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Journal articles on the topic 'Cancer molecular targets'

To see the other types of publications on this topic, follow the link: Cancer molecular targets.

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Weigelt, Britta, and Susana Banerjee. "Molecular targets and targeted therapeutics in endometrial cancer." Current Opinion in Oncology 24, no. 5 (September 2012): 554–63. http://dx.doi.org/10.1097/cco.0b013e328354e585.

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2

Kummar, Shivaani, and James H. Doroshow. "Molecular targets in cancer therapy." Expert Review of Anticancer Therapy 13, no. 3 (March 2013): 267–69. http://dx.doi.org/10.1586/era.12.170.

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3

Lorch, Jochen H. "Molecular Targets for Thyroid Cancer." Oncology Times 35 (June 2013): 2–3. http://dx.doi.org/10.1097/01.cot.0000431825.52663.3e.

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4

Lazo, John S., and Elizabeth R. Sharlow. "Drugging Undruggable Molecular Cancer Targets." Annual Review of Pharmacology and Toxicology 56, no. 1 (January 6, 2016): 23–40. http://dx.doi.org/10.1146/annurev-pharmtox-010715-103440.

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5

Gale, Danielle M. "Molecular targets in cancer therapy." Seminars in Oncology Nursing 19, no. 3 (August 2003): 193–205. http://dx.doi.org/10.1016/s0749-2081(03)00047-0.

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6

Westwell, Andrew D. "Molecular targets and cancer therapeutics." Drug Discovery Today 9, no. 24 (December 2004): 1042–44. http://dx.doi.org/10.1016/s1359-6446(04)03287-8.

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7

William, William N., John V. Heymach, Edward S. Kim, and Scott M. Lippman. "Molecular targets for cancer chemoprevention." Nature Reviews Drug Discovery 8, no. 3 (March 2009): 213–25. http://dx.doi.org/10.1038/nrd2663.

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8

Zaenker, K. S., G. Mustacchi, and E. Mihich. "Molecular targets of cancer chemotherapy." Cancer Chemotherapy and Pharmacology 58, no. 2 (December 24, 2005): 279–82. http://dx.doi.org/10.1007/s00280-005-0170-9.

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9

Rossig, Claudia. "Immune modulation by molecular cancer targets and targeted therapies." OncoImmunology 1, no. 3 (May 2012): 358–60. http://dx.doi.org/10.4161/onci.18401.

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10

Wang, Shihao, Jinqiu Shen, Boyang Zhang, Jiao Tian, Wei Zhao, and Wenzheng Wu. "Molecular mechanism study of cancer treatment based on network pharmacology of lily." Highlights in Science, Engineering and Technology 14 (September 29, 2022): 397–403. http://dx.doi.org/10.54097/hset.v14i.1852.

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OBJECTIVE: To make predictions related to the treatment of cancer by lily. METHODS: A systematic study of the constituents, targets and pathways of lily and cancer treatment was conducted using network pharmacology and molecular docking methods. The active ingredients of lily were screened and selected for investigation using TCMSP, Uniprot and PubChem databases, and the "ingredient-target-pathway" correlation axis was established. PubChem was used to collect the compounds in lily, and the active ingredients and targets with OB≥30% and DL≥0.18 in lily were obtained using the TCMSP Chinese medicine database. The active ingredients that met the criteria were also screened, and the binding patterns of the core targets and active ingredients were verified using molecular docking techniques before the active ingredients in lily were genetically aligned using Uniprot, and the corresponding genes were collated. The genes of different cancers were collated using CTD. Cytoscape 3.9.0 was used to create a map of the active ingredients and their corresponding targets. Finally, the results obtained were used to make predictions related to the treatment of cancer in lily. Results: The herb-compound-target network was obtained through screening. After cross-matching the active targets of the chemical components in lily with various cancers, 42 intersecting targets were obtained. Conclusion: The rank values (degree) of the intersecting targets were analysed and six targets with a degree greater than 5 were found to be PTGS2 (12), MMP1 (10), PPARG (8), HSP90AA1 (8), TP53 (8) and ESR2 (6); the diseases that were closely linked to the targets were Cancer, unspecific (The findings of this paper may provide a reference for the development of relevant targeted drugs and targeted therapeutic approaches in the future.

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11

Horiguchi, Yutaka. "Current Molecular Targets for Urological Cancer." Forum on Immunopathological Diseases and Therapeutics 4, no. 1 (2013): 25–32. http://dx.doi.org/10.1615/forumimmundisther.2013008313.

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12

NAKANO, Shuji. "New Molecular Targets for Cancer Chemotherapy." Internal Medicine 38, no. 2 (1999): 186–90. http://dx.doi.org/10.2169/internalmedicine.38.186.

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13

Eastman, Peggy. "Molecular Targets & Innovative Cancer Therapeutics." Oncology Times 39, no. 1 (January 2017): 34–35. http://dx.doi.org/10.1097/01.cot.0000512069.74279.a1.

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14

Zacharakis, Evangelos, Mahmoud Monem, Jean V. Joseph, and Hiten RH Patel. "Molecular therapeutic targets for bladder cancer." Expert Review of Anticancer Therapy 7, no. 12 (December 2007): 1691–93. http://dx.doi.org/10.1586/14737140.7.12.1691.

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15

Romero, Diana. "From Molecular Targets and Cancer Therapeutics." Nature Reviews Clinical Oncology 17, no. 1 (November 13, 2019): 6. http://dx.doi.org/10.1038/s41571-019-0302-5.

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16

Huntsman, D. "Emerging Molecular Targets in Gynaecological Cancer." Annals of Oncology 25 (September 2014): iv18. http://dx.doi.org/10.1093/annonc/mdu300.1.

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17

Oliff, Allen, Jackson B. Gibbs, and Frank McCormick. "New Molecular Targets for Cancer Therapy." Scientific American 275, no. 3 (September 1996): 144–49. http://dx.doi.org/10.1038/scientificamerican0996-144.

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18

Blagden, Sarah, and Hani Gabra. "Promising molecular targets in ovarian cancer." Current Opinion in Oncology 21, no. 5 (September 2009): 412–19. http://dx.doi.org/10.1097/cco.0b013e32832eab1f.

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19

Tuorkey, Muobarak J. "Molecular targets of luteolin in cancer." European Journal of Cancer Prevention 25, no. 1 (January 2016): 65–76. http://dx.doi.org/10.1097/cej.0000000000000128.

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20

Wolff, Robert A. "Exploiting molecular targets in pancreatic cancer." Hematology/Oncology Clinics of North America 16, no. 1 (February 2002): 139–57. http://dx.doi.org/10.1016/s0889-8588(01)00012-0.

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21

Faria, J., G. Negalha, A. Azevedo, and F. Martel. "Metformin and Breast Cancer: Molecular Targets." Journal of Mammary Gland Biology and Neoplasia 24, no. 2 (March 22, 2019): 111–23. http://dx.doi.org/10.1007/s10911-019-09429-z.

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22

Tucker, Gordon C. "Integrins: Molecular targets in cancer therapy." Current Oncology Reports 8, no. 2 (April 2006): 96–103. http://dx.doi.org/10.1007/s11912-006-0043-3.

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23

Sivaganesh, Vignesh, Nazifa Promi, Salma Maher, and Bela Peethambaran. "Emerging Immunotherapies against Novel Molecular Targets in Breast Cancer." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2433. http://dx.doi.org/10.3390/ijms22052433.

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Immunotherapy is a highly emerging form of breast cancer therapy that enables clinicians to target cancers with specific receptor expression profiles. Two popular immunotherapeutic approaches involve chimeric antigen receptor-T cells (CAR-T) and bispecific antibodies (BsAb). Briefly mentioned in this review as well is the mRNA vaccine technology recently popularized by the COVID-19 vaccine. These forms of immunotherapy can highly select for the tumor target of interest to generate specific tumor lysis. Along with improvements in CAR-T, bispecific antibody engineering, and therapeutic administration, much research has been done on novel molecular targets that can especially be useful for triple-negative breast cancer (TNBC) immunotherapy. Combining emerging immunotherapeutics with tumor marker discovery sets the stage for highly targeted immunotherapy to be the future of cancer treatments. This review highlights the principles of CAR-T and BsAb therapy, improvements in CAR and BsAb engineering, and recently identified human breast cancer markers in the context of in vitro or in vivo CAR-T or BsAb treatment.

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24

Zhang, Wenbiao, Jiacong Ye, Xinling Li, Yinghe Li, and Guokai Feng. "Integrin α6 targeted cancer imaging and therapy." Visualized Cancer Medicine 4 (2023): 4. http://dx.doi.org/10.1051/vcm/2022007.

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Integrins represent ideal targets for molecular imaging and targeted therapy of cancer and their role in cancer has been reviewed extensively elsewhere. Except for αVβ3 and αVβ5, the remaining integrins were not systematically considered and tested as potential therapeutic targets. In recent years, the studies on integrin α6 as a cancer imaging and therapeutic target are increasing, due to their highly expressed in several cancers, and their expression has been associated with poor survival. Integrin α6 appears to be a particularly attractive target for cancer imaging and therapy, and therefore we have developed a wide array of integrin α6-target molecular probes for molecular imaging and targeted therapy of different cancers. Despite the studies on integrin α6 as a cancer imaging and therapeutic target increasing in recent years, most of them were derived from preclinical mouse models, revealing that much more can be done in the future. The development of integrin α6 drugs may now be at an important point, with opportunities to learn from previous research, to explore new approaches. In this review, we will briefly introduce integrin α6 and highlighted the recent advances in integrin α6 targeted imaging and therapeutics in cancer.

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25

Bode, Ann M., and Zigang Dong. "Molecular and cellular targets." Molecular Carcinogenesis 45, no. 6 (2006): 422–30. http://dx.doi.org/10.1002/mc.20222.

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26

Chen, Buze, Xin Jin, Haihong Wang, Qingmei Zhou, Guilin Li, and Xiaoyuan Lu. "Network Pharmacology, Integrated Bioinformatics, and Molecular Docking Reveals the Anti-Ovarian Cancer Molecular Mechanisms of Cinnamon (Cinnamomum cassia (L.) J. Presl)." Natural Product Communications 17, no. 8 (August 2022): 1934578X2211191. http://dx.doi.org/10.1177/1934578x221119118.

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Cinnamon ( Cinnamomum cassia (L.) J. Presl) is a popular natural spice with various pharmacological properties. This study was based on network pharmacology integrating bioinformatics and molecular docking to explore the potential molecular mechanisms of cinnamon in the treatment of ovarian cancer (OC). The chemical composition of cinnamon was collected from the TCMSP database to predict its targets and construct a “cinnamon active component target” network. OC-related genes were retrieved from Genecards and DisGeNET databases. The “disease-target” network was established, and the drug targets were mapped to the disease targets, and the key targets obtained from the mapping were subjected to DAVID analysis to construct a “component-target-pathway” network diagram. The active ingredients of cinnamon were molecularly docked to the core targets to predict the molecular mechanism of cinnamon in the treatment of ovarian cancer. From cinnamon, 105 chemical components were screened and de-duplicated to obtain 15 active components and 74 drug target proteins, and 26 common targets were obtained after mapping drug targets to disease targets. 368 entries were identified by GO enrichment analysis, mainly including biological progresses such as regulation of smooth muscle contraction and regulation of tube diameter, and molecular functions such as antioxidant activity, and peroxidase activity. The KEGG pathway enrichment analysis identified 4 signaling pathways, neuroactive ligand-receptor interaction, HIF-1 signaling pathway, regulation of lipolysis in adipocytes, and complement and coagulation cascades. Molecular docking analysis showed good affinity of these key targets with representative components of OC. There was a stable interaction between DIBP and ADRB2 and NR3C1. There is a stable interaction between oleic acid and C2K, EDN1, ERBB2, PLAU, PLG, PRSS3, PTGS1, PTGS2, SERPINE1 and SLC2A1. Cinnamon exerted its therapeutic effects on OC through multiple pathways and targets.

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27

Ong, Samantha Kah Ling, Muthu K. Shanmugam, Lu Fan, Sarah E. Fraser, Frank Arfuso, Kwang Seok Ahn, Gautam Sethi, and Anupam Bishayee. "Focus on Formononetin: Anticancer Potential and Molecular Targets." Cancers 11, no. 5 (May 1, 2019): 611. http://dx.doi.org/10.3390/cancers11050611.

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Formononetin, an isoflavone, is extracted from various medicinal plants and herbs, including the red clover (Trifolium pratense) and Chinese medicinal plant Astragalus membranaceus. Formononetin’s antioxidant and neuroprotective effects underscore its therapeutic use against Alzheimer’s disease. Formononetin has been under intense investigation for the past decade as strong evidence on promoting apoptosis and against proliferation suggests for its use as an anticancer agent against diverse cancers. These anticancer properties are observed in multiple cancer cell models, including breast, colorectal, and prostate cancer. Formononetin also attenuates metastasis and tumor growth in various in vivo studies. The beneficial effects exuded by formononetin can be attributed to its antiproliferative and cell cycle arrest inducing properties. Formononetin regulates various transcription factors and growth-factor-mediated oncogenic pathways, consequently alleviating the possible causes of chronic inflammation that are linked to cancer survival of neoplastic cells and their resistance against chemotherapy. As such, this review summarizes and critically analyzes current evidence on the potential of formononetin for therapy of various malignancies with special emphasis on molecular targets.

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28

Lim, W. M., S. Nalliah, F. F. L. Chung, K. K. Chan, and C. O. Leong. "Identification of New Molecular Targets for Treatment of Endometrial Cancers." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 203s. http://dx.doi.org/10.1200/jgo.18.82300.

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Background: Current approaches using molecularly targeted drug alone or in combination with cytotoxic agents are associated with varying degrees of response rates and adverse effects. Clearly, there is a need to identify new molecular targets with more selectivity against the endometrial cancer cells. Aim: To perform high throughput screening to identify and validate new molecular targets for treatment of endometrial cancers. Methods: Kinome-wide shRNA library screen was performed on endometrial cancer cell line. The results were validated using viability and apoptosis assay. Immunoblotting assay was conducted to identify the target protein. Results: We identified that the knock-down of endogenous cyclin-dependent kinases regulatory subunit 1B (CKS1B) induced significant cell death in a panel of endometrial cancer cell lines (AN3CA, HEC-1A, HEC-1B, RL-95 and Ishikawa). In contrast, no significant cytotoxicity was observed in the THESC nontransformed endometrial epithelial cells suggesting that CKS1B is mediating a tumor-specific survival pathway. Analysis by immunoblotting assay revealed an increased of p27 protein expression following depletion of endogenous CKS1B in the type 2 endometrial cancer cells (AN3CA and HEC-1A), while no changes was observed in the type 1 (Ishikawa and RL95-2) endometrial cancer cells. These results suggest that CKS1B might regulate the survival of type I and type II endometrial cancer cells through distinct mechanisms. Conclusion: The results demonstrated that inhibition of CKS1B induced significant tumor-specific cell death in endometrial cancer cells. We found that the response is significant in type 2 endometrial cancer cell line and is p27 dependent. This finding suggests that CKS1B could be a potential target for therapeutic intervention and warrant further investigation.

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29

Rouamba, Ablassé, Moussa Compaoré, and Martin Kiendrebeogo. "Molecular targets of honey bee’s products in cancer prevention and treatment." Journal of Herbmed Pharmacology 8, no. 4 (August 1, 2019): 261–68. http://dx.doi.org/10.15171/jhp.2019.38.

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Chemotherapy and radiotherapy are currently the main treatments for cancer but their toxicities on the surrounding normal cells limit their use in cancer therapy. Moreover, many cancers have developed some resistance to the available anticancer chemicals and put in failure the chemotherapy currently used in the cancer treatment. This failure of the targeted monotherapy resulting from bypass mechanisms has obligated researchers to use agents that interfere with multiple cell-signaling pathways. Recently, researches focused on the use of natural products which can target cancer promoting factors genes expression. Of these natural products, honey has been extensively studied. The pharmacological properties of honey include antioxidant, anti-inflammatory, antibacterial, immunomodulatory, estrogenic and anti-cancer effects. The honey bee’s products are potent sources of nutritional components including sugar, amino-acids, water and minerals. Furthermore honey contains chemopreventive compounds such as flavonoids, phenol acids, tannins, vitamins that may interfere with multiple cell’s pathways and hereby reduce the incidence of many types of cancers. However, the molecular mechanisms of honey bee’s products in cancer prevention and treatment are less known. This review highlights the molecular mechanism of honey bioactive compounds in cancer prevention and treatment.

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30

Flaherty, Keith T. "New molecular targets in melanoma." Current Opinion in Oncology 16, no. 2 (March 2004): 150–54. http://dx.doi.org/10.1097/00001622-200403000-00012.

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31

Heaney, Anthony P., and Shlomo Melmed. "Molecular targets in pituitary tumours." Nature Reviews Cancer 4, no. 4 (April 2004): 285–95. http://dx.doi.org/10.1038/nrc1320.

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32

Gupta, Shilpi, Prabhat Kumar, and Bhudev C. Das. "HPV: Molecular pathways and targets." Current Problems in Cancer 42, no. 2 (March 2018): 161–74. http://dx.doi.org/10.1016/j.currproblcancer.2018.03.003.

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33

Nakhjavani, Maryam, Jennifer E. Hardingham, Helen M. Palethorpe, Yoko Tomita, Eric Smith, Tim J. Price, and Amanda R. Townsend. "Ginsenoside Rg3: Potential Molecular Targets and Therapeutic Indication in Metastatic Breast Cancer." Medicines 6, no. 1 (January 23, 2019): 17. http://dx.doi.org/10.3390/medicines6010017.

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Breast cancer is still one of the most prevalent cancers and a leading cause of cancer death worldwide. The key challenge with cancer treatment is the choice of the best therapeutic agents with the least possible toxicities on the patient. Recently, attention has been drawn to herbal compounds, in particular ginsenosides, extracted from the root of the Ginseng plant. In various studies, significant anti-cancer properties of ginsenosides have been reported in different cancers. The mode of action of ginsenoside Rg3 (Rg3) in in vitro and in vivo breast cancer models and its value as an anti-cancer treatment for breast cancer will be reviewed.

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34

Lowe, Leroy, J. William LaValley, and Dean W. Felsher. "Tackling heterogeneity in treatment-resistant breast cancer using a broad-spectrum therapeutic approach." Cancer Drug Resistance 5 (2022): 917–25. http://dx.doi.org/10.20517/cdr.2022.40.

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Tumor heterogeneity can contribute to the development of therapeutic resistance in cancer, including advanced breast cancers. The object of the Halifax project was to identify new treatments that would address mechanisms of therapeutic resistance through tumor heterogeneity by uncovering combinations of therapeutics that could target the hallmarks of cancer rather than focusing on individual gene products. A taskforce of 180 cancer researchers, used molecular profiling to highlight key targets responsible for each of the hallmarks of cancer and then find existing therapeutic agents that could be used to reach those targets with limited toxicity. In many cases, natural health products and re-purposed pharmaceuticals were identified as potential agents. Hence, by combining the molecular profiling of tumors with therapeutics that target the hallmark features of cancer, the heterogeneity of advanced-stage breast cancers can be addressed.

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35

Kelleher, Fergal C., Andrew J. Colebatch, and Aparna Rao. "New Molecular Targets in Lung Adenocarcinoma." Oncology & Hematology Review (US) 09, no. 02 (2013): 122. http://dx.doi.org/10.17925/ohr.2013.09.2.122.

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Lung cancer is designated as either non-small-cell lung cancer (NSCLC) or small-cell lung cancer. There are three subtypes of NSCLC: adenocarcinoma (48 %), squamous cell carcinoma (28 %), and large-cell carcinoma (24 %). Epidermal growth factor receptor(EGFR)mutations, anaplastic lymphoma kinase(ALK)rearrangements, andROS1rearrangements are co-associated with lung adenocarcinoma in never-smokers. Histologically, lung adenocarcinoma is sub-divided into papillary, acinar, bronchioalveolar, and solid subtypes. A superseding molecular subclassification is emerging with important therapeutic implications. Secondary resistance to medications targeting these molecular abnormalities does invariably occur. It is anticipated that strategies including drugs with increased receptor binding affinity, altered medication pharmacodynamic profiles, and combinatorial approaches will emerge.

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36

Park, Woo-Chan, Lee Su Kim, Tae Hyun Kim, Byeong-Woo Park, Ho Yong Park, Byung Joo Song, Jae Bok Lee, Chang Wan Jeon, and Un-Jong Choi. "Molecular Targets for Treatment of Breast Cancer." Journal of Breast Cancer 12, no. 4 (2009): 229. http://dx.doi.org/10.4048/jbc.2009.12.4.229.

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37

Pantano, Francesco, Giulia Ribelli, Michele Iuliani, Marco Fioramonti, Mark Leakos, Alice Zoccoli, Daniele Santini, Giovanni Muto, and Giuseppe Tonini. "New Molecular Targets in Metastatic Prostate Cancer." Journal of Cancer Therapy 07, no. 06 (2016): 388–401. http://dx.doi.org/10.4236/jct.2016.76042.

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38

Ehlerding, E. B., C. G. England, D. G. McNeel, and W. Cai. "Molecular Imaging of Immunotherapy Targets in Cancer." Journal of Nuclear Medicine 57, no. 10 (July 28, 2016): 1487–92. http://dx.doi.org/10.2967/jnumed.116.177493.

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39

Stolfi, Carmine, Roberto Pellegrini, Francesco Pallone, and Giovanni Monteleone. "Molecular Targets of Mesalazine in Colorectal Cancer." Current Cancer Therapy Reviews 4, no. 4 (November 1, 2008): 262–66. http://dx.doi.org/10.2174/157339408786413326.

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40

Humeniuk, Rita, Prasun Mishra, Joseph Bertino, and Debabrata Banerjee. "Molecular Targets for Epigenetic Therapy of Cancer." Current Pharmaceutical Biotechnology 10, no. 2 (February 1, 2009): 161–65. http://dx.doi.org/10.2174/138920109787315123.

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41

Imyanitov, Eugene. "MOLECULAR TARGETS IN LUNG CANCER: CURRENT STATUS." Practical oncology 19, no. 2 (June 30, 2018): 93–105. http://dx.doi.org/10.31917/1902093.

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42

Palozza, Paola. "Carotenoids and Modulation of Cancer: Molecular Targets." Current Pharmacogenomics 2, no. 1 (March 1, 2004): 35–45. http://dx.doi.org/10.2174/1570160043476169.

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43

Shtivelman, Emma, Tomasz M. Beer, and Christopher P. Evans. "Molecular pathways and targets in prostate cancer." Oncotarget 5, no. 17 (August 29, 2014): 7217–59. http://dx.doi.org/10.18632/oncotarget.2406.

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44

Dawson, Nancy A. "New molecular targets in advanced prostate cancer." Expert Review of Anticancer Therapy 6, no. 7 (July 2006): 993–1002. http://dx.doi.org/10.1586/14737140.6.7.993.

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Cindy D. Davis and John A. Milner. "Molecular Targets for Nutritional Preemption of Cancer." Current Cancer Drug Targets 7, no. 5 (August 1, 2007): 410–15. http://dx.doi.org/10.2174/156800907781386560.

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46

Alfonso, L., G. Ai, R. C. Spitale, and G. J. Bhat. "Molecular targets of aspirin and cancer prevention." British Journal of Cancer 111, no. 1 (May 29, 2014): 61–67. http://dx.doi.org/10.1038/bjc.2014.271.

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47

Hodes, R. "Molecular targeting of cancer: Telomeres as targets." Proceedings of the National Academy of Sciences 98, no. 14 (July 3, 2001): 7649–51. http://dx.doi.org/10.1073/pnas.151267698.

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48

SCHALKEN, JACK A. "Validation of molecular targets in prostate cancer." BJU International 96, s2 (December 2005): 23–29. http://dx.doi.org/10.1111/j.1464-410x.2005.05943.x.

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49

Gazdar, Adi F., Kuniharu Miyajima, Jyotsna Reddy, Ubaradka G. Sathyanarayana, Hisayuki Shigematsu, Makoto Suzuki, Takao Takahashi, and Narayan Shivapurkar. "Molecular Targets for Cancer Therapy and Prevention." Chest 125, no. 5 (May 2004): 97S—101S. http://dx.doi.org/10.1378/chest.125.5_suppl.97s-a.

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50

Hong, Liu, Shujun Li, Yu Han, Jianjun Du, Hongwei Zhang, Jipeng Li, Qingchuan Zhao, Kaichun Wu, and Daiming Fan. "Angiogenesis-related molecular targets in esophageal cancer." Expert Opinion on Investigational Drugs 20, no. 5 (March 28, 2011): 637–44. http://dx.doi.org/10.1517/13543784.2011.571203.

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