scholarly journals Antitumor Effect of Fever Range Whole Body Hyperthermia with Curcumin in Breast Cancer-induced Mice

2019 ◽  
Vol 8 (2S2) ◽  
pp. 297-301
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Combination Treatment ◽  
Tumor Volume ◽  
Whole Body ◽  
Tumor Growth Inhibition ◽  
Tumor Treatment ◽  
Treatment Groups ◽  
Whole Body Hyperthermia ◽  
Cancer Types

Breast cancer is a complex and heterogeneous disease and also one of the major cancer types among female worldwide. Fever range whole-body hyperthermia and curcumin as a single treatment have been tested against breast cancer and showed some promising anti-tumor effect. However, their combination as an effective anti- tumor treatment against breast cancer has never been explored. The effects of combined wholebody fever range hyperthermia and curcumin on tumor growth was examined in this study. Mice were inoculated with EMT6 cells subcutaneously and allocated to 4 treatment groups: (i) control (control), (ii) curcumin (50mg/kg bodyweight), (iii) twice fever range whole-body hyperthermia 39.0°C (± 0.5) for 15 minutes, (iv) a combination of curcumin (50mg/kg bodyweight) and twice fever range whole-body hyperthermia 39.0°C (± 0.5) for 15 minutes. Following treatment, mice body weight and tumor volume were measured. The greatest tumor growth inhibition exhibited in combination treatment (68.45%, p<0.05) and showed no general toxicity. As conclusion, the combination treatment can be a potential anti-tumor treatment of breast cancer.

scholarly journals Effects of Steady Low-Intensity Exercise on High-Fat Diet Stimulated Breast Cancer Progression Via the Alteration of Macrophage Polarization

2020 ◽  
Vol 19 ◽  
pp. 153473542094967
Author(s):  
Min Kyoon Kim ◽  
Yesl Kim ◽  
SeungHwa Park ◽  
Eunju Kim ◽  
Yerin Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
High Fat Diet ◽  
Tumor Volume ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
High Fat ◽  
Low Intensity ◽  
M2 Macrophage Polarization ◽  
Low Intensity Exercise

Physical inactivity and high-fat diet, especially high saturated fat containing diet are established risk factors for breast cancer that are amenable to intervention. High-fat diet has been shown to induce tumor growth and metastasis by alteration of inflammation but steady exercise has anti-tumorigenic effects. However, the mechanisms underlying the effects of physical activity on high-fat diet stimulated breast cancer initiation and progression are currently unclear. In this study, we examined how the intensity of physical activity influences high fat diet-stimulated breast cancer latency and progression outcomes, and the possible mechanisms behind these effects. Five-week-old female Balb/c mice were fed either a control diet or a high-fat diet for 8 weeks, and then 4T1 mouse mammary tumor cells were inoculated into the mammary fat pads. Exercise training occurred before tumor cell injection, and tumor latency and tumor volume were measured. Mice with a high-fat diet and low-intensity exercise (HFLE) had a longer tumor latency period, slower tumor growth, and smaller tumor volume in the final tumor assessment compared with the control, high-fat diet control (HFDC), and high-fat diet with moderate-intensity exercise (HFME) groups. Steady low- and moderate-intensity exercise had no effect on cell proliferation but induced apoptosis by activating caspase-3 through the alteration of Bcl-2, Bcl-xL, and Bax expression. Furthermore, steady exercise reduced M2 macrophage polarization in breast tumor tissue, which has been linked to tumor growth. The myokine, myostatin, reduced M2 macrophage polarization through the inhibition of the JAK-STAT signaling pathway. These results suggest that steady low-intensity exercise could delay breast cancer initiation and growth and reduce tumor volume through the induction of tumor cell apoptosis and the suppression of M2 macrophage polarization.

Enhanced tumor growth in experimental whole body hyperthermia

1983 ◽  
Vol 24 (2) ◽  
pp. 119-123 ◽  
Author(s):  
Alan G. Wile ◽  
Maurice Y. Nahabedian ◽  
G. Robert Mason
Keyword(s):  
Tumor Growth ◽  
Whole Body ◽  
Whole Body Hyperthermia

scholarly journals Deep Learning Based Automated Orthotopic Lung Tumor Segmentation in Whole-Body Mouse CT-Scans

Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4585
Author(s):  
Wouter R. P. H. van de Worp ◽  
Brent van der Heyden ◽  
Georgios Lappas ◽  
Ardy van Helvoort ◽  
Jan Theys ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Deep Learning ◽  
Tumor Growth ◽  
Tumor Volume ◽  
Learning Algorithm ◽  
Lung Tumor ◽  
Whole Body ◽  
Ct Scans ◽  
Therapeutic Effects ◽  
Deep Learning Algorithm

Lung cancer is the leading cause of cancer related deaths worldwide. The development of orthotopic mouse models of lung cancer, which recapitulates the disease more realistically compared to the widely used subcutaneous tumor models, is expected to critically aid the development of novel therapies to battle lung cancer or related comorbidities such as cachexia. However, follow-up of tumor take, tumor growth and detection of therapeutic effects is difficult, time consuming and requires a vast number of animals in orthotopic models. Here, we describe a solution for the fully automatic segmentation and quantification of orthotopic lung tumor volume and mass in whole-body mouse computed tomography (CT) scans. The goal is to drastically enhance the efficiency of the research process by replacing time-consuming manual procedures with fast, automated ones. A deep learning algorithm was trained on 60 unique manually delineated lung tumors and evaluated by four-fold cross validation. Quantitative performance metrics demonstrated high accuracy and robustness of the deep learning algorithm for automated tumor volume analyses (mean dice similarity coefficient of 0.80), and superior processing time (69 times faster) compared to manual segmentation. Moreover, manual delineations of the tumor volume by three independent annotators was sensitive to bias in human interpretation while the algorithm was less vulnerable to bias. In addition, we showed that besides longitudinal quantification of tumor development, the deep learning algorithm can also be used in parallel with the previously published method for muscle mass quantification and to optimize the experimental design reducing the number of animals needed in preclinical studies. In conclusion, we implemented a method for fast and highly accurate tumor quantification with minimal operator involvement in data analysis. This deep learning algorithm provides a helpful tool for the noninvasive detection and analysis of tumor take, tumor growth and therapeutic effects in mouse orthotopic lung cancer models.

Development of orally bioavailable prodrugs of fulvestrant for the treatment of metastatic/advanced breast cancer.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e13027-e13027
Author(s):  
Parva Purohit ◽  
Pathik Brahmkshatriya ◽  
Vishalgiri Goswami
Keyword(s):  
Breast Cancer ◽  
Oral Delivery ◽  
Tumor Volume ◽  
Estrogen Therapy ◽  
Xenograft Model ◽  
Fold Increase ◽  
Tumor Growth Inhibition ◽  
Pharmacokinetic Studies ◽  
Hormone Receptor Positive ◽  
Mcf 7

e13027 Background: Fulvestrant, a potent, selective estrogen receptor degrader, is a primary drug of choice for treating advanced metastatic hormone receptor-positive breast cancer in postmenopausal women following anti-estrogen therapy. However, the existing therapy limits to inconvenient intramuscular injections due to low solubility, weak permeation, high metabolism, and poor pharmacokinetics profile. Additionally, it takes 30 days to reach maximal steady-state plasma concentration, limiting clinical efficacy. To overcome these issues, we modulated physicochemical properties of fulvestrant, enabling its oral delivery to improve bioavailability. Methods: Structurally diverse pro-moieties were appended on fulvestrant to improve solubility and ADME profile. Thermodynamic solubility, plasma/liver microsomal stability, and Caco-2 permeability studies were performed to identify lead molecules. Pharmacokinetic studies were performed for selected molecules in mice. Antitumor activity of once-daily oral dose of three molecules was evaluated in female nude mice using the MCF-7 xenograft model. The efficacy of lead molecules was compared with subcutaneously administered faslodex in terms of percentage tumor growth inhibition. Results: Several prodrugs of fulvestrant were synthesized and evaluated for their intrinsic properties suitable for increasing bioavailability of fulvestrant. Remarkable improvements (̃500 to 2000-fold increase) were achieved in solubility and permeability. The PoC established an increase in systemic plasma exposure of fulvestrant upon oral administration of prodrugs in mice with enhanced bioavailability (1.5-8.7-fold) as compared to fulvestrant given subcutaneously (Table). Herewith, we report the identification of KSHN001022, KSHN001075, and KSHN001126, the prodrugs of fulvestrant, which showed enhanced efficacy with better tumor volume reduction (̃48-88% regression in tumor volume) as compared to that of fulvestrant (78%) in the estrogen-dependent MCF-7 xenograft model. Conclusions: KSHN001 lead candidates demonstrated significantly higher bioavailability, hence, provides a novel strategy to deliver fulvestrant orally to pursue the potential benefits in patients with advanced metastatic disease.[Table: see text]

scholarly journals DRES-07. TMZ-LEV- IFN COCKTAIL REGIMEN SIGNIFICANTLY INHIBITED THE GROWTH OF GLIOMA IN VIVO

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi72-vi73
Author(s):  
Xiang-rong Ni ◽  
Jing Wang ◽  
Fu-rong Chen ◽  
Hai-ping Cai ◽  
Yan-jiao Yu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Tumor Growth ◽  
Tumor Volume ◽  
Control Group ◽  
First Line ◽  
Killing Effect ◽  
Treatment Groups ◽  
Mgmt Protein ◽  
Tumor Killing

Abstract OBJECTIVE Temozolomide (TMZ), is the first line chemotherapeutic drug for glioma. Previous studies have suggested that interferon (IFN) and levetiracetam (LEV) could respectively reverse the resistance of TMZ by down-regulating MGMT expression. This study, we aim to investigate the therapeutic effect of a cocktail chemotherapy regimen combining TMZ, LEV, IFN in vivo. METHODS Glioma cell lines U251 and SKMG-4 (MGMT protein expression positive), U138 and GSC-1(MGMT protein expression negative) were used for producing xenograft tumors. The xenograft tumors were established by subcutaneously injecting 1×106 glioma cells into female BALB/C nude mice and divided into 5 treatment groups: Control, TMZ, TMZ+IFN, TMZ+LEV, TMZ+LEV+IFN. The treatment with TMZ (50 mg/kg, i.p.), IFN (2×105 IU, s.c.), LEV (150 mg/kg, i.p.) once a day for five consecutive days and xenograft tumors were measured every two days. RESULTS We identified that U138, U251, SKMG-4 tumor growth among TMZ, TMZ+IFN, TMZ+LEV, TMZ+LEV+IFN were all significantly inhibited (P< 0.05), compared with the control. As for U251 and SKMG-4, tumor killing effect of all 4 treatment groups were not different (P > 0.05). In the treatment of mice bearing U138 glioma, the tumor weight of TMZ+LEV+IFN (0.2688±0.1169 g) group was the lowest and significantly lower than that of TMZ+LEV (0.6574±0.08174g, P=0.0261), TMZ+IFN(0.6108±0.07317 g, P=0.0381), and TMZ (0.9054±0.07154 g, P=0.0017) group. Glioma stem cells GSC-1 was highly resistant to TMZ, tumor volume of TMZ group was not different from control group (P >0.05). While compared with TMZ (1.993±0.1274 g) group, in TMZ+IFN (1.506±0.1223g, P=0.0203), TMZ+LEV (1.178±0.1807g, P=0.0042), and TMZ+LEV+IFN (1.049±0.2171 g, P=0.0038) groups, GSC-1 tumor growth were significantly inhibited(P< 0.05). CONCLUSION Our data demonstrate that both IFN and LEV can sensitize TMZ effect on glioma in vivo, even for MGMT(+) tumors, and TMZ-LEV-IFN cocktail regimen seems the best. Key words: glioma, TMZ, LEV, IFN

scholarly journals Regulation of Parathyroid Hormone-Related Peptide by Estradiol: Effect on Tumor Growth and Metastasis in Vitro and in Vivo

Endocrinology ◽  
2005 ◽  
Vol 146 (7) ◽  
pp. 2885-2894 ◽  
Author(s):  
S. A. Rabbani ◽  
P. Khalili ◽  
A. Arakelian ◽  
H. Pizzi ◽  
G. Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Growth ◽  
Tumor Volume ◽  
In Vivo Studies ◽  
Promoting Effect ◽  
X Ray ◽  
Tumor Bearing ◽  
Tumor Growth And Metastasis

Abstract We evaluated the capacity of estradiol (E2) to regulate PTHrP production, cell growth, tumor growth, and metastasis to the skeleton in breast cancer. In estrogen receptor (ER)-negative human breast cancer cells, MDA-MB-231, and cells transfected with full-length cDNA encoding ER (S-30), E2 caused a marked decrease in cell growth and PTHrP production, effects that were abrogated by anti-E2 tamoxifen. E2 also inhibited PTHrP promoter activity in S-30 cells. For in vivo studies, MDA-MB-231 and S-30 cells were inoculated into the mammary fat pad of female BALB/c nu.nu mice. Animals receiving S-30 cells developed tumors of significantly smaller volume compared with MDA-MB-231 tumor-bearing animals. This change in tumor volume was reversed when S-30 cells were inoculated into ovariectomized (OVX) hosts. Inoculation of MDA-MB-231 cells into the left ventricle resulted in the development of lesions in femora and tibia as determined by x-ray analysis. In contrast, these lesions were significantly smaller in volume and number in animals inoculated with S-30, and this lower incidence was reversed in OVX animals. Bone histological analysis showed that the tumor volume to tissue volume ratio was comparable with that seen by x-ray. Immunohistochemical analysis showed that PTHrP production was inhibited in S-30 group and restored to levels comparable to that seen in MDA-MB-231 tumor-bearing animals when S-30 cells were inoculated in OVX animals. Collectively these studies show that E2 production is inversely correlated with PTHrP production and that the growth-promoting effect of PTHrP has a direct impact on tumor growth at both nonskeletal and skeletal sites.

Oral Dosing of the Novel Proteasome Inhibitor CEP-18770 Shows Marked Anti-Myeloma Effects in SCID-Hu Models of Multiple Myeloma.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1840-1840
Author(s):  
Eric Sanchez ◽  
Mingjie Li ◽  
Jeffrey A Steinberg ◽  
Cathy S Wang ◽  
Jing Shen ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Proteasome Inhibitor ◽  
Tumor Volume ◽  
Single Agent ◽  
Volume Growth ◽  
Oral Formulation ◽  
Clinical Development ◽  
Scid Mice ◽  
Control Group ◽  
Treatment Groups

Abstract Abstract 1840 Poster Board I-866 Introduction: Currently, there is no orally administered proteasome inhibitor (PI) which has been FDA approved for the treatment of any cancer. The first PI in clinical development, bortezomib, was approved in 2003 following two successful single-agent phase II trials in relapsed multiple myeloma (MM). In contrast to bortezomib which is administered by intravenous bolus, CEP-18770 is a PI that is active as an oral formulation. Furthermore, the efficacy of orally administered CEP-18770 in multiple MM models has not been reported. In this study, we determined the effects of orally administered CEP-18770 therapy at escalating doses either daily or twice weekly in severe combined immunodeficient (SCID) mice bearing human MM that has been serially passaged in SCID mice from bone marrow derived from a MM patient before (LAGκ-1A) and after resistance (LAGκ-1B) to bortezomib developed. Materials and Methods: Each naïve SCID mouse received a 20 — 40 mm3 MM tumor piece which was surgically implanted into the left hind limb superficial gluteal muscle. Seven days post-implantation mice were bled, human IgG levels were measured by ELISA and animals were randomized into treatment groups. CEP-18770 was administered via oral gavage either daily at 5 mg/kg or twice weekly at 10 mg/kg (M, W) throughout the study. Each week, mice were bled for hIgG levels (where applicable) and tumors were measured using standard calipers. Data graphed is the mean ± SEM with n = 15 mice/group. Results: Single-agent CEP-18770 administered orally significantly inhibited tumor growth in bortezomib-sensitive LAGκ-1A-bearing mice. A significant inhibition of both human paraprotein secretion and reduction of tumor volume was observed as soon as three weeks following initiation of treatment with CEP-18770 at 10 mg/kg twice weekly (hIgG: P = 0.0011 and tumor volume: P = 0.001). Furthermore, tumor volume growth to 700 mm3 was delayed by 94% (day 32.5 for control compared to day 63) among animals receiving this treatment regimen when compared to animals receiving no treatment. At day 35, daily administration of the PI at 5 mg/kg also resulted in significant tumor inhibition (hIgG: P < 0.0001 and tumor volume: P < 0.0001). Reductions of tumor growth by 75%, 95%, 97% and 98% on days 28, 35, 42 and 49 respectively, were observed when compared to the control group. The effect of single-agent CEP-18770 dosed orally in SCID mice bearing nonsecretory bortezomib-resistant LAGκ-1B tumors was also evaluated. Four weeks following initiation of treatment, 5 mg/kg administered daily or 10 mg/kg twice weekly, resulted in a significant reduction in tumor volume (P = 0.0327 and P = 0.0018 respectively). Tumor volume growth to 300 mm3 was delayed by 36% (day 31 for control compared to day 42 for CEP-18770-treated group) in animals receiving 5 mg/kg daily compared to animals receiving no treatment. Tumor volume at 220 mm3 was delayed by 50% (day 28 for control compared to day 42 for CEP-18770-treated mice) among animals receiving 10 mg/kg twice weekly when compared to the untreated control group. Reductions of tumor growth by 78%, 73%, 74% and 70% on days 35, 42, 49 and 56 respectively, were observed when compared to the control group. Moreover, body weights measured at treatment cessation were not significantly different between pre- and post-treatment levels for both treatment groups and MM tumor types. Conclusions: The results of these studies show a marked reduction of tumor size and delay of tumor growth, when compared to the control group, following oral administration of CEP-18770 in LAGκ-1A and LAGκ-1B-bearing mice. The potential availability of an oral PI will greatly enhance the convenience of administration of drugs in this class as bortezomib has only shown efficacy when given intravenously. Other PIs that are bioavailable and active orally in preclinical studies in the treatment of MM are now in early clinical development. The data presented in our study provide further support for clinical development of CEP-18770 as an oral formulation for the treatment of MM. Disclosures: Berenson: Cephalon, Inc.: Consultancy, Honoraria, Research Funding, Speakers Bureau.

Azurin, highly potent and selective anticancer agent for breast cancer

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 13106-13106
Author(s):  
T. Yamada ◽  
R. Mehta ◽  
D. Majumdar ◽  
A. M. Chakrabarty ◽  
T. K. Das Gupta
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Tumor Volume ◽  
Tumor Regression ◽  
Treated Group ◽  
Redox Protein ◽  
The Mean ◽  
The Difference ◽  
Mcf 7

13106 Background: The use of live or attenuated pathogenic bacteria in the treatment of cancer dates back to the late nineteen hundreds when William B. Coley first reported that inducing Streptococcal infection resulted in tumor regression. However, the hazards of using live bacteria are obvious. Similarly, the results of using attenuated bacteria have been spotty and enthusiasm for it has waxed and waned. Recently, we have shown that redox protein azurin (14 kDa) secreted by an opportunistic pathogen, Pseudomonas aeruginosa, is not only cytotoxic to cancer cells in vitro but also produces tumor regression in athymic mice without producing any toxicity (PNAS, 99, 14098–14103, 2002; Science’s STKE, 158, tw416, 2002). Methods: In this study, we show the effect of 1mg/kg of azurin injected i.p. starting 72 hours after inoculation of 5x107 MCF-7 breast cancer cells in estradiol pretreated nude mice for 28 days (n = 20, control = 10, azurin-treated = 10). Results: Univariate analysis of the data showed the difference in tumor growth rates between control animals and azurin-treated animals was significant. For instance, 22 days after the start of treatment, the mean tumor volume in azurin-treated animals was only 22% of the mean tumor volume in the control mice (i.e., 0.0267 cm3 + 0.124 cm3 respectively, P = 0.0179 Kruskal-Wallis test). At the end of the experiment on the 29th day there was a reduction in the tumor volume by 85% in the treated group. We used a multivariate model, where the tumor growth over time was taken to be exponential with coefficients that were subject specific mixed effect (For control, tumor volumes = exp (−4.23 + 0.06 time) while for the treated group it was tumor volume = exp (−4.23 + 0.03 time)). The difference is statistically significant (P = 0.0456). Taken together, this in vivo data shows azurin exerts an inhibitory effect in the growth and progression of MCF-7 tumor xenotransplants. During the 28 days of treatment, treated animals did not show any sign of toxicity. Conclusions: Bacterial redox protein azurin can be explored as a novel therapeutic agent for treatment of breast cancer. Recently, we have prepared a truncated version of azurin which has 28 amino acids. It appers that this chemically synthesized peptide (2.8 kDa) has similar properties as azurin. No significant financial relationships to disclose.

Effect of the antiprogesterone RU-38486 on meningioma implanted into nude mice

1987 ◽  
Vol 66 (4) ◽  
pp. 584-587 ◽  
Author(s):  
Jeffrey J. Olson ◽  
David W. Beck ◽  
Janet A. Schlechte ◽  
Pao-Min Loh
Keyword(s):  
Tumor Growth ◽  
Nude Mice ◽  
Binding Proteins ◽  
Tumor Volume ◽  
Growth Index ◽  
Control Group ◽  
Content Type ◽  
Treatment Groups ◽  
Steroid Binding Proteins

✓ Meningiomas have been shown to have steroid-binding proteins. In vitro, estradiol, progesterone, and the antiestrogen tamoxifen stimulate tumor growth. However, incubation of tumor cells with an antiprogesterone agent results in tumor inhibition. In this investigation, a human meningioma was implanted subcutaneously in athymic nude mice. Two treatment groups were established, one receiving the antiprogesterone agent RU-38486 (10 mg/kg/day in suspension) and the other receiving only vehicle. After 3 months, the tumor growth index (defined as the tumor volume at 3 months divided by the initial tumor volume) was 0.25 ± 0.46 (mean ± standard deviation) in the group receiving antiprogesterone and was 1.54 ± 0.58 in the control group (p = 0.041). Further investigation of the effect of antiprogestational agents on the growth and hormone-binding proteins of other meningiomas will better define the mechanism of their effects.

scholarly journals Effects of Enoxaparin Emulsion on Dimethylbenzanthracene-induced Breast Cancer in Female Rats

2018 ◽  
Vol 5 (4) ◽  
pp. 23
Author(s):  
Bolandpayeh M ◽  
Hassanpour-Ezzati M ◽  
Mousavi Z
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Tumor Volume ◽  
Positive Control ◽  
Female Rats ◽  
Positive Control Group ◽  
Control Group ◽  
Dependent Manner ◽  
Angiogenic Proteins ◽  
Dose Dependent

Introduction: Enoxaparin is an anticoagulant medication. Anticoagulation inhibits tumor cell-mediated release of angiogenic proteins and diminishes angiogenic response. Angiogenesis is an important event in various cancers such as breast cancer. Angiogenesis provide oxygen and nutrients to tumor cells and causes tumor progression. The aim of the present study was to evaluate the anti-angiogenesis effect of an enoxaparin cream on breast cancer induced by dimethylbenzanthracene in rats. Methods: In this experimental in vivo study, 50 Wistar female rats were divided into negative control (vehicle), positive control (cream base), and 3 groups with enoxaparin treatment (40, 60, and 80 mg/ml). After one month of treatment along with breast cancer induction by dimethylbenzanthracene, breast tissue samples were isolated and stained with hematoxylin-eosin, and tumor growth suppression rate was calculated. Tumor size (length and width) was measured using a clipper, and the tumor volume was calculated using the following formula: V = (L × W × W)/2, where V is tumor volume, W is tumor width, L is tumor length. The data were analyzed using one-way ANOVA and Tukey’s post hoc test. Results: Tumor suppression was significantly increased in enoxaparin treatment groups compared to the positive control group (40 mg/ml of enoxaparin treated versus positive control group; P = 0.017, 60 mg/ml of enoxaparin treated versus positive control; P = 0.015, 40 mg/ml of enoxaparin treated versus positive control; P = 0.009, 60 mg/ml of enoxaparin treated versus 40 mg/ml of enoxaparin treated; P = 0.019, and 80 mg/ml of enoxaparin treated versus 40 mg/ml of enoxaparin treated; P = 0.011 in a dose-dependent manner. Conclusion: Enoxaparin inhibits breast cancer in a dose-dependent manner. The application of enoxaparin cream in patients with breast cancer may considerably reduce tumor growth. 

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