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| EDITORIAL |
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| Year : 2014 | Volume
: 1
| Issue : 2 | Page : 60-61 |
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Aiming targeted therapy in oral cancer
Sachin C. Sarode
Associate Editor, Journal of Dental Research and Review, Department of Oral and Maxillofacial Pathology, Dr. D.Y. Patil Dental College and Hospital, Dr. D.Y. Patil Vidyapeeth, Pune, Maharashtra, India
| Date of Web Publication | 5-Jun-2014 |
Correspondence Address:
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2348-2915.133903
How to cite this article:
Sarode SC. Aiming targeted therapy in oral cancer. J Dent Res Rev 2014;1:60-1 |
"Curing cancer is certainly more complicated than landing on the moon"
-Peter Krammer
German Cancer Researcher
Oral squamous cell carcinoma (OSCC) is the most common malignant neoplasm of the oral cavity, which is usually preceded by premalignant disorders. [1],[2] Despite recent advances in surgery, radiation and chemotherapy, prognosis for OSCC remains dismal with minimal improvement seen in the last few decades. It is generally agreed that understanding of the molecular mechanisms underlying the pathogenesis and progression of OSCC is crucial for the development of more rational and successful techniques for effective treatment.
In recent years, science has made a great progress in understanding the biology of cancer. We now know that cancer initiation and progression are a highly complex process that involves activation and/or inactivation of numerous signaling pathways. The most pronounced pathways are related to inflammation mediated carcinogenesis. [3] This knowledge has brought us into a new era of cancer therapeutics called "targeted therapy." These targeted therapy drugs act by:
- Blocking the specific enzyme and growth factor receptor
- Modifying the function of proteins
- Helping the immune system to destroy cancer cells
- Blocking an angiogenesis.
The molecules under target in oral cancer are cyclooxygenase-2, epidermal growth factor receptor, phosphoinositide-3-kinase/Akt/mammalian target of rapamycin (mTOR) axis, signal transducers and activators of transcription pathways, peroxisome proliferator-activated receptor gamma etc. [3] Accordingly, common drugs, which are used in clinical practice or are under-investigation include etuximab, panitumumab, erlotinib, sorafenib, sunitinib malate, imatinibmesylate, bevacizumab, trastuzumab, lapatinib, and mTORs.
Nanotechnology in targeted therapy is a hot area of research in cancer therapeutics but is still in a stage of infancy. The basic rationale is that nanometer-sized particles, such as biodegradable micelles, semiconductor quantum dots and iron oxide nano-crystals, when linked with bio-targeting ligands, such as monoclonal antibodies, peptides or small molecules, can be used to target malignant tumors with high affinity and specificity. [4]
Despite extensive intellectual advancement in cancer therapeutics, we are still lingering in the dark. We have not yet identified a consistent molecular target for OSCC. It appears that cancer cells are more intelligent in deceiving the targeted drug molecule. The reason could be attributed to the relatively rapid acquisition of resistance to such treatments that is observed in virtually all cases. This significantly limits their utility and remains a substantial challenge to the clinical management of advanced cancers. As molecular mechanisms of resistance have begun to be elucidated, new strategies to overcome or prevent the development of resistance have begun to emerge. In some cases, specific mutational mechanisms contribute directly to the acquired drug resistance, and in other cases, it appears that nonmutational and possibly epigenetic mechanisms play a significant role. On the top of it, unpredictable behavior such as tumor cell cannibalism [5],[6] and microbial interactions with signaling pathways [7] baffle us in understanding the tumor biology.
In conclusion, targeted therapy appears to be the future of cancer therapeutics. However, the development of resistance, heterogeneity and unpredictable behavior of cancer cell raise a question about how soon we will achieve this goal. It appears that treatment alone cannot win this war against cancer. Prevention and early detection may hold the key to success. [8]
| References | |  |
| 1. | Sarode SC, Sarode GS, Karmarkar S, Tupkari JV. A new classification for potentially malignant disorders of the oral cavity. Oral Oncol 2011;47:920-1. 
[PUBMED] |
| 2. | Sarode SC, Sarode GS, Tupkari JV. Oral potentially malignant disorders: Precising the definition. Oral Oncol 2012;48:759-60.
[PUBMED] |
| 3. | Sarode SC, Sarode GS, Patil A. Therapeutic aspects of the inflammation mediated oral carcinogenesis. Oral Oncol 2014;50:e13-4.
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| 4. | Akhter S, Ahmad I, Ahmad MZ, Ramazani F, Singh A, Rahman Z, et al. Nanomedicines as cancer therapeutics: Current status. Curr Cancer Drug Targets 2013;13:362-78.
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| 5. | Sarode GS, Sarode SC, Karmarkar S. Complex cannibalism: An unusual finding in oral squamous cell carcinoma. Oral Oncol 2012;48:e4-6.
[PUBMED] |
| 6. | Sarode SC, Sarode GS. Neutrophil-tumor cell cannibalism in oral squamous cell carcinoma. J Oral Pathol Med 2014; doi:10.1111/jop.12157.
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| 7. | Sarode GS, Sarode SC. E6 oncoprotein interaction with paxillin and FAK. Oral Oncol 2014;50:e17.
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| 8. | Sarode SC, Sarode GS, Karmarkar S. Early detection of oral cancer: Detector lies within. Oral Oncol 2012;48:193-4.
[PUBMED] |
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