Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5885_Библиотеки_им_академика_М_И_Перельмана
.pdf
284
https://t.me/medicina_free
TABLE 12.2 (Continued)
Activity Cell Line Mechanism of Action
Human breast cancer Resveratrol increased the cytoplasmic
MDA-MB-231 cells concentration of calcium in cancer cells
Ovarian, (Kueck et al., 2007) Abrogating Akt phosphorylation.
breast, (Li et al., 2006)
uterine, (Sexton et al., 2006)
prostate, (Aziz et al., 2006)
and multiple myeloma cells
(Bhardwaj et al., 2007)
Biomarkers as Targeted Herbal Drug Discovery
and activate p53 causing the proapoptotic
gene’s transcription (Van Ginkel et al.,
2015).
Progression of tumor implies the growth in size and increase in a number of cells
in the tumor. This progression implicates various processes such as that lead to
tumor metastasis. It has been seen that several genes are mutated or deleted
physiologically that sustain the development of aggressive tumors. The invasion of healthy cells and metastasis of cancerous cells include the destruction
of the extracellular matrix (ECM) and the basement membrane, by proteolytic
enzymes, such as matrix metalloproteinases (MMPs). Out of all these enzymes,
MMP-2 and MMP-9 are highly expressed within different types of malignant
tumors modifying the cellular invasion and its metastatic properties (Nelson et
al., 2000). Tissue inhibitor metalloproteinase proteins (TIMPs), on the other
hand, are a protein group comprising TIMP-1, -2, -3, and -4 acting as natural
MMP inhibitors (Jinga et al., 2006). Invasive tumors require new blood vessels
which are fulfilled via angiogenesis. During the process of angiogenesis, endothelial cells can be activated by several growth factors, like fibroblast growth
factor (FGF) and VEGF. Obstructing the development of newly formed blood
vessels causes the supply of nutrients and oxygen to be reduced and, as a result,
the size of the tumor and metastasis may also be reduced (see Table 12.3).
Resveratrol has also been reported to possess a significant anti-cancer
property in various pre-clinical animal models (see Table 12.4). Table 12.4
summarizes the major outcomes of several research studies.
285 Resveratrol-Loaded Phytomedicines for Management of Cancer
https://t.me/medicina_free
TABLE 12.3 The Anti-Tumor Progression Potential of Resveratrol and its Mode of Action
Activity Cell Line Mechanism of Action
Anti-tumor
progression
Liver cancer HepG2
cells
Liver cancer Hep3B
cells
Breast cancer
MDA-MB231 cells
Human ovarian
cancer cells
A549 lung cancer
cells
Pancreatic cancer
PANC-1 cells
Up-regulated TIMP-1 protein expression and
down-regulated MMP-9 activity (Weng et al.,
2010).
Activities of MMP-2 and MMP-9 were decreased,
along with a rise in the protein expression level of
TIMP-2 (Weng et al., 2010).
Inhibition of the epidermal growth factor (EGF)induced elevation of cell migration, and of the
expression of MMP-9 (Lee et al., 2011).
Abrogating the activation of the PI3K/Akt and
MAPK signaling pathways (Cao et al., 2004).
Inhibited TGF--induced EMT by augmenting
the expression of E-cadherin and attenuating the
expression of vimentin and fibronectin, as well as
the EMT-inducing transcription factors Slug and
Snail (Wang et al., 2013).
By regulating factors related to EMT (vimentin,
E-cadherin, N-cadherin, MMP-2, and MMP-9)
and modulating the activation of PI3K/Akt/NF-kB
pathways (Lee et al., 2013).
TABLE 12.4 Enlists the Outcomes of In Vivo Study Involving Resveratrol
Cancer Model Animal Model Outcome
Skin DMBA/TPA model in female
CD-1 mice
Mouse xenograft models of A431
cells
DMBA/TPA model in CD-1 mice Skin tumor incidence decreases.
UVB-mediated
photocarcinogenesis in female
SKH-1 mice
Incidence decreases.
Number of tumors per mouse
decreases (Jang et al., 1997).
Xenograft volume decreases.
Free radical scavenging Incidence
decreases.
Number of tumors per mouse
decreases (Hao et al., 2013).
Apoptosis increases; p53 increases;
Bax increases; cytochrome C
increases; APAF increases; Bcl2
decreases (Soleas et al., 2002).
Decrease hyperplasia; p53
increases.
286
https://t.me/medicina_free
TABLE 12.4 (Continued)
Cancer Model Animal Model Outcome
Breast Spontaneous mammary tumor in Onset of tumorigenesis decreases.
female FVB/N HER-2/neu mice
DMBA-induced mammary Suppressed tumor growth Cell
carcinogenesis in female Sprague- proliferation decreases, Apoptosis
Dawley rats increases (Whitsett et al., 2006)
Female HER-2/neu Delays the development and
transgenic mice model
Prostate Athymic nude mice Tumor volume decreases.
xenograft models of PC-3 cells Cell proliferation decreases.
Male nude mice Tumor growth decreases.
xenograft models with Progression, local invasion
Du145-EV-Luc decreases.
or Du145-MTA1 Spontaneous metastasis decreases.
shRNA-Luc in anterior prostate Angiogenesis decreases.
Lung Female C57BL/6 mice] Tumor volume/weight decreases.
xenograft models of LLC tumors Metastasis to lung decreases
C57BL/6 mice implanted with Angiogenesis decreases. Apoptosis
Lewis’s lung carcinoma lung increases (Lee et al., 2006).
tumor model
Liver Male Donryu rats Tumor weight decreases.
xenograft models of AH109A Metastasis decreases (Miura et al.,
cells 2007).
Biomarkers as Targeted Herbal Drug Discovery
Cox2 decreases; ODC decreases;
surviving decreases mRNA and
protein (Afaq et al., 2003).
Tumor volume decreases.
Multiplicity decreases.
Apoptosis increases (Provinciali et
al., 2005).
reduces the metastatic growth of
spontaneous mammary tumors.
Apoptosis increases, decreases
HER-2/neu mRNA and protein
(Provinciali et al., 2005).
Apoptosis increases.
Number of blood vessels decreases
(Ganapathy et al., 2010).
Apoptosis increases (Li et al.,
2013).
(Kimura et al., 2001).
287 Resveratrol-Loaded Phytomedicines for Management of Cancer
https://t.me/medicina_free
TABLE 12.4 (Continued)
Cancer Model Animal Model Outcome
DENA-initiated and PB-promoted
hepatocyte nodule formation in
female
Sprague-Dawley rats
Male Wistar rats implanted with
AH-130 hepatoma cells
Tumor growth decreases.
Apoptosis increases.
Cell proliferation decreases.
Bcl2 decreases; Bax increases
(Bishayee et al., 2009).
Tumor weight decreases.
Apoptosis increases.
Increases cells at G2/M (Kowalczyk
et al., 2013).
In recent years, a number of approaches have been developed to encounter
the molecular-level changes in the pathophysiology of carcinogenesis. The
latest approach includes nano-diagnostic and nanotherapeutic modalities, like
lipid nanoparticles, nanohybrids, and polymeric nanoparticles (Gharpure et
al., 2015; Pacardo et al., 2015; Stylianopoulos et al., 2015). These nanocarrier modalities as drug delivery vehicles have elucidated promising results in
preclinical and initial clinical trials (Eetezadi et al., 2015; Fernandes et al.,
2015; Johnstone et al., 2016). Nanocarrier drug delivery systems have excellent salient features, including but not limited to improved stability, enhanced
solubility, and increased surface area: volume ratio. Moreover, these carriers
add extra edge as their surface properties are modifiable and can be adjusted
to achieve manageable pharmacological and physicochemical characteristics,
hence reducing impediments in attaining effective cancer chemotherapy
(Kumari et al., 2016). In addition, an improved therapeutic index and moderated toxicity to normal healthy cells are also attained through nanotherapeutic
carriers (Kumari et al., 2016). It is remarkable that active and passive targeting
could be used to deliver drugs to specific sites. These characteristic features
of nanocarriers are imperative for typical biologically active compounds like
polyphenols for their rendition into novel therapeutic modalities. Irrespective
of the assuring progress in basic cancer biology in preclinical studies, polyphenols possess inappropriate pharmacological properties like low bioavailability due to inept systemic access, and therefore high doses are required for
elucidation of optimum therapeutic effect (Siddiqui et al., 2012). Although the
288
https://t.me/medicina_free
Biomarkers as Targeted Herbal Drug Discovery
biological effectiveness of polyphenols has been established through in vitro
studies, similar results could not be reproduced in the in vivo studies and it
was due to their instability in the physiological conditions of temperature, pH,
and enzyme system. It was then proposed that the development of polyphenol
loaded nanotherapeutics could resolve this issue by addressing the instability
and systemic access of the active ingredient, resveratrol. Sooner a series of
studies were carried out to evaluate the biologically active polyphenol combination with nano-sized carriers. The outcome from these studies revealed many
solutions to overcome the shortcomings of conventional anticancer therapy
and develop a clinically efficient anticancer treatment.
Some of the research studies have recorded intense toxicity of curcuminloaded poloxamer nanocarriers in HeLa (Sahu et al., 2011) and ovarian
cancer cells (Saxena et al., 2013). Moreover, resveratrol and doxorubicin
(DOX) containing poloxamer nano-formulations exhibited a synergistic
effect on ovarian cancer in mice (Carlson et al., 2014). Kim et al. (2015)
reported that a combination of resveratrol-quercetin elucidated similar
effect in ovarian tumors (Kim et al., 2015). In addition, resveratrol was
encapsulated into PEG-polycaprolactone conjugate was used to encapsu-
late resveratrol and the surface modication of the resulting micelles was
carried out using a polipoprotein and used to treat glioblastoma (Wang et
al., 2015) as well as breast cancer. Finally, other studies mentioned that
epigallocatechin gallate (EGCG) was delivered in colon cancer using
PEG-polylactic acid (PLA) (Haratifar et al., 2014) and in pancreatic cancer
using casein micelles as carriers (Sun et al., 2014) (see Table 12.5).
In another set of studies we found that resveratrol was nanoencapsulated
in bovine serum albumin (Guo et al., 2015), gelatin (Karthikeyan et al., 2015),
PLGA (Kumar et al., 2016), and PLGA-PEG derivatives (Sanna et al., 2013),
and reported a signicant elevation in the anticancer activity of resveratrol
against prostate, ovarian, breasts, and lung cancer (Guo et al., 2015; Karthikeyan
et al., 2015; Kumar et al., 2016; Sanna et al., 2013). Transferrin was used to
modify the surface of resveratrol loaded PLGA-PEG nanoparticles for active
targeting of glioma cancer cells in vivo (Guo et al., 2013).
Nanoparticles loaded with EGCG, resveratrol, quercetin, and 5-uorouracil
can be designed with enhanced stability and in vitro anticancer activity can be
elucidated in various types of cancer including cancer of the stomach, prostate,
ovaries, alimentary canal, and breast. The stability can be adjusted using several
natural polymers, such as gelatin, PEG, and PLGA, alone or in combination
with synthetic polymers, like chitosan (CS), and casein. Polyphenol-loaded
polymeric conjugates for the treatment of cancer are summarized in Table 12.5.
TABLE 12.5 Enumerates Different Types of Nanoparticles Prepared Using Resveratrol and Synergistic Agents
https://t.me/medicina_free
Sl. Type of Nano Components of Method Resveratrol + Model Used
No. Formulation Nanoparticles Synergistic Agent
1. Nanovesicles Poloxamers F127 Thin-layer evaporation Resveratrol + curcumin + Ovarian cancer SKOV-3 Healthy mice
Doxorubicin (Carlson et al., 2014)
2. Poloxamers F127 Thin-layer evaporation Resveratrol + quercetin + Ovarian cancer SKOV-3 Healthy mice
Doxorubicin (Cote et al., 2015)
3. Apolipoprotein-E3 Recombinant DNA Resveratrol Glioblastoma A-172 (Kim et al., 2015)
4. Polycaprolactone- Thin-layer evaporation Resveratrol Breast cancer MCF-7 (Wang et al., 2015)
PEG-Succinate
5. Nanoparticles PLGA-PEG Nanoprecipitation Resveratrol Prostate cancer DU-145, LNCaP (Guo et
al., 2015)
6. Bovine Serum Nanoprecipitation Resveratrol Lung cancer NCI-H460 (Karthikeyan et
Albumin al., 2015)
7. Bovine Serum Nanoprecipitation Resveratrol Ovarian Cancer SKOV-3 (Kumar et al.,
Albumin 2016)
8. PLGA Emulsion method Resveratrol Breast cancer MCF-7 (Sanna et al., 2013)
9. Maleimide-PEG- Self-assembly Resveratrol Glioblastoma CT26, U87 CT26 Xenograft
Polylactic acid mice (Guo et al., 2013)
10. Polymeric PEG Condensation method Resveratrol + Cervical cancer HeLa (Wang et al., 2016)
conjugates Bicalutamide
11. PEG Condensation method Resveratrol + Breast cancer MCF-7 (Wang et al., 2016)
Bicalutamide
12. Carbon-based Graphene oxide Reduction method Resveratrol Ovarian cancer A2780 (Gurunathan et al.,
nanohybrids 2015)
Resveratrol-Loaded Phytomedicines for Management of Cancer
289
290
https://t.me/medicina_free
Biomarkers as Targeted Herbal Drug Discovery
Curcumin-gemcitabine combination was encapsulated in PEG conjugates
by a condensation reaction in the presence of carbodiimide for the treatment of
pancreatic cancer (Li et al., 2009). PEG conjugates containing only curcumin
have been formulated for prostate cancer (Safavy et al., 2007) and glioma
cancer (Dey et al., 2015). Using the same conjugation technique, Wang et al.
reported synergistic cytotoxicity by resveratrol-bicalutamide-PEG conjugates
in breast and cervical cancer cells (Wang et al., 2016) and in hepatic cancer cells
using quercetin-paclitaxel-carboxymethyl CS conjugates (Wang et al., 2014).
There is a multitude of polymeric conjugates which include nanoparticles loaded with resveratrol, quercetin, and curcumin in combination with
standard anticancer drugs like paclitaxel, gemcitabine, or bortezomib for the
treatment of hepatic, pancreatic, prostate, glioma, and breast cancer.
From the remarkable reports of resveratrol involved in preclinical and clinical
anticancer studies, it can be deduced that resveratrol can attenuate carcinogenesis at various stages. As validated by experimental in vivo and in vitro studies,
which are further supported by some clinical trial studies it can be stated that
resveratrol has substantial potential as an anti-cancer agent and is involved in
both prevention and therapy of a wide range of cancerous conditions. Resveratrol has many molecular targets and it acts on different protective and common
pathways that are generally distorted in cancerous tumors. This suggests that
resveratrol is a suitable anticancer agent and produces the pharmacological
effect in conjunction with diverse chemotherapeutics and targeted therapies.
The ability of resveratrol to prevent carcinogenesis includes the placation of
oxidative stress, inflammation, and inhibition of cancer cell proliferation, and
the activation of tightly regulated cell-death mechanisms.
Since resveratrol has complex involvement in the cellular processes,
more studies must be carried out to understand better ways resveratrol could
be exploited to prevent the carcinogenesis. Moreover, resveratrol has poor
bioavailability in human subjects, and it has been a serious concern in transforming the outcomes of basic research to formulating therapeutic agents.
Though clinical trials have revealed positive and benecial outcomes, there
are many conicts which still need to be addressed. To enhance the bioavail-
ability of resveratrol and to make it a potential anticancer agent, research
that is more active should be directed toward the novel drug delivery system
of resveratrol, its formulations, and its metabolism. Moreover, the possible
interactions of resveratrol with other compounds also must be ruled out.
291 Resveratrol-Loaded Phytomedicines for Management of Cancer
https://t.me/medicina_free
• anticancer
• cancer
• chemoprevention
•
• nanoformulation
• phytomedicine
• resveratrol
Afaq, F., Adhami, V. M., & Ahmad, N., (2003). Prevention of short-term ultraviolet Bradiation-
mediated damages by resveratrol in SKH-1 hairless mice. Toxicol. Appl. Pharmacol., 186,
28–37.
Aggarwal, B. B., Bhardwaj, A., Aggarwal, R. S., Seeram, N. P., Shishodia, S., & Takada, Y.,
(2004). Role of resveratrol in prevention and therapy of cancer: Preclinical and clinical
studies. Anticancer Res., 24, 2783–2840.
Aggarwal, B. B., Van, K. M. E., Iyer, L. H., Harikumar, K. B., & Sung, B., (2009). Molecular
targets of nutraceuticals derived from dietary spices: Potential role in suppression of
inflammation and tumorigenesis. Exp. Biol. Med., 234, 825–849.
Aggarwal, B. B., Vijayalekshmi, R. V., & Sung, B., (2009). Targeting inflammatory pathways
for prevention and therapy of cancer: Short-term friend, long-term foe. Clin. Cancer Res.,
15, 425–430.
Athar, M., Back, J. H., Kopelovich, L., Bickers, D. R., & Kim, A. L., (2009). Multiple
molecular targets of resveratrol: Anticarcinogenic mechanisms. Archives of Biochemistry
and Biophysics, 486(2), 95–102.
Athar, M., Back, J. H., Tang, X., Kim, K. H., Kopelovich, L., Bickers, D. R., & Kim, A. L.,
(2007). Resveratrol: A review of preclinical studies for human cancer prevention. Toxicol.
App. Pharmacol., 224(3), 274–283.
Attia, S. M., (2012). Influence of resveratrol on oxidative damage in genomic DNA and
apoptosis induced by cisplatin. Mutat. Res., 741, 22–31.
Aziz, M. H., Nihal, M., Fu, V. X., Jarrard, D. F., & Ahmad, N., (2006). Resveratrol-caused
apoptosis of human prostate carcinoma LNCaP cells is mediated via modulation of
phosphatidylinositol 30-kinase/Akt pathway and Bcl-2 family proteins. Mol. Cancer Ther.,
5, 1335–1341.
Bai, Y., Mao, Q. Q., Qin, J., Zheng, X. Y., Wang, Y. B., Yang, K., Shen, H. F., & Xie, L. P.,
(2010). Resveratrol induces apoptosis and cell cycle arrest of human T24 bladder cancer
cells in vitro and inhibits tumor growth in vivo. Cancer Sci., 101, 488–493.
Barzilai, A., & Yamamoto, K., (2004). DNA damage responses to oxidative stress. DNA
Repair, 3, 1109–1115.
292
https://t.me/medicina_free
Baur, J. A., Pearson, K. J., Price, N. L., Jamieson, H. A., Lerin, C., Kalra, A., Prabhu, V. V.,
Allard, J. S., Lopez-Lluch, G., Lewis, K., et al., (2006). Resveratrol improves health and
survival of mice on a high-calorie diet. Nature, 444, 337–342.
Beedanagari, S. R., Bebenek, I., Bui, P., & Hankinson, O., (2009). Resveratrol inhibits dioxin-
induced expression of human CYP1A1 and CYP1B1 by inhibiting recruitment of the aryl
hydrocarbon receptor complex and RNA polymerase II to the regulatory regions of the
corresponding genes. Toxicol. Sci., 110, 61–67.
Benitez, D. A., Pozo-Guisado, E., Alvarez-Barrientos, A., Fernandez-Salguero, P. M., &
Castellon, E. A., (2007). Mechanisms involved in resveratrol-induced apoptosis and cell
cycle arrest in prostate cancer-derived cell lines. J. Androl., 28, 282–293.
Bernhard, D., Tinhofer, I., Tonko, M., Hubl, H., Ausserlechner, M. J., Greil, R., Kofler, R.,
& Csordas, A., (2000). Resveratrol causes arrest in the S-phase prior to Fas-independent
apoptosis in CEM-C7H2 acute leukemia cells. Cell Death Differ., 7, 834–842.
Bhardwaj, A., Sethi, G., Vadhan-Raj, S., Bueso-Ramos, C., Takada, Y., Gaur, U., Nair, A.
S., et al., (2007). Resveratrol inhibits proliferation, induces apoptosis, and overcomes
chemo resistance through down-regulation of STAT3 and nuclear factor-kB-regulated
antiapoptotic and cell survival gene products in human multiple myeloma cells. Blood,
109, 2293–2302.
Bishayee, A., & Dhir, N., (2009). Resveratrol-mediated chemoprevention of diethylnitrosamine-
initiated hepatocarcinogenesis: Inhibition of cell proliferation and induction of apoptosis.
Chem. Biol. Interact., 179, 131–144.
Bishayee, A., & Sethi, G., (2016). Bioactive natural products in cancer prevention and
therapy: Progress and promise. Semin. Cancer Biol., 40, 41, 1–3.
Bishayee, A., (2009). Cancer prevention and treatment with resveratrol: From rodent studies
to clinical trials. Cancer Prev. Res., 2, 409–418.
Bishayee, A., Politis, T., & Darvesh, A. S., (2010). Resveratrol in the chemoprevention and
treatment of hepatocellular carcinoma. Cancer Treat. Rev., 36, 43–53.
Cai, Y. J., Wei, Q. Y., Fang, J. G., Yang, L., Liu, Z. L., Wyche, J. H., & Han, Z., (2004).
The 3, 4-dihydroxyl groups are important for trans-resveratrol analogs to exhibit enhanced
antioxidant and apoptotic activities. Anticancer Res., 24, 999–1002.
Cao, Z., Fang, J., Xia, C., Shi, X., & Jiang, B. H., (2004). trans-3,4,50-Trihydroxystibene
inhibits hypoxia-inducible factor 1and vascular endothelial growth factor expression in
human ovarian cancer cells. Clin. Cancer Res., 10, 5253–5263.
Carlson, L. J., Cote, B., Alani, A. W., & Rao, D. A., (2014). Polymeric micellar codelivery of
resveratrol and curcumin to mitigate in vitro doxorubicin induced cardiotoxicity. J. Pharm.
Sci., 103, 2315–2322.
Carter, L. G., D’Orazio, J. A., & Pearson, K. J., (2014). Resveratrol and cancer: Focus on in
vivo evidence. Endocr. Relat. Cancer, 21, R209–R225.
Chai, E. Z., Siveen, K. S., Shanmugam, M. K., Arfuso, F., & Sethi, G., (2015). Analysis of
the intricate relationship between chronic inflammation and cancer. Biochem. J., 468, 1–15.
Chen, Z. H., Hurh, Y. J., Na, H. K., Kim, J. H., Chun, Y. J., Kim, D. H., Kang, K. S., et
al., (2004). Resveratrol inhibits TCDD-induced expression of CYP1A1 and CYP1B1 and
catechol estrogen-mediated oxidative DNA damage in cultured human mammary epithelial
cells. Carcinogenesis, 25, 2005–2013.
Ciolino, H. P., & Yeh, G. C., (1999). Inhibition of aryl hydrocarbon-induced cytochrome
P-450 1A1 enzyme activity and CYP1A1 expression by resveratrol. Mol. Pharmacol., 56,
760–767.
Biomarkers as Targeted Herbal Drug Discovery
293 Resveratrol-Loaded Phytomedicines for Management of Cancer
https://t.me/medicina_free
Clement, M. V., Hirpara, J. L., Chawdhury, S. H., & Pervaiz, S., (1998). Chemo preventive
agent resveratrol, a natural product derived from grapes, triggers CD95 signaling-dependent
apoptosis in human tumor cells. Blood, 92, 996–1002.
Colin, D., Lancon, A., Delmas, D., Lizard, G., Abrossinow, J., Kahn, E., Jannin, B., &
Latruffe, N., (2008). Antiproliferative activities of resveratrol and related compounds in
human hepatocyte derived HepG2 cells are associated with biochemical cell disturbance
revealed by fluorescence analyses. Biochimie., 90, 1674–1684.
Cote, B., Carlson, L. J., Rao, D. A., & Alani, A. W. G., (2015). Combinatorial resveratrol and
quercetin polymeric micelles mitigate doxorubicin induced cardiotoxicity in vitro and in
vivo. J. Control Release, 213, 128–133.
Cucciolla, V., Borriello, A., Oliva, A., Galletti, P., Zappia, V., & Della, R. F., (2007).
Resveratrol: From basic science to the clinic. Cell Cycle, 6, 2495–2510.
Delmas, D., Rebe, C., Lacour, S., Filomenko, R., Athias, A., Gambert, P., Cherkaoui-Malki,
M., Jannin, B., Dubrez-Daloz, L., Latruffe, N., et al., (2003). Resveratrol-induced apoptosis
is associated with Fas redistribution in the rafts and the formation of a death-inducing
signaling complex in colon cancer cells. J. Boil. Chem., 278, 41482–41490.
Dey, S., Ambattu, L. A., Hari, P. R., Rekha, M. R., & Sreenivasan, K., (2015). Glutathione-
bearing fluorescent polymer-curcumin conjugate enables simultaneous drug delivery and
label-free cellular imaging. Polym. UK, 75, 25–33.
Eetezadi, S., Ekdawi, S. N., & Allen, C., (2015). The challenges facing block copolymer
micelles for cancer therapy, in vivo barriers, and clinical translation. Adv. Drug Deliv. Rev.,
91, 7–22.
Fernandes, E., Ferreira, J. A., Andreia, P., Luís, L., Barroso, S., Sarmento, B., & Santos, L. L.,
(2015). New trends in guided nanotherapies for digestive cancers, a systematic review. J.
Control Release, 209, 288–307.
Ferry-Dumazet, H., Garnier, O., Mamani-Matsuda, M., Vercauteren, J., Belloc, F., Billiard,
C., Dupouy, M., Thiolat, D., Kolb, J. P., Marit, G., et al., (2002). Resveratrol inhibits
the growth and induces the apoptosis of both normal and leukemic hematopoietic cells.
Carcinogenesis, 23, 1327–1333.
Filippi-Chiela, E. C., Villodre, E. S., Zamin, L. L., & Lenz, G., (2011). Autophagy interplay
with apoptosis and cell cycle regulation in the growth inhibiting effect of resveratrol in
glioma cells. PLoS One, 6, e20849.
Fruehauf, J. P., & Meyskens, F. L. Jr., (2007). Reactive oxygen species: A breath of life or
death? Clin. Cancer Res., 13, 789–794.
Galati, G., Teng, S., Moridani, M. Y., Chan, T. S., & O’Brien, P. J., (2000). Cancer
chemoprevention and apoptosis mechanisms induced by dietary polyphenolics. Drug
Metab. Drug Interact, 17, 311–349.
Ganapathy, S., Chen, Q., Singh, K. P., Shankar, S., & Srivastava, R. K., (2010). Resveratrol
enhances antitumor activity of TRAIL in prostate cancer xenografts through activation of
FOXO transcription factor. PLoS One, 5, e15627.
Gartel, A. L., & Tyner, A. L., (2002). The role of the cyclin-dependent kinase inhibitor p21 in
apoptosis. Mol. Cancer Ther., 1, 639–649.
Gatouillat, G., Balasse, E., Joseph-Pietras, D., Morjani, H., & Madoulet, C., (2010).
Resveratrol induces cell-cycle disruption and apoptosis in chemoresistant B16 melanoma.
J. Cell. Biochem., 110, 893–902.
Gharpure, K. M., Wu, S. Y., Li, C., Lopez-Berestein, G., & Sood, A. K., (2015). Nanotechnology,
future of oncotherapy. Clin. Cancer Res., 21, 3121–3130.
Соседние файлы в папке Библиотека им академика М.И. Перельмана