 2019): 2982. http://dx.doi.org/10.1182/blood-2019-126578.

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Myelodysplastic syndromes (MDS) are heterogeneous bone marrow failure neoplasms marked by cytopenias, reduced quality of life and predilection to transform into AML. While several treatments for AML have recently been approved, the available treatments for MDS are lacking, and adaptation of AML therapy to MDS is complicated. This is due, in part, to the heterogeneity of MDS. Despite this heterogeneity, most clonal cells in MDS have an imbalance of mitochondrial-controlled BCL2 family proteins resulting in dysregulated apoptosis. These anti- (or pro-) apoptotic proteins compete for ligand to block (or promote) apoptosis, providing an opportunity to selectively target anti-apoptotic proteins and advance therapy for MDS. Venetoclax (VEN), a newly FDA-approved therapy that specifically inhibits the anti-apoptotic protein BCL2, has yielded response rates of up to 50-70% in elderly AML including impressive responses in transformed MDS which previously failed DNMTi (DiNardo et al, 2019, Wei et al, 2019). Upregulation of the anti-apoptotic protein, induced myeloid cell leukemia-1 (MCL1), is a known resistance mechanism in AML resistant or refractory to BCL2 inhibition (Pan et al, 2014), and MCL1 increases when some MDS samples are treated with BCL2 inhibitors (Jilg et al, 2016). Therefore, strategic inhibition of BCL2 and/or MCL1 is a logical therapeutic approach in MDS. We have shown efficacy of MCL1 inhibitors in the laboratory against AML patient samples that are dependent on MCL1 protein or resistant to BCL2 inhibition, including AML cells that arose from MDS (Ramsey et al, 2018). Here, our goal was to determine the sensitivity of MDS cells to inhibition of specific anti-apoptotic proteins, elucidate the characteristic determinants of response, and investigate synergy with combined BCL2 and MCL1 inhibition. We cultured MDS patient samples and determined the in vitro sensitivity of 35 MDS patient samples to selective BCL2, BCL-XL and MCL1 inhibitors using CellTiter-Glo to determine the relative cell viability concentrations (GI50) for each selective inhibitor after 48 hours of exposure. While there was little sensitivity to BCL-XL inhibition across all samples, we detected a gradient of low to high response to the BCL2 inhibitor with low to higher blast count MDS subtypes; higher blast count MDS (EB1 and EB2) were more sensitive than low blast count subtypes (RS-SLD/MLD and MLD). Interestingly, nearly all MDS subtypes were sensitive to the selective MCL1 inhibitor, S63845. To determine if there were any correlations between sensitivity to specific inhibitors and mutational status, a targeted NGS panel of 37 commonly mutated genes in myeloid disease was conducted on all samples. As expected, we observed an increased number of SF3B1 mutations in the lower blast count MDS-RS patient samples. Likewise, though there were only two samples in this cohort containing mutations in PTPN11, one was completely resistant to BCL2 inhibition.(Stevens et al, ASH 2018) Otherwise, we did not observe any correlation between specific mutations and BH3 dependence. Since upregulation of MCL1 is seen in VEN treated MDS cells and is a known resistance mechanism for VEN treatment in AML, we treated these same patient samples with VEN+S63845 to determine any synergistic benefit of combining these drugs. While there were differential responses to VEN monotherapy between subtypes, all MDS subtypes exhibited response benefit to the addition S63845 to VEN. Drug synergy was confirmed with the Zero Interaction Potency model. These results were further corroborated by increased annexin-V staining and reduced colony formation in methylcellulose. Toxicity experiments in the MISTRG immunocompromised animal model indicate that the combination of selective inhibitors of MCL1 and BCL2 are tolerated, and treatment of MDS within these xenografts is underway and will be presented. Overall, our data suggests that higher blast count MDS subtypes (EB1 and EB2) are more likely to respond to VEN monotherapy than low blast count subtypes, while all MDS subtypes may respond to MCL1 inhibition. Moreover, drug synergy can be obtained across all subtypes of MDS by combining BCL2 and MCL1 inhibitors. BCL2 inhibition is changing the standard of care in AML, thus, refining the design of clinical trials testing BCL2 and MCL1 inhibitors in MDS and the precision of patient selection for therapy is a great priority. Disclosures Savona: Boehringer Ingelheim: Patents & Royalties; Celgene Corporation: Membership on an entity's Board of Directors or advisory committees; AbbVie: Membership on an entity's Board of Directors or advisory committees; TG Therapeutics: Membership on an entity's Board of Directors or advisory committees, Research Funding; Sunesis: Research Funding; Incyte Corporation: Membership on an entity's Board of Directors or advisory committees, Research Funding; Karyopharm Therapeutics: Consultancy, Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Selvita: Membership on an entity's Board of Directors or advisory committees; Takeda: Membership on an entity's Board of Directors or advisory committees, Research Funding.
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49

Saud Sunny, S., N. Islam, and A. T. M. Asaduzzaman. "AB0546 DETERMINANTS OF VASCULITIS IN SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1400.2–1400. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4274.

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BackgroundAmong the manifestations of SLE, vasculitic presentation is common. This study was aimed to identify the predictors of vasculitis in SLE patients.ObjectivesTo identify the determinants of vasculitis in SLE patients.MethodsThe study was conducted in the Department of Rheumatology, BSMMU, Dhaka from December 2019 to January 2021. A total 168 consecutive confirmed cases of SLE patients were enrolled. The patients were evaluated for the features of vasculitic rashes, digital gangrene, mesenteric vasculitis, mononeuritis multiplex. The cutaneous vasculitis was confirmed by a dermatologist. Study subjects were grouped into vasculitic and no vasculitic groups. The disease activity and damage were assessed using SLEDAI and SLICC/ACR DI. The rate of vasculitis was expressed in percentage. The multivariate logistic regression analysis was done to determine the independent predictors of vasculitis in SLE. P value <0.05 was considered significant.ResultsRate of lupus vasculitis was 14.3%. The features shown significant difference between vasculitic and no vasculitic groups were: ACLE (79.2% vs. 18.8%, p<0.001), oral ulcer (70.8% vs. 13.2%, p<0.001), alopecia (83.3% vs. 27.1%, p<0.001), Raynaud’s phenomenon (20.8% vs. 5.6%, p=0.011), fever (54.2% vs. 25.0%, p=0.002), arthritis (70.8% vs. 29.9%, p<0.001), pregnancy loss (68.8% vs. 32.7%, p=0.003), lupus nephritis (25.0% vs. 45.1%, p=0.032), seizure (8.3% vs. 0.7%, p=0.027), pleurisy (8.3% vs. 0.7%, p=0.027), leucopenia (8.3% vs. 1.4%, p=0.049), anti ds-DNA positivity (87.5% vs. 62.5%, p=0.008), hypocomplementemia (87.5% vs. 59%, p=0.003), higher mean SLEDAI (p<0.001) and SLICC/ACR damage index score (p<0.001). Though not significant the rate of antiphospholipid antibody positivity was high (69.2% vs. 42.9%, p=0.052) in vasculitis group. In multivariate logistic regression analysis, higher SLEDAI score (OR = 1.296, 95% CI =1.114-1.508) was positively and lupus nephritis (OR= 0.055, 95% CI =0.007-0.413) was negatively associated with lupus vasculitis.ConclusionIn SLE, vasculitic presentation is common. Higher the SLEDAI score greater the chance of lupus vasculitis.References[1]Aringer, M., Costenbader, K., Daikh, D., Brinks, R., Mosca, M., Ramsey-Goldman, R., et al., (2019). 2019 European League Against Rheumatism/American College of Rheumatology Classification Criteria for Systemic Lupus Erythematosus. Arthritis & Rheumatology, 71(9), pp.1400-1412.[2]Drenkard, C., Villa, A., Reyes, E., Abello, M. and Alarcón-Segovia, D. (1997). Vasculitis in systemic lupus erythematosus. Lupus, 6(3), pp.235-242.[3]Ramos-Casals, M., Nardi, N., Lagrutta, M., Brito-Zerón, P., Bové, A., Delgado, et al., (2006). Vasculitis in Systemic Lupus Erythematosus. Medicine, 85(2), pp.95-104.Table 1.Comparison of clinical features of Lupus vasculitis and without vasculitis (n=168)Clinical featuresLupus vasculitis (n=24) n (%)Without vasculitis (n=144) n (%)p-valueFever13 (54.2)36 (25.0)0.002γSLE specific skin lesionsACLE19 (79.2)27(18.8)<0.001γSCLE1 (4.2)6(4.2)0.500*SLE non-specific skin lesionsOral ulcer17 (70.8)19 (13.2)<0.001γAlopecia20 (83.3)39 (27.1)<0.001γ Raynaud’s5 (20.8)8 (5.6)0.011*Arthritis17 (70.8)43 29.9)<0.001γLupus nephritisa6 (25.0)65 (45.1)0.032γNeuro psychiatricSeizure2 (8.3)1 (0.7)0.027*Psychosis1 (4.2)2 (1.4)0.186*SerositisPleurisyPericarditis2 (8.3)1 (4.2)1 (0.7)3 (2.1)0.027*0.231*Pregnancy loss11/16 (68.8)32/98 (32.7)0.003γDVT1 (4.2)6 (4.2)0.500*APS3 (12.5)11 (7.6)0.213*AVN1 (4.2)2 (1.4)0.186*Pulmonary HTN2 (8.3)3 (2.1)0.074** Fisherʼs eхact test; γ chi-Square test, p < 0.05 is considered statistically significant, n: Number, %: Percent.ACLE: Acute Cutaneous Lupus Erythematosus, SCLE: Sub-acute Cutaneous Lupus Erythematosus, DVT: Deep Vein Thrombosis, APS: Anti Phospholipid Antibody Syndrome, AVN: Avascular necrosis, HTN: Hypertension,a: all diagnosed cases of lupus nephritis, presented with or without flareAcknowledgementsWe acknowledge all of our patients for their kind participation in this study. We also acknowledge Prof. Syed Atiqul Haq, Prof. Minhaj Rahim Choudhury, Prof. Abu Shahin, Dr. Md. Masudul Hasaan, Dr. Shamim Ahmed, Dr. Abul Kalam Azad, Department of rheumatology, BSMMU for their support and kind help during the work. At the end we acknowledge BSMMU authority for their support in conducting the study.Disclosure of InterestsNone declared
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Cook, Katherine L., Ramsey Jenshcke, Karen Corleto, Carol Fabian, Stephen Hursting, Bruce Kimler, Danilo Landrock, and Erin Giles. "Abstract PS07-08: Bazedoxifene plus conjugated estrogen reduces mammary proliferation markers and improves adipocyte size, gut microbiome, and metabolic health: Findings from a preclinical model of obesity and breast cancer risk." Cancer Research 84, no. 9_Supplement (May 2, 2024): PS07–08—PS07–08. http://dx.doi.org/10.1158/1538-7445.sabcs23-ps07-08.

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Abstract Background: Many women at high risk for breast cancer will not take tamoxifen or aromatase inhibitors for cancer prevention due to concern of side effects including hot flashes. Further, tamoxifen has detrimental metabolic effects in some overweight/obese women. Duavee®, a tissue-selective complex of bazedoxifene + conjugated estrogen, is FDA-approved for relief of hot-flashes and prevention of osteoporosis. Preclinical studies suggest favorable metabolic effects and potential for breast cancer risk reduction. In a single arm clinical trial, BZA+CE reduced Ki-67 and mammographic density (PMID: 31420361), and this combination is currently being assessed further in a Phase IIB trial of postmenopausal high risk women with vasomotor symptoms. Here, we examined the modifying effects of obesity on response to BZA+CE in a rodent model of obesity and breast cancer risk. Methods: Rats received carcinogen at 7-weeks of age to induce mammary tumors and were fed a high-fat diet (46% kcal fat) to promote obesity. Lean and obese rat were selected based on adiposity at 16 weeks. Separate cohorts of lean and obese ovary-intact or ovariectomized (OVX) rats were randomized to a daily dose of BZA+CE or placebo control for 8 weeks. We assessed tumor development throughout the study and end of study RNA from mammary glands was analysed by gene expression microarray (Affymetrix). We also analyzed body weight/composition, markers of metabolic health (circulating glucose, insulin, adiponectin), as well as changes in the gut microbiome (metagenomic sequencing on DNA isolated from baseline and end-of-study fecal samples) in response to BZA+CE. Results: BZA+CE improved metabolic health in both ovary intact and OVX rats, including reduced body weight and % body fat, particularly in the visceral regions. These effects were greater in obese rats compared to lean. BZA+CE reduced the number of large adipocytes and increased small (insulin sensitive) adipocytes in the mammary adipose, indicating benefical changes in local tumor microenvironment. We found no evidence that Duavee® promoted tumor development or growth in ovary-intact or OVX’d rats. Gene set enrichment analysis (GSEA) of microarray data showed enrichment of cell proliferation pathways in MG from obese rats and these same pathways were downregulated with BZA+CE, consistent with anti-cancer effects. Analysis of the microbiome found that BZA+CE increased proportional abudance of Odoribacter laneus in the gut, regardless of lean/obese or intact/OVX status. Previous studies have demonstrated that this bacterim improves glucose control and reduces inflammatory cytokines when administered to obese mice, suggesting a possible mechanistic link in this study. Conclusions: Unlike traditional SERMs that can have negative metabolic effects, BZA+CE improved whole body and mammary gland metabolic health and reduced expression of cell proliferation pathways, particularly in obese rats. Prelminary data suggest that changes in the gut microbiome could contribute, at least in part, to these effects. Together this supports BZA+CE (Duavee) as an agent with potential beneficial effects on breast cancer risk reduction and improvements in metabolic health in women with obesity. Further analyses will guide assessment of outcomes in an ongoing parallel clinical study in postmenopausal women at high risk for breast cancer. Citation Format: Katherine L. Cook, Ramsey Jenshcke, Karen Corleto, Carol Fabian, Stephen Hursting, Bruce Kimler, Danilo Landrock, Erin Giles. Bazedoxifene plus conjugated estrogen reduces mammary proliferation markers and improves adipocyte size, gut microbiome, and metabolic health: Findings from a preclinical model of obesity and breast cancer risk [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PS07-08.
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