Anti-cancer properties -
And the benefits keep coming; as natural sources of glucosinolates, they also contain antibacterial and antiviral properties, inactivate carcinogens, help reprogram cancer cells to die off, and prevent tumor formation and metastasis. These powerhouse chemicals are known to break down during the chewing and digestion process into biologically active compounds that prevent cancer cells growth, which are referred to as indoles, thiocyanates and isothiocyanates.
Cruciferous vegetables are known to be cancer fighters and some of the best vitamin C foods widely available. Nearly all members of the brassica family of cruciferous vegetables are nutrient-dense sources of a family of phytochemicals called isothiocyanates that are linked to cancer prevention.
In addition to isothiocyanates, cruciferous veggies like cabbage and broccoli also contain sulforaphanes and indoles — two types of strong antioxidants and stimulators of detoxifying enzymes that protect the structure of DNA.
Add one or two kinds — including broccoli, cauliflower , cabbage or Brussels sprouts — to three mostly plant-based diet meals daily in the form of roasted veggies, soups or stir fries, or dip them into hummus or Greek yogurt for a healthy, fast snack.
The ORAC scores of nearly all berries are very high, making them some of the top high-antioxidant foods in the world. Berries are especially rich in proanthocyanidin antioxidants, which have been observed to have anti-aging properties in several animal studies and are capable of lowering free radical damage.
High amounts of phenols, zeaxanthin, lycopene, cryptoxanthin, lutein and polysaccharides are other berry benefits. to increase immunity and energy, so look for those in powder or dried form in health food stores and online.
Carotenoids alpha-carotene, beta-carotene, lycopene , lutein, cryptoxanthin, etc. are derivatives of vitamin A found in many citrus fruits, sweet potatoes , berries, pumpkin, squashes and other plant foods. One of the most researched is beta-carotene , an essential nutrient for immune functioning, detoxification, liver health, and fighting cancers of the skin, eyes and organs.
Two nutrients that give these foods their signature dark hues include lutein and zeaxanthin, which have been shown to help prevent eye and skin-related disorders since they act as antioxidants that filter harmful high-energy blue wavelengths, protecting healthy cells in the process.
When it comes to carbohydrate-rich veggies, studies show that complex carbs, including sweet potatoes, carrots, beets, other tubers and whole-grain foods, is related to a reduced risk of several types of cancer, particularly of the upper digestive tract.
This is likely due to a favorable role of fiber, but the issue is still open to discussion. In contrast, refined grain intake and high glycemic load foods are not apart of an anti-cancer diet. These have been associated with increased risk of different types of cancer, including breast and colorectal.
A molecular compound found in colorful, spicy peppers, capsaicin is a top cancer-fighting food and is found to have positive effects on shrinking tumors, preventing metastasis new tumors found away from the original cancer site , causing apoptosis in various cancer models and even potentially preventing cancer from occurring in the first place.
Also, pineapple is now recognized in the scientific community as one of the top cancer-fighting foods. In studies, bromelain has been found to have natural anti-cancer effects, including promoting apoptotic cell death and preventing tumor growth.
Studies have linked bromelain to increased protection against breast and lung cancer, and the journal Anticancer Drugs published results from a clinical trial that suggested it affects malignant peritoneal mesothelioma — a rare cancer caused by asbestos exposure.
Along with easy-to-use black pepper, turmeric absorption is enhanced and better able to fight inflammation. You can also take curcumin supplements; aim for 1, milligrams daily. Meanwhile, the seeds of the cilantro plant, called coriander, possess anti-inflammatory properties that may play a role in disease and even cancer.
Ashwagandha benefits include its ability to inhibit the proliferation of cancer cells. Perhaps most striking is the Chinese root spice galangal , suggested by a growing body of scientific research, is its ability to fight and potentially prevent a broad number of cancers and tumors.
See our list of healing herbs and spices. Detoxifying with rich sources of selenium , zinc and B vitamins helps purify blood; produce the bile needed to digest fats; balance hormones naturally; and store essential vitamins, minerals and iron.
These mineral-rich foods can help counteract the effects of alcohol, prescription drugs, hormone disruptions, high triglyceride levels, low potassium, obesity and viral infections.
One of the easiest ways to consume more probiotics is in their most natural state, which includes raw milk products such as cheese, kefir and yogurt.
Raw and cultured are key here, since fermentation produces probiotics but high heat processing used to pasteurize dairy can damage many of the vital nutrients, including the enzymes, proteins and probiotics.
Most dairy today is loaded with hormones, antibiotics, pain killers and pesticide residue so buying organic is also important.
Aim for six ounces of cultured dairy daily probiotic yogurt , cottage cheese, goat milk kefir or amasai. Cottage cheese, which is rich in sulfur protein and saturated fats, was found to be especially beneficial as part of the Budwig diet for cancer protocol.
You can also increase your probiotic food intake without dairy by consuming cultured vegetables like kimchi , sauerkraut, coconut kefir, kombucha or natto.
Cultured dairy is also a great source of calcium. Calcium , particularly when combined with vitamin D3 form, may reduce the incidence of cancer. Calcium seems to be especially beneficial for preventing cancer and rectal cancers.
Some studies have also found that it helps reduce breast cancer and ovarian cancer risk. Sunlight exposure and marine oils such as cod liver oil or krill oil are great sources of vitamin D that help with calcium absorption. Calcium should ideally be obtained from foods like organic dairy products.
Chia seeds and flaxseeds are two of the most nutrient-dense seeds in the world. It used to treat breast cancer. Some of the research has been showed that it has an effective anticancer property against breast cancer [1].
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Download as PDF Printable version. Extracts from Camptotheca the "happy tree" or "cancer tree" were used to develop the chemotherapeutic drug Topotecan Plant sources of anti-cancer agents are plants, the derivatives of which have been shown to be usable for the treatment or prevention of cancer in humans.
Journal of Ethnopharmacology. doi : PMID Archived from the original on Retrieved Bangladesh Journal of Pharmacology. Trends in Pharmacological Sciences.
PMC Autophagy is a housekeeping process by which cells may dispose of old or damaged cytoplasmic organelles and proteins, and also serves an adaptive function under conditions of nutrient stress by allowing cells to recycle endogenous biosynthetic substrates such as amino acids.
Autophagy is considered Type II programmed cell death apoptosis is type I and necrosis is type III and, thus has come under interest as a potential process that may be exploited in the development of anti-cancer chemotherapeutics.
Programmed cell death type II: Autophagy is a catabolic process by which cells degrade their own components via the lysosomal system. In response to cellular or nutrient stress, double-layered autophagosomes containing cytoplasmic proteins and organelles are formed following envelopment by a membrane derived from the endoplasmic reticulum.
Upon fusion with lysosomes, the contents of these autophagolysosomes are degraded. Autophagy is important as a housekeeping function to promote cell survival and may also function as a pathway of programmed cell death.
The possible roles of autophagy in carcinogenesis as well as tumor regression in response to therapy are still being elucidated, with seemingly conflicting studies suggesting that induction of autophagy enhances cell death in certain tumor types while mediating chemotherapeutic resistance in others.
On one hand, there is evidence that autophagy may be employed by cancer cells to facilitate growth under the stressful metabolic conditions commonly encountered in the tumor microenvironment such as hypoxia and decreased availability of glucose and other nutrients due to poor vascularization [ — ].
In addition, the induction of autophagy as an adaptive response mediating resistance to chemotherapy has been observed in multiple tumor types including malignant gliomas, lymphoma, breast, lung and hepatocelluar carcinomas [ — ].
On the other hand, there is genomic evidence that disruption of autophagy is associated with tumorigenesis, as suggested by the mono-allelic deletion of the autophagy-related gene beclin-1 in a high percentage of breast and ovarian cancers [ ].
In addition it was found that monoallelic deletion of beclin-1 resulted in increased cellular proliferation, decreased autophagy as measured by expression of the autophagosome membrane protein LC3, and accelerated the development of hepatitis B-induced premalignant lesions [ ].
Conversely, transfection of beclin-1 into MCF-7 breast cancer cells which express a very low baseline level of the protein inhibited the cellular proliferation and tumorigenicity in a nude mouse xenograft model [ ]. While autophagy appears to play a role in mediating chemoresistance in certain cancers as described above, there is also data supporting that autophagy may also induce non-apoptotic cell death in response to chemotherapy.
In human MCF-7 estrogen-receptor positive breast cancer, both tamoxifen and paclitaxel were found to induce autophagic cell death in cell culture [ , ].
Arsenic trioxide was found to induce autophagic cell death in malignant glioma, leukemia and fibrosarcoma cells, and in leukemia this effect was accompanied by up-regulation of beclin-1 [ — ].
The small molecule tyrosine kinase inhibitor imatinib has been shown to induce cellular autophagy, an effect that may sensitize drug-resistant Kaposi sarcoma cells [ , ]. Interestingly, imatinib's induction of autophagy seems to decrease its effectiveness in chronic myelogenous leukemia CML and blocking of autophagy lead to increased apoptotic cell death [ ].
Studies done in malignant glioma cells have also yielded varying results; while autophagy induced by arsenic trioxide resulted in increased cell death, treatment with temolozamide and etoposide led to an increase in ATP that exerted a protective effect [ , ].
Likewise, there is controversy regarding the effect of autophagy induction on radiation sensitivity. Studies in breast cancer have suggested that vitamin D-dependant radiosensitization is mediated through autophagy, while autophagy has demonstrated both radiosensitizing and dampening effects in malignant gliomas [ — ].
Curcumin has been shown to be an inducer of autophagic cell death in chronic myelogenous leukemia, esophageal cancer and malignant glioma cells [ — ].
While the current data on autophagy and cancer is far from providing a consensus, it is evident that regulation of this process may play an important role in tumorigenesis and response to therapy thus making pharmacologic modulators of autophagy attractive candidates for further study.
The stimulation of new blood vessel growth is an essential step for tumor growth and metastasis in order to provide for the metabolic needs of rapidly proliferating malignant cells.
Angiogenesis is regulated by a variety of pro-angiogenic genes and signaling molecules including vascular endothelial growth factor VEGF , basic fibroblast growth factor bFGF , epidermal growth factor EGF , platelet-derived growth factors, hypoxia-inducible factors, angiopoetin-1 and 2, and matrix metalloproteinases [ ].
The role of angiogenesis in tumor growth has been targeted by newer chemotherapeutic agents such as bevacizumab, an anti-VEGF monoclonal antibody that is FDA approved for metastatic forms of various cancers including colon, non-small cell lung, HER2-negative breast cancer and renal cell carcinoma.
In addition to bevacizumab, sorafenib and sunitinib are novel small-molecule inhibitors of multiple receptor tyrosine kinase RTK pathways involved in signal transduction from angiogenic receptors such as VEGFR and PDGF-R that are approved for renal cell carcinoma as well as hepatocellular carcinoma and gastrointestinal stromal tumor, respectively [ ].
Curcumin has demonstrated an anti-angiogenic effect in vivo in xenograft models of various tumors including glioblastoma, hepatocelluar carcinoma, prostate and ovarian carcinomas [ , — ]. Curcumin has been shown to regulate a variety of pro-angiogenic growth factors, enzymes and transcription factors including bFGF, VEGF, angiopoetin-1 and 2, COX-2, matrix metalloproteinase-9 MMP-9 , AP-1 and NF-κB [ — ].
Curcumin has also been shown to inhibit the angiogenic response to FGF-2 stimulation in mouse endothelial cells and decrease the expression of MMP-9, an enzyme involved in tissue remodeling that is important for the growth of new blood vessels [ ].
In addition, curcumin treatment decreased the levels of the angiogenic biomarkers COX-2 and VEGF in hepatocelluar carcinoma cells, and resulted in a reduction in tumor neocapillary density compared to the untreated cells [ ].
In addition to its inhibitory effects on angiogenesis, curcumin has also been demonstrated to affect a number of cellular adhesion molecules involved in the processes of tumor growth and metastasis. A study of curcumin in metastatic melanoma demonstrated a dose dependant reduction in binding to extracellular matrix proteins, decreased expression of alpha5beta1 and alpha v beta3 integrin receptors and increased expression of various anti-metastatic proteins including tissue inhibitor metalloproteinase TIMP-2 , nonmetastatic gene 23 Nm23 and E-cadherin [ ].
E-cadherin expression is important in maintaining the integrity of intercellular adhesion though binding to various catenins including β-catenin , and loss of E-cadherin is associated with an increased tendency for tumor metastasis [ ].
Anti-metastatic effects of curcumin have also been demonstrated in the MDA-MB breast cancer cell line, resulting in decreased expression of matrix metalloproteinases, ICAM-1 and chemokine receptor 4 CXCR4 and suppressed cell migration and invasion [ ].
In addition, curcumin was shown to decrease the ability of paclitaxel-resistant breast cancer cells to form lung metastases via suppression of various anti-apoptotic proteins including XIAP, Bcl-2 and IAP1 and 2 , proliferative COX-2, c-myc and cyclin D1 , and metastatic proteins MMP-9, VEGF and ICAM-1 [ ].
As many pro-angiogenic and pro-metastatic genes are regulated by NF-κB including COX-2, VEGF, ICAM-1 and MMP-9 among others , curcumin's suppressive effect on NF-κB activation likely plays a key role in mediating the compound's anti-angiogenic and anti-tumorigenic effects. Curcumin has been studied in various in vitro and vivo models of head and neck squamous cell carcinoma with promising results.
An overview of current literature supporting the spice's utility in the treatment of head and neck cancer including as a chemopreventive agent, as well as future directions for study is presented below.
Studies of curcumin in various head and neck cancer cell lines have demonstrated decreased cell growth and survival, concomitant with the compound's effects on molecular pathways involved in cellular proliferation.
Expression of constitutively active NF-κB and IκK has been observed in multiple oral squamous cell carcinoma cell lines, and curcumin treatment was shown to suppress growth and survival of these cell lines via inhibition of NF-κB activation [ 43 ].
Signal-transducer-and-activator-of-transcription-3 STAT3 is a signaling protein observed to be overexpressed in multiple head and neck cancers, and curcumin was shown to suppress the IL-6 mediated phosphorylation of STAT3 as well as inhibiting nuclear localization [ ].
In another study, Chakravarti et al [ ] demonstrated that curcumin suppressed the growth of immortalized oral mucosal epithelial cells and squamous cell carcinoma cells UMSCC22B and SCC4 while having minimal effect on normal oral epithelial cells. Curcumin was shown to reduce the efficiency of the eIF4F translational complex of these immortalized cells via suppression of phosphorylation of 4E-BP1, eIF4G, eIF4B and Mnk1, as well as a reduction in the total levels of eIF4E and Mnk1.
Our laboratory has studied the effects of curcumin in several head and neck squamous cell carcinoma cell lines: CCL23 laryngeal , CAL27, UM-SCC14A and UM-SCC1 oral [ 48 , 53 , ].
The growth suppressive effect was shown to be mainly mediated via the effects of curcumin on the NF-κB pathway. Curcumin was shown to decrease the expression of NF-κB and also inhibited its nuclear localization; this observation was supported by a concomitant decrease in phospho-IκB-α expression [ 46 ].
In addition, the expression levels of multiple NF-κB regulated gene products including cyclin D1, MMP-9, COX-2, Bcl-2, Bcl-xL, Il-6, IL-8, Mcl-1L and Mcl-1S were reduced [ 48 , 53 ].
It has been demonstrated that the curcumin-induced suppression of the NF-κB pathway in head and neck cancer cells is due to inhibition of IκK inhibitor kappa B kinase , thus blocking the phosphorylation of IκB-α and resulting in NF-κB sequestration in the cytoplasm.
We have shown dose-dependent suppression of IL-6 and IL-8 following curcumin treatment in CCL23, CAL27, UM-SCC1 and UM-SCC14A cell lines via inhibition of IκK activity [ ]. Furthermore, the curcumin-induced inhibition of IκK was found to take place via an AKT-independent mechanism [ 53 ].
The data on curcumin's effect on the AKT pathway is varying; while it has been shown to act independently of AKT in HNSCC as well as melanoma, curcumin suppresses the AKT pathway in other tumors such as malignant gliomas and pancreatic cancer [ 96 , , ].
AKT another kinase of transcription, also known as protein kinase B is a protein kinase involved in signal transduction from oncogenes and growth factors. The AKT signaling cascade is stimulated by EGFR, and represents one pathway by which NF-κB may be activated [ ]. The finding that curcumin suppresses NF-κB independently of the AKT pathway in HNSCC is of clinical significance, as it acts via a different mechanism than cetuximab and the two agents could potentially be used in combination for treating head and neck cancers.
Curcumin has demonstrated in vivo growth suppressive effects on head and neck squamous cell carcinoma using nude mouse xenograft models. The lipophilic nature of curcumin and relative insolubility in aqueous solutions, combined with short half life and low bioavailability following oral administration has presented a significant challenge in developing an effective delivery system for its use as a chemotherapeutic agent [ ].
In an effort to overcome this obstacle, various strategies are being tried including the use of piperine as an adjuvant agent to slow curcumin breakdown as well as the development of liposomal, phospholipid and nanoparticulated formulations of the compound to enable intravenous administration [ ].
Liposomal formulations of curcumin have been studied in various cancers including pancreatic, colorectal and prostate [ — ]. Intravenous liposomal curcumin has been studied by our laboratory in mouse xenograft tumors of the oral cancer cell lines CAL27 and UM-SCC-1, and was found to be both nontoxic as well as effective at suppressing tumor growth.
Xenograft mouse tumors were stratified into groups receiving no treatment, treatment with empty liposomes or treatment with liposome encapsulated curcumin and a statistically significant growth suppressive effect was observed in the liposomal curcumin group [ 53 ]. The presence of curcumin in mouse serum and liver was confirmed using liquid chromatography-mass spectrophotometry, demonstrating increased systemic absorption of liposomal curcumin relative to a DMSO-suspension of curcumin.
Immunohistochemistry of the tumor samples revealed decreased expression of NF-κB in the liposomal curcumin-treated tumors relative to both the liposomal control and untreated groups, while the staining intensity of pAKT did not show a significant difference among the three treatment groups, further supporting the in vitro findings that curcumin's growth suppressive effects are related to the suppression of NF-κB in an AKT-independent manner [ 53 ].
A recent study by Clark et al [ ] has shown chemopreventive effects of curcumin in mouse xenograft models of oral squamous cell carcinoma. These authors have demonstrated an inhibitory effect on tumor growth following treatment of the mice with an oral curcumin solution both prior to inoculation of SCC40 tongue squamous cell carcinoma cells as well as when curcumin was initiated after tumor formation.
In addition, curcumin oral solution was studied in a mouse model of oral carcinogenesis in which the tobacco derivative 4-nitroquinoloneoxide was painted inside the animal's mouths several times weekly, with or without concurrent oral curcumin solution.
In the mice receiving concurrent curcumin, tumor-free and overall survival times were significantly increased. Finally, curcumin was found to decrease migration and invasion of malignant oral squamous cells via a downregulation in MMP-9 expression. While studies of curcumin as a single agent in the treatment of head and neck cancer have shown promising results, there is significant interest in potentially using the compound as an adjuvant agent in combination with standard platinum-based chemotherapy for the treatment of head and neck tumors.
Data from our laboratory in both CAL27 and UMSCC-1 cell lines demonstrated an increased growth suppressive effect in cells treated with a combination of liposomal curcumin and cisplatin, both in vitro as well as in mouse xenograft tumor models [ ].
While treatment with either curcumin or cisplatin in vitro resulted in cell death, a combination of curcumin and suboptimal concentrations of cisplatin demonstrated a significant growth suppressive effect compared to treatment with either agent alone. Curcumin's suppressive effect was again shown to derive from the inhibition of cytoplasmic and nuclear IκK, leading to inhibition of NF-κB activity.
There was no effect on pAKT, supporting an AKT-independent mechanism for NF-κB inhibition. Cisplatin treatment led to cellular senescence, an effect mediated through increased expression of p16 and p53 [ 7 ].
Differing mechanisms of curcumin and cisplatin suggest potential for the clinical use of subtherapeutic doses of cisplatin in combination with curcumin to accomplish effective suppression of tumor growth while minimizing cisplatin's toxic side effects.
In addition to the potential synergistic effect of curcumin with platinum based chemotherapy, the spice may also have potential utility as an enhancer of radiation therapy. A recent study by Khafif et al [ ] compared the effects of curcumin and single-dose radiation alone and in combination in the HNSCC cell lines SCC-1, SCC-9, A and KB.
In vitro growth suppression with either curcumin or radiation was observed in all four cell lines, and the combination of both therapies resulted in an additive growth suppressive effect. In addition, curcumin was shown to decrease COX-2 expression and inhibit EGFR phosphorylation in SCC-1 cells.
In vivo experiments using orthotopic mouse models of SCC-1 tumors also supported the additive effects of curcumin and radiation therapy. While curcumin has exhibited varying effects on radiation sensitivity in different cancer cell types, its effect as a radiosensitizer has been supported in several other tumors in addition to HNSCC including prostate, colorectal and ovarian cancers [ — ].
As discussed in this review, curcumin has demonstrated powerful anti-cancer effects in a variety of malignancies via its effects on a host of biological pathways involved in tumorigenesis and cellular growth. Continuing investigation into the molecular pathways affected by curcumin is indicated to further define the effects of the compound on growth signaling pathways, apoptotic and non-apoptotic cell death, oncogene and tumor suppressor regulation.
Translating this abundance of molecular data into eventual clinical applications is a paramount goal of future research. In head and neck cancers, a promising area of study centers around the use of curcumin to treat platinum-refractory tumors, which are associated with a poorer prognosis and have a tendency for disease recurrence.
Some work has been done in the area of characterizing putative 'cancer stem cells' in a variety of tumor types including HNSCC, breast, colorectal and prostate cancers [ — ]. Cancer stem cells are not true multipotent stem cells, but are a sub-population of highly tumorigenic cells that are theorized to contribute to chemoresistance and recurrence [ ].
CD44 is a cell surface marker that has been shown to be highly expressed in putative head and neck cancer stem cells [ — ]. Our laboratory has demonstrated a population of CD44 High putative stem cells within the UM-SCC1 cell line that possess increased tumorigenicity, growth rate and resistance to cisplatin treatment relative to CD44 Low cells [ ].
Investigating the growth suppressive properties of curcumin in these highly tumorigenic cells could be an initial study in quantifying the utility of the compound in chemotherapy-resistant head and neck cancers, and may have applications in other types of chemoresistant malignancies as well.
The solubility of curcumin in an intravenous delivery system is a major consideration in formulating the compound as a suitable chemotherapeutic agent. While our laboratory and others have shown increased therapeutic efficacy of liposomal curcumin, it is possible that other delivery systems may yield superior bioavailability and therapeutic results.
In addition to curcumin, multiple other biologically targeted agents are currently being studied in head and neck cancer.
As previously mentioned EGFR is overexpressed in many head and neck cancers and therefore represents a promising potential therapeutic target. The anti-EGFR monoclonal antibody cetuximab is approved both in combination with radiotherapy as well as a single agent for platinum-resistant HNSCC, but is also being investigated in combination with standard chemotherapeutic regimens.
However, acquired resistance to EGFR inhibition by cetuximab has emerged as a therapeutic challenge [ ]. In addition to targeting the extracellular EGF receptor, tyrosine kinase inhibitors erlotinib, gefitinib, lapatinib that block intracellular EGFR phosphorylation and inhibit downstream signal transduction are also being studied in HNSCC.
A Phase II study of erlotinib in patients with recurrent or metastatic head and neck cancer showed an increase in disease stabilization Table 2 [ ]. A Phase III trial of gefitinib alone compared to methotrexate monotherapy in recurrent HNSCC failed to show a significant survival increase, but a more recent study of gefitinib added to concurrent chemoradiation showed a favorable response that correlated to the number of EGFR copies in the various tumors [ , ].
Targeted therapies against the vascular endothelial growth factor receptor VEGF are also being evaluated in HNSCC. The anti-VEGF monoclonal antibody bevacizumab in combination with paclitaxel showed increased anti-tumor effects in mouse xenograft tumor models of HNSCC compared to either agent alone [ ].
As such employing rapamycin derivatives such as everolimus, deforolimus and temserolimus may prove useful in the treatment of refractory head and neck cancers. Analysis of the radiosensitizing effect of CCI in mouse xenograft models of both cisplatin sensitive FaDu and resistant SCC40 head and neck squamous cell carcinoma showed increased survival relative to radiotherapy alone.
In addition, the antitumor effects of CCI plus radiotherapy were superior when compared to conventional chemoradiotherapy with cisplatin in both the FaDu and SCC40 xenograft tumors [ ].
In addition to the major pathways discussed above, several other novel biologic agents are under investigation in head and neck cancer that merit brief mention. It is currently FDA approved for treatment of advanced primary renal cell carcinoma and hepatocellular carcinoma. Pemetrexed is a folate antimetabolite currently FDA approved in combination with cisplatin for malignant mesothelioma.
A Phase I study of pemetrexed in combination with cisplatin for HNSCC showed no enhancement in cisplatin-related toxicities or alteration of the cisplatin pharmacokinetics [ ].
Bortezomib is a proteosome inhibitor that is FDA approved for the treatment of multiple myeloma and mantle cell lymphoma. The cytoplasmic to nuclear translocation and activation of NF-κB is a proteosome-dependant process, and bortezomib has been shown to inhibit nuclear activation of the RelA and NF-κB1 subunits in HNSCC [ ].
In addition bortezomib has been found to induce apoptosis in HNSCC cells via up-regulation of the pro-apoptotic proteins Bik and Bim, and the combination of bortezomib and cisplatin resulted in a synergistic tumoricidal effect in HNSCC [ ].
The need for alternative and less toxic therapies for head and neck squamous cell carcinoma is clear. While some promising results from such targeted therapies have been obtained, the complexity of interaction between these signaling pathways may contribute to the limited clinical response seen with the use of single-agent biologic therapies.
As a natural product, curcumin is both non-toxic as well as diversified in its inhibitory effects on a multitude of pathways involved in carcinogenesis and tumor formation.
While the compound alone has shown some anti-tumor effects in HNSCC, curcumin's lack of systemic toxicity and broad-reaching mechanism of action may make it best suited as an adjuvant therapy for head and neck cancers that are resistant to currently available therapies.
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