Sandy Chang

15.3k total citations · 4 hit papers
88 papers, 11.3k citations indexed

About

Sandy Chang is a scholar working on Molecular Biology, Physiology and Oncology. According to data from OpenAlex, Sandy Chang has authored 88 papers receiving a total of 11.3k indexed citations (citations by other indexed papers that have themselves been cited), including 71 papers in Molecular Biology, 66 papers in Physiology and 21 papers in Oncology. Recurrent topics in Sandy Chang's work include Telomeres, Telomerase, and Senescence (64 papers), DNA Repair Mechanisms (47 papers) and CRISPR and Genetic Engineering (16 papers). Sandy Chang is often cited by papers focused on Telomeres, Telomerase, and Senescence (64 papers), DNA Repair Mechanisms (47 papers) and CRISPR and Genetic Engineering (16 papers). Sandy Chang collaborates with scholars based in United States, China and Japan. Sandy Chang's co-authors include Ronald A. DePinho, Asha S. Multani, Geoffrey J. Gottlieb, Yibin Deng, K. Lenhard Rudolph, Sunil R. Hingorani, David A. Tuveson, Lifu Wang, Ralph H. Hruban and Anil K. Rustgi and has published in prestigious journals such as Nature, Science and Cell.

In The Last Decade

Sandy Chang

86 papers receiving 11.1k citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice

2005 1.8k citations Asha S. Multani, Sandy Chang et al. profile →
Longevity, Stress Response, and Cancer in Aging Telomerase-Deficient Mice

1999 1.1k citations K. Lenhard Rudolph, Sandy Chang et al. Cell profile →
Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice

2000 873 citations Sandy Chang, Ronald A. DePinho et al. Nature profile →
Endogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects

2004 626 citations Sandy Chang, Ronald A. DePinho et al. profile →

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name	h						Papers	Cites
Sandy Chang United States	46	7.6k	4.9k	3.2k	1.4k	964	88	11.3k
Agata Smogorzewska United States	40	12.2k 1.6×	5.4k 1.1×	2.6k 0.8×	1.8k 1.3×	1.1k 1.2×	71	14.7k
James W. Horner United States	33	6.5k 0.9×	2.0k 0.4×	3.1k 1.0×	1.3k 0.9×	891 0.9×	42	10.0k
Jan Karlseder United States	42	7.3k 1.0×	5.6k 1.1×	876 0.3×	613 0.4×	1.1k 1.2×	67	9.4k
Daniel S. Peeper Netherlands	47	8.9k 1.2×	3.5k 0.7×	4.6k 1.4×	2.6k 1.9×	436 0.5×	115	14.1k
Elinor Ng Eaton United States	16	9.4k 1.3×	3.0k 0.6×	8.1k 2.5×	3.6k 2.6×	407 0.4×	19	15.9k
Scott L. Weinrich United States	22	7.6k 1.0×	8.4k 1.7×	1.5k 0.5×	728 0.5×	830 0.9×	36	12.6k
Manuel Collado Spain	34	5.8k 0.8×	3.2k 0.7×	2.4k 0.7×	1.4k 1.0×	542 0.6×	78	9.2k
Walter D. Funk United States	38	5.4k 0.7×	2.8k 0.6×	1.7k 0.5×	482 0.4×	404 0.4×	66	7.9k
Tracy M. Bryan Australia	36	5.8k 0.8×	3.7k 0.8×	1.7k 0.5×	821 0.6×	515 0.5×	65	8.6k
Mila E. McCurrach United States	20	7.3k 1.0×	2.1k 0.4×	3.6k 1.1×	1.3k 0.9×	318 0.3×	21	9.6k

Countries citing papers authored by Sandy Chang

Since Specialization

Citations

This map shows the geographic impact of Sandy Chang's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Sandy Chang with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Sandy Chang more than expected).

Fields of papers citing papers by Sandy Chang

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Sandy Chang. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Sandy Chang. The network helps show where Sandy Chang may publish in the future.

Co-authorship network of co-authors of Sandy Chang

This figure shows the co-authorship network connecting the top 25 collaborators of Sandy Chang. A scholar is included among the top collaborators of Sandy Chang based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Sandy Chang. Sandy Chang is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

Sort: Min cites: Since: Top N: Style:

20 of 20 papers shown

Chen, Cong, Peili Gu, Jian Wu, et al.. (2017). Structural insights into POT1-TPP1 interaction and POT1 C-terminal mutations in human cancer. Nature Communications. 8(1). 14929–14929. 75 indexed citations

Rai, Rekha, Yong Chen, Ming Lei, & Sandy Chang. (2016). TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions. Nature Communications. 7(1). 10881–10881. 108 indexed citations

Gu, Peili & Sandy Chang. (2013). Functional characterization of human CTC1 mutations reveals novel mechanisms responsible for the pathogenesis of the telomere disease Coats plus. Aging Cell. 12(6). 1100–1109. 58 indexed citations

Akbay, Esra A., Christopher G. Peña, Yuji Nakada, et al.. (2012). Cooperation between p53 and the telomere-protecting shelterin component Pot1a in endometrial carcinogenesis. Oncogene. 32(17). 2211–2219. 24 indexed citations

Flynn, Rachel Litman, Richard C. Centore, Roderick J. O’Sullivan, et al.. (2011). TERRA and hnRNPA1 orchestrate an RPA-to-POT1 switch on telomeric single-stranded DNA. Nature. 471(7339). 532–536. 264 indexed citations

Yang, Gong, Bin Chang, Fan Yang, et al.. (2010). Aurora Kinase A Promotes Ovarian Tumorigenesis through Dysregulation of the Cell Cycle and Suppression of BRCA2. Clinical Cancer Research. 16(12). 3171–3181. 111 indexed citations

Lam, Yung C., Shamima Akhter, Peili Gu, et al.. (2010). SNMIB/Apollo protects leading‐strand telomeres against NHEJ‐mediated repair. The EMBO Journal. 29(13). 2230–2241. 98 indexed citations

Rai, Rekha, Hong Zheng, Hua He, et al.. (2010). The function of classical and alternative non‐homologous end‐joining pathways in the fusion of dysfunctional telomeres. The EMBO Journal. 29(15). 2598–2610. 153 indexed citations

Buis, Jeffrey, Yipin Wu, Yibin Deng, et al.. (2008). Mre11 Nuclease Activity Has Essential Roles in DNA Repair and Genomic Stability Distinct from ATM Activation. Cell. 135(1). 85–96. 269 indexed citations

10.

Cosme‐Blanco, Wilfredo & Sandy Chang. (2008). Dual roles of telomere dysfunction in initiation and suppression of tumorigenesis. Experimental Cell Research. 314(9). 1973–1979. 25 indexed citations

11.

Akli, Saïd, Carolyn S. Van Pelt, Tuyen Bui, et al.. (2007). Overexpression of the Low Molecular Weight Cyclin E in Transgenic Mice Induces Metastatic Mammary Carcinomas through the Disruption of the ARF-p53 Pathway. Cancer Research. 67(15). 7212–7222. 61 indexed citations

12.

Cosme‐Blanco, Wilfredo, Alexander J. Lazar, Sen Pathak, et al.. (2007). Telomere dysfunction suppresses spontaneous tumorigenesis in vivo by initiating p53‐dependent cellular senescence. EMBO Reports. 8(5). 497–503. 156 indexed citations

13.

Bhatia, Bobby, Asha S. Multani, Lubna Patrawala, et al.. (2007). Evidence that senescent human prostate epithelial cells enhance tumorigenicity: Cell fusion as a potential mechanism and inhibition by p16INK4a and hTERT. International Journal of Cancer. 122(7). 1483–1495. 38 indexed citations

14.

Guo, Xiaolan, Yibin Deng, Yahong Lin, et al.. (2007). Dysfunctional telomeres activate an ATM‐ATR‐dependent DNA damage response to suppress tumorigenesis. The EMBO Journal. 26(22). 4709–4719. 197 indexed citations

15.

Wong, Kwok‐Kin, Sandy Chang, & Ronald A. DePinho. (2006). 5 Modeling Cancer and Aging in the Telomerase-deficient Mouse. Cold Spring Harbor Monograph Archive. 45. 109–138. 3 indexed citations

16.

Akli, Saïd, Asha S. Multani, Hannah F. Wingate, et al.. (2004). Tumor-Specific Low Molecular Weight Forms of Cyclin E Induce Genomic Instability and Resistance to p21, p27, and Antiestrogens in Breast Cancer. Cancer Research. 64(9). 3198–3208. 117 indexed citations

17.

Ranganathan, Velvizhi, Walter Heine, David Ciccone, et al.. (2001). Rescue of a telomere length defect of Nijmegen breakage syndrome cells requires NBS and telomerase catalytic subunit. Current Biology. 11(12). 962–966. 94 indexed citations

18.

Chang, Sandy, Katryn J. Stacey, Jianmin Chen, et al.. (1999). Mechanisms of regulation of the MacMARCKS gene in macrophages by bacterial lipopolysaccharide. Journal of Leukocyte Biology. 66(3). 528–534. 21 indexed citations

19.

Myat, Monn Monn, Sandy Chang, Enrique Rodríguez-Boulan, & Alan Aderem. (1998). Identification of the basolateral targeting determinant of a peripheral membrane protein, MacMARCKS, in polarized cells. Current Biology. 8(12). 677–683. 24 indexed citations

20.

Aksoy, Serap, Suzanne Williams, Sandy Chang, & Frank F. Richards. (1990). SLACS retrotransposon fromTrypanosoma brucei gambienseis similar to mammalian LINEs. Nucleic Acids Research. 18(4). 785–792. 74 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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