Huda H. Al‐Khalaf

1.1k total citations
30 papers, 850 citations indexed

About

Huda H. Al‐Khalaf is a scholar working on Molecular Biology, Oncology and Cancer Research. According to data from OpenAlex, Huda H. Al‐Khalaf has authored 30 papers receiving a total of 850 indexed citations (citations by other indexed papers that have themselves been cited), including 21 papers in Molecular Biology, 19 papers in Oncology and 8 papers in Cancer Research. Recurrent topics in Huda H. Al‐Khalaf's work include Cancer-related Molecular Pathways (13 papers), Epigenetics and DNA Methylation (6 papers) and RNA modifications and cancer (6 papers). Huda H. Al‐Khalaf is often cited by papers focused on Cancer-related Molecular Pathways (13 papers), Epigenetics and DNA Methylation (6 papers) and RNA modifications and cancer (6 papers). Huda H. Al‐Khalaf collaborates with scholars based in Saudi Arabia, United States and Canada. Huda H. Al‐Khalaf's co-authors include Abdelilah Aboussekhra, Mai Almohanna, Siti‐Faujiah Hendrayani, Falah Almohanna, Hazem Ghebeh, Shreeram C. Nallar, Dhananjaya V. Kalvakolanu, Abdelbaset Mohamed Elasbali, Gadah Albasher and Bader Almuzzaini and has published in prestigious journals such as Nucleic Acids Research, Journal of Biological Chemistry and PLoS ONE.

In The Last Decade

Huda H. Al‐Khalaf

29 papers receiving 844 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Huda H. Al‐Khalaf Saudi Arabia 17 457 353 223 88 86 30 850
Angela Kueck United States 11 425 0.9× 415 1.2× 229 1.0× 93 1.1× 39 0.5× 14 895
Miaoqing Zhao China 16 425 0.9× 171 0.5× 199 0.9× 67 0.8× 50 0.6× 75 792
Xinzheng Dai China 18 407 0.9× 196 0.6× 196 0.9× 83 0.9× 48 0.6× 29 877
Beibei Liu China 13 477 1.0× 164 0.5× 225 1.0× 79 0.9× 22 0.3× 46 711
Yuanjun Jiang China 18 365 0.8× 117 0.3× 175 0.8× 66 0.8× 41 0.5× 47 734
Falah Almohanna Saudi Arabia 18 470 1.0× 457 1.3× 199 0.9× 46 0.5× 172 2.0× 49 1.1k
Sanjay Kansra United States 18 419 0.9× 171 0.5× 78 0.3× 61 0.7× 29 0.3× 31 770
Jiaming Huang China 17 518 1.1× 216 0.6× 433 1.9× 81 0.9× 18 0.2× 51 932
Junfeng Zhang China 16 391 0.9× 206 0.6× 268 1.2× 84 1.0× 34 0.4× 35 814
Céline Van Themsche Canada 18 544 1.2× 246 0.7× 228 1.0× 41 0.5× 40 0.5× 25 894

Countries citing papers authored by Huda H. Al‐Khalaf

Since Specialization
Citations

This map shows the geographic impact of Huda H. Al‐Khalaf'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 Huda H. Al‐Khalaf with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Huda H. Al‐Khalaf more than expected).

Fields of papers citing papers by Huda H. Al‐Khalaf

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Huda H. Al‐Khalaf. 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 Huda H. Al‐Khalaf. The network helps show where Huda H. Al‐Khalaf may publish in the future.

Co-authorship network of co-authors of Huda H. Al‐Khalaf

This figure shows the co-authorship network connecting the top 25 collaborators of Huda H. Al‐Khalaf. A scholar is included among the top collaborators of Huda H. Al‐Khalaf 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 Huda H. Al‐Khalaf. Huda H. Al‐Khalaf is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
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Aboussekhra, Abdelilah, et al.. (2023). Ionizing radiation normalizes the features of active breast cancer stromal fibroblasts and suppresses their paracrine pro-carcinogenic effects. Translational Oncology. 37. 101780–101780. 3 indexed citations
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Al‐Khalaf, Huda H. & Abdelilah Aboussekhra. (2019). AUF1 positively controls angiogenesis through mRNA stabilization-dependent up-regulation of HIF-1α and VEGF-A in human osteosarcoma. Oncotarget. 10(47). 4868–4879. 15 indexed citations
5.
Al‐Khalaf, Huda H., et al.. (2018). Senescent Breast Luminal Cells Promote Carcinogenesis through Interleukin-8-Dependent Activation of Stromal Fibroblasts. Molecular and Cellular Biology. 39(2). 32 indexed citations
6.
Al‐Khalaf, Huda H. & Abdelilah Aboussekhra. (2016). p16INK4A induces senescence and inhibits EMT through microRNA‐141/microRNA‐146b‐5p‐dependent repression of AUF1. Molecular Carcinogenesis. 56(3). 985–999. 22 indexed citations
7.
Al‐Mazrou, Amer, et al.. (2016). PAC down-regulates estrogen receptor alpha and suppresses epithelial-to-mesenchymal transition in breast cancer cells. BMC Cancer. 16(1). 540–540. 22 indexed citations
8.
Al‐Mazrou, Amer, et al.. (2015). PAC exhibits potent anti‐colon cancer properties through targeting cyclin D1 and suppressing epithelial‐to‐mesenchymal transition. Molecular Carcinogenesis. 55(3). 233–244. 22 indexed citations
9.
Zou, Minjing, Essa Y. Baitei, Roua A. Al‐Rijjal, et al.. (2015). TSH overcomes BrafV600E-induced senescence to promote tumor progression via downregulation of p53 expression in papillary thyroid cancer. Oncogene. 35(15). 1909–1918. 49 indexed citations
10.
Al‐Khalaf, Huda H. & Abdelilah Aboussekhra. (2014). MicroRNA-141 and MicroRNA-146b-5p Inhibit the Prometastatic Mesenchymal Characteristics through the RNA-binding Protein AUF1 Targeting the Transcription Factor ZEB1 and the Protein Kinase AKT. Journal of Biological Chemistry. 289(45). 31433–31447. 53 indexed citations
11.
Al‐Khalaf, Huda H. & Abdelilah Aboussekhra. (2013). p16INK4A Positively Regulates p21WAF1 Expression by suppressing AUF1-dependent mRNA decay. PLoS ONE. 8(7). e70133–e70133. 32 indexed citations
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Al‐Khalaf, Huda H. & Abdelilah Aboussekhra. (2012). Survivin expression increases during aging and enhances the resistance of aged human fibroblasts to genotoxic stress. AGE. 35(3). 549–562. 14 indexed citations
15.
Al‐Khalaf, Huda H., Siti‐Faujiah Hendrayani, & Abdelilah Aboussekhra. (2011). The Atr Protein Kinase Controls UV-Dependent Upregulation of p16INK4A Through Inhibition of Skp2-Related Polyubiquitination/Degradation. Molecular Cancer Research. 9(3). 311–319. 13 indexed citations
16.
Al‐Khalaf, Huda H., Siti‐Faujiah Hendrayani, & Abdelilah Aboussekhra. (2011). ATR controls the p21WAF1/Cip1 protein up‐regulation and apoptosis in response to low UV fluences. Molecular Carcinogenesis. 51(12). 930–938. 13 indexed citations
17.
Al‐Khalaf, Huda H., Bolesław Lach, Ayman Allam, et al.. (2007). Expression of survivin and p16INK4a/Cdk6/pRB proteins and induction of apoptosis in response to radiation and cisplatin in meningioma cells. Brain Research. 1188. 25–34. 19 indexed citations
18.
Al‐Khalaf, Huda H., Bolesław Lach, Ayman Allam, et al.. (2007). The p53/p21 DNA damage-signaling pathway is defective in most meningioma cells. Journal of Neuro-Oncology. 83(1). 9–15. 17 indexed citations
19.
Almohanna, Mai, et al.. (2006). The p16INK4a tumor suppressor controls p21WAF1 induction in response to ultraviolet light. Nucleic Acids Research. 35(1). 223–233. 67 indexed citations
20.
Hassounah, Maher, Bolesław Lach, Ayman Allam, et al.. (2005). Benign tumors from the human nervous system express high levels of survivin and are resistant to spontaneous and radiation-induced apoptosis. Journal of Neuro-Oncology. 72(3). 203–208. 16 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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