Arvind Kumar Shukla
@pusan.ac.kr
Department of Biomedical Convergence Engineering
Pusan National University
Arvind Kumar Shukla is working on the molecular mechanism of cancer stem cell biology. He is the main focus in the fabrication of functional tissue and organ development by 3D bioprinting, with a study on stem cells & cancer signaling pathways, and also focuses on various cancer drug delivery methods that are used and tested clinically for treatment.
EDUCATION
Pusan National University (February 2020–February 2024)
Location: Busan, South Korea
Doctor of Philosophy: Biomedical Convergence Engineering (3D Bioprinting, Organ-on-a-chip (OOC), Stem Cells, Cancer).
Dr. D.Y. Patil University (July 2012–July 2014)
Location: Mumbai, India
Master of Science: Genetic Engineering (HIV, Stem Cells, Cancer)
University of Mumbai (February 2008–July 2012)
Location: Mumbai, India
Bachelor of Science: Zoology and Environmental Science
RESEARCH, TEACHING, or OTHER INTERESTS
Cell Biology, Molecular Biology, Genetics, General Pharmacology, Toxicology and Pharmaceutics
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
Gabriella Marfe, Stefania Perna, Giovanna Mirone, and Arvind Kumar Shukla
CRC Press
Arvind Kumar Shukla, Ge Gao, and Byoung Soo Kim
MDPI AG
Induced pluripotent stem cells (iPSCs) are essentially produced by the genetic reprogramming of adult cells. Moreover, iPSC technology prevents the genetic manipulation of embryos. Hence, with the ensured element of safety, they rarely cause ethical concerns when utilized in tissue engineering. Several cumulative outcomes have demonstrated the functional superiority and potency of iPSCs in advanced regenerative medicine. Recently, an emerging trend in 3D bioprinting technology has been a more comprehensive approach to iPSC-based tissue engineering. The principal aim of this review is to provide an understanding of the applications of 3D bioprinting in iPSC-based tissue engineering. This review discusses the generation of iPSCs based on their distinct purpose, divided into two categories: (1) undifferentiated iPSCs applied with 3D bioprinting; (2) differentiated iPSCs applied with 3D bioprinting. Their significant potential is analyzed. Lastly, various applications for engineering tissues and organs have been introduced and discussed in detail.
Raj Kumar Mongre, Chandra Bhushan Mishra, Arvind Kumar Shukla, Amresh Prakash, Samil Jung, Md Ashraf-Uz-Zaman, and Myeong-Sok Lee
MDPI AG
GLOBOCAN 2020 estimated more than 19.3 million new cases, and about 10 million patients were deceased from cancer in 2020. Clinical manifestations showed that several growth factor receptors consisting of transmembrane and cytoplasmic tyrosine kinase (TK) domains play a vital role in cancer progression. Receptor tyrosine kinases (RTKs) are crucial intermediaries of the several cellular pathways and carcinogenesis that directly affect the prognosis and survival of higher tumor grade patients. Tyrosine kinase inhibitors (TKIs) are efficacious drugs for targeted therapy of various cancers. Therefore, RTKs have become a promising therapeutic target to cure cancer. A recent report shows that TKIs are vital mediators of signal transduction and cancer cell proliferation, angiogenesis, and apoptosis. In this review, we discuss the structure and function of RTKs to explore their prime role in cancer therapy. Various TKIs have been developed to date that contribute a lot to treating several types of cancer. These TKI based anticancer drug molecules are also discussed in detail, incorporating their therapeutic efficacy, mechanism of action, and side effects. Additionally, this article focuses on TKIs which are running in the clinical trial and pre-clinical studies. Further, to gain insight into the pathophysiological mechanism of TKIs, we also reviewed the impact of RTK resistance on TKI clinical drugs along with their mechanistic acquired resistance in different cancer types.
Chaima Amri, Arvind Kumar Shukla, and Jin-Ho Lee
MDPI AG
The effectiveness of cancer treatment strongly depends on the early detection of the disease. Currently, the most common diagnostic method, tissue biopsy, takes time and can be damaging to the patient. Circulating cancer biomarkers such as circulating tumor DNA, micro-RNA (miRNA), tumor proteins, exosomes, and circulating tumor cells have repeatedly demonstrated their viability as targets for minimally invasive cancer detection through liquid biopsies. However, among other things, achieving a great sensitivity of detection is still challenging due to the very low concentration of biomarkers in fluid samples. This review will discuss how the recent advances in nanoparticle-based biosensors are overcoming these practical difficulties. This report will be focusing mainly on optical transduction mechanisms of metal nanoparticles (M-NPs), quantum dots (QDs), and upconversion nanoparticles (UCNPs).
Giovanna Mirone, Stefania Perna, Arvind Shukla, and Gabriella Marfe
Wiley
Regorafenib, an oral small‐molecule multi kinase inhibitor, is able to block Vascular Endothelial Growth Factor Receptors (VEGFR‐1, 2, and 3), Platelet‐Derived Growth Factor Receptors (PDGF), Fibroblast Growth Factor (FGF) receptor 1, Raf, TIE‐2, and the kinases KIT, RET, and BRAF. Different studies have displayed its antitumor activity in several cancer models (both in vitro and in vivo), particularly in colorectal and gastrointestinal stromal cancers. The mechanism of resistance to regorafenib is largely unknown. In our investigation, we have generated regorafenib‐resistant SW480 cells (Reg‐R‐SW480 cells) by culturing such cells with increasing concentration of regorafenib. Examination of intracellular signaling found that Akt signaling was activated in Reg‐R‐SW480 cells but not in wild–type SW480 cells, after regorafenib treatment as measured by Western Blot. The Notch pathway is a fundamental signaling system in the development and homeostasis of tissues since it regulates different cellular process such as proliferation, differentiation, and apoptosis and it can be a potential driver of resistance to a wide array of targeted therapies. In this study, we found that Notch‐1 was significantly up‐regulated in resistant tumor cells as well as HES1 and HEY. Additionally, inhibition of Notch‐1 in resistant cells partially restored sensitivity to regorafenib treatment in vitro. Collectively, these data suggest a key role of Notch‐1 in mediating the resistant effects of regorafenib in colorectal cancer cells, and also provide a rationale to improve the therapeutic efficacy of regorafenib. J. Cell. Physiol. 231: 1097–1105, 2016. © 2015 Wiley Periodicals, Inc.
Giovanna Mirone, Arvind Shukla, and Gabriella Marfe
Elsevier BV
Gabriella Marfe, Giovanna Mirone, Arvind Shukla, and Carla Stefano
Bentham Science Publishers Ltd.
Sphingosine kinases (Sphk1 and 2) regulate the prodution of sphingosine-1-phosphate (S1P), that is key molecule in cancer development. SphK1, which is commonly overexpressed in malignant tumours, significantly contributes to the pathogenesis of various types of cancer as well as to resistance to different Tyrosine Kinase inibitors (TKIs). Even, SphK2 may promote apoptosis and inhibit cell growth but its role has not yet been fully understood in pathologic conditions. Different growth factorsinduced activation of receptor tyrosine kinases (RTKs) results in production of Sphk1 which catalyzes the phosphorylation of sphingosine. Such enzyme, in turn, is involved in many cellular processes by its five receptors. These are able to transactivate RTKs through amplification of a positive-feedback signaling loop. In conclusion, development of pharmacological inhibitors of SphK1 has been limited by the lack of completely understanding of the enzymatic activation mechanisms of SphK1.