Kakali Dhar

846 total citations
17 papers, 693 citations indexed

About

Kakali Dhar is a scholar working on Molecular Biology, Oncology and Immunology. According to data from OpenAlex, Kakali Dhar has authored 17 papers receiving a total of 693 indexed citations (citations by other indexed papers that have themselves been cited), including 17 papers in Molecular Biology, 5 papers in Oncology and 5 papers in Immunology. Recurrent topics in Kakali Dhar's work include Connective Tissue Growth Factor Research (11 papers), Biomarkers in Disease Mechanisms (5 papers) and Hedgehog Signaling Pathway Studies (3 papers). Kakali Dhar is often cited by papers focused on Connective Tissue Growth Factor Research (11 papers), Biomarkers in Disease Mechanisms (5 papers) and Hedgehog Signaling Pathway Studies (3 papers). Kakali Dhar collaborates with scholars based in United States, Switzerland and India. Kakali Dhar's co-authors include Sushanta K. Banerjee, Snigdha Banerjee, Smita Mehta, Gopal Dhar, Inamul Haque, Peter J. Van Veldhuizen, K. Sengupta, Sandipto Sarkar, Donald R. Campbell and Suman Kambhampati and has published in prestigious journals such as Biochemistry, Cancer Research and Scientific Reports.

In The Last Decade

Kakali Dhar

17 papers receiving 676 citations

Peers

Kakali Dhar

ONCOL

IMMUN

CMN

Sung-Wuk Jang South Korea

Smita Mehta United States

Gopal Dhar United States

Yiwen Jiang China

Hee-Young Jeon South Korea

Ting Dai China

Karl Deacon United Kingdom

Jeong Yoon Song South Korea

Babette Aicher Germany

Sung-Wuk Jang South Korea

Kakali Dhar

341 ×0.7

126 ×0.5

ONCOL

106 ×1.0

IMMUN

80 ×0.8

70 ×1.0

CMN

Citations per year, relative to Kakali Dhar Kakali Dhar (= 1×) peers Sung-Wuk Jang

Countries citing papers authored by Kakali Dhar

Since Specialization

Citations

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

Fields of papers citing papers by Kakali Dhar

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Kakali Dhar. 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 Kakali Dhar. The network helps show where Kakali Dhar may publish in the future.

Co-authorship network of co-authors of Kakali Dhar

This figure shows the co-authorship network connecting the top 25 collaborators of Kakali Dhar. A scholar is included among the top collaborators of Kakali Dhar 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 Kakali Dhar. Kakali Dhar 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:

17 of 17 papers shown

Maity, Gargi, Arnab Ghosh, Inamul Haque, et al.. (2019). CYR61/CCN1 Regulates dCK and CTGF and Causes Gemcitabine-resistant Phenotype in Pancreatic Ductal Adenocarcinoma. Molecular Cancer Therapeutics. 18(4). 788–800. 30 indexed citations

Haque, Inamul, Arnab Ghosh, Snigdha Banerjee, et al.. (2018). Leptin-induced ER-α-positive breast cancer cell viability and migration is mediated by suppressing CCN5-signaling via activating JAK/AKT/STAT-pathway. BMC Cancer. 18(1). 99–99. 45 indexed citations

Das, Amlan, Kakali Dhar, Gargi Maity, et al.. (2017). Deficiency of CCN5/WISP-2-Driven Program in breast cancer Promotes Cancer Epithelial cells to mesenchymal stem cells and Breast Cancer growth. Scientific Reports. 7(1). 1220–1220. 22 indexed citations

Maity, Gargi, Smita Mehta, Inamul Haque, et al.. (2014). Pancreatic Tumor Cell Secreted CCN1/Cyr61 Promotes Endothelial cell migration and Aberrant Neovascularization. Scientific Reports. 4(1). 4995–4995. 35 indexed citations

Maity, Gargi, Sandipto Sarkar, Kakali Dhar, et al.. (2014). Abstract 2330: Transcription factor MAZ promotes cell growth and aggressive behavior of human pancreatic cancer cells. Cancer Research. 74(19_Supplement). 2330–2330. 1 indexed citations

Srinivasan, Harini, et al.. (2013). Novel method to differentiate 3T3 L1 cells in vitro to produce highly sensitive adipocytes for a GLUT4 mediated glucose uptake using fluorescent glucose analog. Journal of Cell Communication and Signaling. 7(2). 129–140. 42 indexed citations

Haque, Inamul, Smita Mehta, Kakali Dhar, et al.. (2011). Cyr61/CCN1 signaling is critical for epithelial-mesenchymal transition and stemness and promotes pancreatic carcinogenesis. Molecular Cancer. 10(1). 8–8. 92 indexed citations

Banerjee, Snigdha, Smita Mehta, Archana De, et al.. (2011). Abstract 1314: Estrogen receptor-α is activated in breast ductal epithelial cells by CCN5 in CCN5-conditional tri-transgenic mice. Cancer Research. 71(8_Supplement). 1314–1314. 1 indexed citations

Kambhampati, Suman, Snigdha Banerjee, Kakali Dhar, et al.. (2010). 2-Methoxyestradiol Inhibits Barrett's Esophageal Adenocarcinoma Growth and Differentiation through Differential Regulation of the β-Catenin–E-Cadherin Axis. Molecular Cancer Therapeutics. 9(3). 523–534. 10 indexed citations

10.

Dhar, Kakali, Gopal Dhar, Inamul Haque, et al.. (2010). Tumor cell-derived PDGF-B potentiates mouse mesenchymal stem cells-pericytes transition and recruitment through an interaction with NRP-1. Molecular Cancer. 9(1). 209–209. 61 indexed citations

11.

Dhar, Animesh, Smita Mehta, Gopal Dhar, et al.. (2009). Crocetin inhibits pancreatic cancer cell proliferation and tumor progression in a xenograft mouse model. Molecular Cancer Therapeutics. 8(2). 315–323. 94 indexed citations

12.

Dhar, Gopal, Snigdha Banerjee, Kakali Dhar, et al.. (2008). Gain of Oncogenic Function of p53 Mutants Induces Invasive Phenotypes in Human Breast Cancer Cells by Silencing CCN5/WISP-2. Cancer Research. 68(12). 4580–4587. 53 indexed citations

13.

Banerjee, Snigdha, Smita Mehta, Inamul Haque, et al.. (2008). VEGF-A₁₆₅ Induces Human Aortic Smooth Muscle Cell Migration by Activating Neuropilin-1-VEGFR1-PI3K Axis. Biochemistry. 47(11). 3345–3351. 45 indexed citations

14.

Dhar, Kakali, Snigdha Banerjee, Gopal Dhar, K. Sengupta, & Sushanta K. Banerjee. (2007). Insulin-like Growth Factor-1 (IGF-1) Induces WISP-2/CCN5 via Multiple Molecular Cross-talks and Is Essential for Mitogenic Switch by IGF-1 Axis in Estrogen Receptor–Positive Breast Tumor Cells. Cancer Research. 67(4). 1520–1526. 35 indexed citations

15.

Banerjee, Snigdha, K. Sengupta, Kakali Dhar, et al.. (2006). Breast cancer cells secreted platelet‐derived growth factor‐induced motility of vascular smooth muscle cells is mediated through neuropilin‐1. Molecular Carcinogenesis. 45(11). 871–880. 74 indexed citations

16.

Sengupta, K., Snigdha Banerjee, Kakali Dhar, et al.. (2006). WISP-2/CCN5 Is Involved As a Novel Signaling Intermediate in Phorbol Ester-Protein Kinase Cα-Mediated Breast Tumor Cell Proliferation. Biochemistry. 45(35). 10698–10709. 17 indexed citations

17.

Banerjee, Snigdha, K. Sengupta, Neela K. Saxena, Kakali Dhar, & Sushanta K. Banerjee. (2005). Epidermal Growth Factor Induces WISP-2/CCN5 Expression in Estrogen Receptor-α-Positive Breast Tumor Cells through Multiple Molecular Cross-talks. Molecular Cancer Research. 3(3). 151–162. 36 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.

Explore authors with similar magnitude of impact