Relevant bibliographies by topics / Enzymes; Breast cancer

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Enzymes; Breast cancer'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Enzymes; Breast cancer.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Enzymes; Breast cancer"

1

Wright, Roni H. G., and Miguel Beato. "Role of the NUDT Enzymes in Breast Cancer." International Journal of Molecular Sciences 22, no. 5 (February 25, 2021): 2267. http://dx.doi.org/10.3390/ijms22052267.

Full text
Abstract:
Despite global research efforts, breast cancer remains the leading cause of cancer death in women worldwide. The majority of these deaths are due to metastasis occurring years after the initial treatment of the primary tumor and occurs at a higher frequency in hormone receptor-positive (Estrogen and Progesterone; HR+) breast cancers. We have previously described the role of NUDT5 (Nudix-linked to moiety X-5) in HR+ breast cancer progression, specifically with regards to the growth of breast cancer stem cells (BCSCs). BCSCs are known to be the initiators of epithelial-to-mesenchyme transition (EMT), metastatic colonization, and growth. Therefore, a greater understanding of the proteins and signaling pathways involved in the metastatic process may open the door for therapeutic opportunities. In this review, we discuss the role of NUDT5 and other members of the NUDT family of enzymes in breast and other cancer types. We highlight the use of global omics data based on our recent phosphoproteomic analysis of progestin signaling pathways in breast cancer cells and how this experimental approach provides insight into novel crosstalk mechanisms for stratification and drug discovery projects aiming to treat patients with aggressive cancer.
APA, Harvard, Vancouver, ISO, and other styles
2

Suzuki, Takashi, Yasuhiro Miki, Yasuhiro Nakamura, Takuya Moriya, Kiyoshi Ito, Noriaki Ohuchi, and Hironobu Sasano. "Sex steroid-producing enzymes in human breast cancer." Endocrine-Related Cancer 12, no. 4 (December 2005): 701–20. http://dx.doi.org/10.1677/erc.1.00834.

Full text
Abstract:
It is well known that sex steroids are involved in the growth of breast cancers, and the great majority of breast carcinomas express estrogen (ER), progesterone (PR), and androgen (AR) receptors. In particular, recent studies have demonstrated that estrogens and androgens are locally produced in breast carcinoma tissues, and total blockade of in situ estrogen production potentially leads to an improvement in prognosis of breast cancer patients. Therefore, it is important to obtain a better understanding of sex steroid-producing enzymes in breast carcinoma tissues. In this review, we summarize recent studies on the expression and regulation of enzymes related to intratumoral production of estrogens (aromatase, 17β-hydroxysteroid dehydrogenase type 1 (17βHSD1), and steroid sulfatase (STS) etc) and androgens (17βHSD5 and 5α-reductase) in human breast carcinoma tissues, and discuss the biological and/or clinical significance of these enzymes. The cellular localization of aromatase in breast carcinoma tissues still remains controversial. Therefore, we examined localization of aromatase mRNA in breast carcinoma tissues by laser capture microdissection/real time-polymerase chain reaction. Aromatase mRNA expression was detected in both carcinoma and intratumoral stromal cells, and the expression level of aromatase mRNA was higher in intratumoral stromal cells than in carcinoma cells in the cases examined. We also examined an association among the immunoreactivity of enzymes related to intratumoral estrogen production and ERs in breast carcinoma tissues, but no significant association was detected. Therefore, the enzymes responsible for the intratumoral production of estrogen may not always be the same among breast cancer patients, and not only aromatase but also other enzymes such as STS and 17βHSD1 may have important therapeutic potential as targets for endocrine therapy in breast cancer patients.
APA, Harvard, Vancouver, ISO, and other styles
3

Adnan Yasseen, Hadeel, Rawand Tajuldeen Sahib, and Shaho Abdulrehman Ezzaddin. "MITOCHONDRIAL ENZYMES CORRELATION WITH BREAST CANCER CLINICOPATHOLOGICAL PARAMETERS/ A STUDY IN SULAIMANI CITY-IRAQ." Journal of Sulaimani Medical College 8, no. 1 (April 15, 2018): 37–46. http://dx.doi.org/10.17656/jsmc.10149.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Wiebe, John P. "Progesterone metabolites in breast cancer." Endocrine-Related Cancer 13, no. 3 (September 2006): 717–38. http://dx.doi.org/10.1677/erc.1.01010.

Full text
Abstract:
In the 70 years since progesterone (P) was identified in corpus luteum extracts, its metabolism has been examined extensively in many tissues and cell lines from numerous species. In addition to the reproductive tissues and adrenals, every other tissue that has been investigated appears to have one or more P-metabolizing enzyme, each of which is specific for a particular site on the P molecule. In the past, the actions of the P metabolizing enzymes generally have been equated to a means of reducing the P concentration in the tissue microenvironment, and the products have been dismissed as inactive waste metabolites. In human breast tissues and cell lines, the following P-metabolizing enzymes have been identified: 5α-reductase, 3α-hydroxysteroid oxidoreductase (3α-HSO), 3β-HSO, 20α-HSO, and 6α-hydroxylase. Rather than providing diverse pathways for inactivating and controlling the concentration of P in breast tissue microenvironments, it is proposed that the enzymes act directly on P to produce two types of autocrines/paracrines with opposing regulatory roles in breast cancer. Evidence is reviewed which shows that P is directly converted to the 4-pregnenes, 3α-hydroxy-4-pregnen-20-one (3α-dihydroprogesterone; 3αHP) and 20α-dihydroprogesterone (20αHP), by the actions of 3α-HSO and 20α-HSO respectively and to the 5α-pregnane, 5α-pregnane-3,20-dione(5α-dihydroprogesterone; 5αP), by the irreversible action of 5α-reductase. In vitro studies on a number of breast cell lines indicate that 3αHP promotes normalcy by downregulating cell proliferation and detachment, whereas 5αP promotes mitogenesis and metastasis by stimulating cell proliferation and detachment. The hormones bind to novel, separate, and specific plasma membrane-based receptors and influence opposing actions on mitosis, apoptosis, and cytoskeletal and adhesion plaque molecules via cell signaling pathways. In normal tissue, the ratio of 4-pregnenes:5α-pregnanes is high because of high P 3α- and 20α-HSO activities/expression and low P 5α-reductase activity/expression. In breast tumor tissue and tumorigenic cell lines, the ratio is reversed in favor of the 5α-pregnanes because of altered P-metabolizing enzyme activities/expression. The evidence suggests that the promotion of breast cancer is related to changes in in situ concentrations of cancer-inhibiting and -promoting P metabolites. Current estrogen-based theories and therapies apply to only a fraction of all breast cancers; the majority (about two-thirds) of breast cancer cases are estrogen-insensitive and have lacked endocrine explanations. As the P metabolites, 5αP and 3αHP, have been shown to act with equal efficacy on all breast cell lines tested, regardless of their tumorigenicity, estrogen sensitivity, and estrogen receptor/progesterone receptor status, it is proposed that they offer a new hormonal basis for all forms of breast cancer. New diagnostic and therapeutic possibilities for breast cancer progression, control, regression, and prevention are suggested.
APA, Harvard, Vancouver, ISO, and other styles
5

Raza, Uzma, Aziza Khannum, and Shahnawaz Jamali. "LIVER ENZYMES." Professional Medical Journal 22, no. 06 (June 10, 2015): 745–51. http://dx.doi.org/10.29309/tpmj/2015.22.06.1242.

Full text
Abstract:
Objective: To study the effect of breast cancer treatment on liver enzymes indiabetic and cardiac breast cancer females. Study Design: Cross-sectional type of study.Setting: Liaquat National Hospital Karachi. Period: January 2008 to January 2010. Patientsand Methods: Total 47 breast cancer patients. Out of these, 22 were diabetic and 25 werecardiac patients, visiting the oncology OPD of the hospital. Patients with metastasis to distantorgans were excluded from the study. Treatment was carried under the supervision of anoncologist. Samples were collected twice during the study. First sample was collected at diseasepresentation before starting any type of treatment and second time, sample was collected14 weeks after the last chemotherapy dose. Statistical analysis: Data was analyzed usingstatistical package (SPSS version 11.0). “Students t-test”and analysis of variance (ANOVA) wasused to analyze the means and standard deviations of quantitative/continuous variables. Inall statistical analysis p<0.05 was considered significant. Results: In all patient groups aftertreatment alkaline phosphatase was significantly high as compared to that before treatment(p<0.05) whereas alanine transaminase increased significantly without including Tamoxifenin the treatment. Variation pattern of liver enzyme was the same in both patient groups.Conclusions: Altered profile of liver enzyme was similar in both patient groups therefor thevariations cannot be attributed to hyperglycemia in diabetic females and the alterations in liverenzymes were attributed to liver damage by chemotherapy and fatty infiltration of liver inducedby Tamoxifen.
APA, Harvard, Vancouver, ISO, and other styles
6

Brueggemeier, Robert W., Jeanette A. Richards, and Trevor A. Petrel. "Aromatase and cyclooxygenases: enzymes in breast cancer." Journal of Steroid Biochemistry and Molecular Biology 86, no. 3-5 (September 2003): 501–7. http://dx.doi.org/10.1016/s0960-0760(03)00380-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Tappel, Al. "Lysosomal enzymes and initiation of breast cancer." Medical Hypotheses 64, no. 2 (January 2005): 288–89. http://dx.doi.org/10.1016/j.mehy.2004.07.025.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Jansson, Agneta. "17Beta-hydroxysteroid dehydrogenase enzymes and breast cancer." Journal of Steroid Biochemistry and Molecular Biology 114, no. 1-2 (March 2009): 64–67. http://dx.doi.org/10.1016/j.jsbmb.2008.12.012.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Wang, Shu-Ching M., Dennis H. Dowhan, and George E. O. Muscat. "Epigenetic arginine methylation in breast cancer: emerging therapeutic strategies." Journal of Molecular Endocrinology 62, no. 3 (April 2019): R223—R237. http://dx.doi.org/10.1530/jme-18-0224.

Full text
Abstract:
Breast cancer is a heterogeneous disease, and the complexity of breast carcinogenesis is associated with epigenetic modification. There are several major classes of epigenetic enzymes that regulate chromatin activity. This review will focus on the nine mammalian protein arginine methyltransferases (PRMTs) and the dysregulation of PRMT expression and function in breast cancer. This class of enzymes catalyse the mono- and (symmetric and asymmetric) di-methylation of arginine residues on histone and non-histone target proteins. PRMT signalling (and R methylation) drives cellular proliferation, cell invasion and metastasis, targeting (i) nuclear hormone receptor signalling, (ii) tumour suppressors, (iii) TGF-β and EMT signalling and (iv) alternative splicing and DNA/chromatin stability, influencing the clinical and survival outcomes in breast cancer. Emerging reports suggest that PRMTs are also implicated in the development of drug/endocrine resistance providing another prospective avenue for the treatment of hormone resistance and associated metastasis. The complexity of PRMT signalling is further underscored by the degree of alternative splicing and the scope of variant isoforms (with distinct properties) within each PRMT family member. The evolution of PRMT inhibitors, and the ongoing clinical trials of PRMT inhibitors against a subgroup of solid cancers, coupled to the track record of lysine methyltransferases inhibitors in phase I/II clinical trials against cancer underscores the potential therapeutic utility of targeting PRMT epigenetic enzymes to improve survival outcomes in aggressive and metastatic breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
10

Makar, Subhajit, Abhrajyoti Ghosh, Ashok Kumar, and Sushil K. Singh. "Recent Studies on Aromatase and Sulfatase Involved in Breast Cancer and their Inhibitors." Current Enzyme Inhibition 16, no. 1 (May 4, 2020): 20–44. http://dx.doi.org/10.2174/1573408016666200325120248.

Full text
Abstract:
Enzyme aromatase uses several androgen substrates for the biosynthesis of estrogen, i.e. conversion of androstenedione to estrone and testosterone to biologically potent estradiol. Aromatase inhibitors (AIs) such as anastrozole, letrozole and exemestane have been established in standard endocrine therapy of breast cancer, by interfering with estrogen signaling cascade. Steroid sulphatase (STS) regulates the level of active oestrogens and androgens in human target organs and steroidogenic tissues, which have a key role in hormone dependent breast cancers (HDBC). Sulfatase is still under the exploration stage and is yet to emerge as a potential therapeutic target in breast cancer. The discovery of estrone 3-O-sulfamate (EMATE), a highly potent irreversible STS inhibitor, accelerated the development of potent steroidal and nonsteroidal STS inhibitors. Attempts are also being made for the development of dual inhibitors of AI and STS, as an alternative approach to overcome the acquired resistance. This review includes the molecular structures and biochemistry of aromatase and sulphatase enzymes. The advances in the development of inhibitors of the two enzymes have also been outlined.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Enzymes; Breast cancer"

1

Gunnarsson, Cecilia. "Steroid converting enzymes in breast cancer /." Linköping : Univ, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med908s.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

RICH, WENDY LEA. "Interrelationships Of The Estrogen-Producing Enzymes Network In Breast Cancer." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1230581012.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Palmebäck, Wegman Pia. "Studies of tamoxifen resistance in breast cancer." Doctoral thesis, Linköpings universitet, Cellbiologi, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-8943.

Full text
Abstract:
Oestrogen is one of the most important hormonal regulators and is known to play a key role in the development and growth of breast cancer. The majority of tumours have a hormone dependent growth, and this is indicated by the presence of oestrogen receptors (ERs). About two thirds of breast cancers occur after the menopause when the ovaries have ceased to produce oestrogen and despite the low levels of circulating oestrogen’s the tumour concentrations of oestrone, oestradiol and their sulfates have been shown to be significant. Patients with hormone dependent tumours are candidates for treatment with the anti-oestrogen tamoxifen, which acts by competing with oestrogen for binding to the ER thereby, diminish the transcription of oestrogen regulated genes. The drug is mainly metabolised by cytochrome P450 enzymes in the liver and to a lesser extent locally in the breast, where upon several produced metabolites have higher affinity for the ER than the mother substance. Patients treated with tamoxifen have in general a prolonged disease-free survival. Even if most patients respond well to tamoxifen about 30-50 % either fail to respond or become resistant by incompletely understood mechanisms. Therefore, the aim of this thesis was to investigate possible mechanisms responsible for tamoxifen resistance. In paper I and II we studied genetic variants of enzymes participating in the metabolism of tamoxifen and assessed whether these variants correlated to breast cancer prognosis and/or to the benefit of tamoxifen. The results indicate an influence of CYP2D6, CYP3A5, and SULT1A1 genotypes in tamoxifen response. Further, tamoxifen has shown to compete with oestrogen for the binding to ER. In paper III we measured the expression levels of enzymes involved in the local synthesis of oestrogens in order to see if they correlated to clinical outcome. The protein expression of stromal aromatase was shown to have a prognostic significance, especially in ER-positive patients. Finally, tamoxifen and its ER-active metabolites have shown to induce both cell cycle arrest and apoptosis and one central mediator in these processes is the tumour suppressor protein p53. The proapoptotic activity of p53 is dependent on a proline rich domain containing a common Pro-to-Arg polymorphism. In paper IV we examined the value of this genetic variant as a predictive marker for anti-cancer therapy and found that patients carrying the Pro-allele might be good responders of tamoxifen therapy. The present thesis further indicates the complexity of the mechanisms underlying tamoxifen resistance. In summary, genetic variants of metabolic enzymes, genetic variants in p53, as well as expression levels of enzymes involved in local oestrogen synthesis, may have influence on breast cancer prognosis and may be useful markers in the prediction of tamoxifen response.
APA, Harvard, Vancouver, ISO, and other styles
4

Sandri, Maria Ines. "Studies of the expression and regulation of topoisomerase II." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364213.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Xintaropoulou, Chrysi. "Targeting aerobic glycolysis in breast and ovarian cancer." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29525.

Full text
Abstract:
Cancer cells, unlike normal tissue, frequently rely on glycolysis for the production of energy and the metabolic intermediates required for their growth regardless of cellular oxygenation levels. This metabolic reconfiguration, termed the Warburg effect, provides a potential strategy to preferentially target tumours from a therapeutic perspective. The present study sought to investigate the glycolytic phenotype of breast and ovarian cancer, and assess the possibility of exploiting several glycolytic targets therapeutically. Initially the growth dependency of breast and ovarian cancer cells on the availability of glucose was established. An array of 10 compounds reported to inhibit key enzymes of the glycolytic pathway were investigated and compared against an extended panel of breast and ovarian cancer cell line models. All inhibitors investigated, targeted against multiple points of the pathway, were shown to block the glycolytic pathway as demonstrated by glucose accumulation in the culture media combined with decreased lactate secretion, and attenuated breast and ovarian cancer cell proliferation in a concentration dependent manner. Furthermore their mechanism of action was investigated by flow cytometric analysis and their antiproliferative effect was associated with induction of apoptosis and G0/G1 cell cycle arrest. The glycolytic inhibitors were further assessed in combination strategies with established chemotherapeutic and targeted agents and several synergistic interactions, characterised by low combination index values, were revealed. Among them, 3PO (a novel PFKFB3 inhibitor) enhanced the effect of cisplatin in both platinum sensitive and platinum resistant ovarian cancer cells suggesting a strategy for treatment of platinum resistant disease. Furthermore robust synergy was identified between IOM-1190 (a novel GLUT1 inhibitor) and metformin, an antidiabetic inhibitor of oxidative phosphorylation, resulting in strong inhibition of breast cancer cell growth. This combination is proposed for the treatment of highly aggressive triple negative breast tumours. An additional objective of this research was to investigate the effect of the oxygen level on sensitivity to glycolysis inhibition. Breast cancer cells were found to be more sensitive to glycolysis inhibition in high oxygen conditions. This enhanced resistance at low oxygen levels was associated with upregulation of the targeted glycolytic enzymes as demonstrated at both the mRNA (by gene expression microarray profiling, Illumina BeadArrays) and protein level (by Western blotting). Manipulation of LDHA (Lactate Dehydrogenase A) by siRNA knockdown provided further evidence that downregulation of this target was sufficient to significantly suppress breast cancer cell proliferation. Finally, the expression of selected glycolytic targets was examined in a clinical tissue microarray set of a large cohort of ovarian tumours using quantitative immunofluorescence technology, AQUA. The role of the glycolytic phenotype in ovarian cancer was suggested and interesting associations between the glycolytic profile and clear cell and endometrioid ovarian cancers revealed. Increased PKM2 (Pyruvate kinase isozyme M2) and LDHA expression were demonstrated in clear cell tumours and also low expression of these enzymes was significantly correlated with improved survival of endometrioid ovarian cancer patients. Taken together the findings of this study support the glycolytic pathway as a legitimate target for further investigation in breast and ovarian cancer treatment.
APA, Harvard, Vancouver, ISO, and other styles
6

Segersten, Ulrika. "Vitamin D Hydroxylating Enzymes and Analogues in Parathyroid Tumors and Breast Cancer." Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6008.

Full text
Abstract:

In hyperparathyroidism (HPT) raised serum concentrations of ionized calcium is caused by increased secretion of parathyroid hormone (PTH) by parathyroid tumors. Active vitamin D, 1α,25-dihydroxyvitamin D3, is known to suppress PTH secretion and to reduce proliferation of parathyroid tumor cells.

The aim of this thesis was to examine expression of vitamin D hydroxylating enzymes, regulating the activation and inactivation of vitamin D and to study effects of vitamin D analogues, in parathyroid tumors and breast cancer.

The vitamin D activating enzyme, CYP27B1/25-hydroxyvitamin D3 1α-hydroxylase (1α-hydroxylase) and the vitamin D inactivating enzyme CYP24A1/25-hydroxyvitamin D3 24-hydroxylase (24-hydroxylase) were expressed in parathyroid tumors and breast cancer.

The parathyroid tumors had raised expression levels of 1α-hydroxylase and reduced levels of 24-hydroxylase in comparison to normal parathyroid glands, indicating ability for endogenous activation of vitamin D. The expression of 1α-hydroxylase may be of therapeutic advantage for local activation of non-1α-hydroxylated vitamin D analogues in tumor cells, thereby reducing unwanted hypercalcemic effects.

Three of five selected low calcemic vitamin D analogues had as efficient PTH suppressing effect, in bovine parathyroid cells, as three vitamin D analogues used clinically for treatment of secondary HPT.

The non-1α-hydroxylated vitamin D analogue EB1285 showed antiproliferative and PTH suppressive effects as well as transcriptional activity in parathyroid and breast tumor cells, respectively.

Ketoconazole, an inhibitor of vitamin D hydroxylating enzymes, suppressed PTH secretion and potentiated the effect of vitamin D analogues. Combined treatment with vitamin D analogues and specific 24-hydroxylase inhibitors may be important for future therapy.

APA, Harvard, Vancouver, ISO, and other styles
7

Kopsida, Maria. "Targeting histone deacetylase (HDACs) enzymes with novel bisnaphthalimidopropyl derivatives (BNIPs) as alternative breast cancer therapies." Thesis, Robert Gordon University, 2018. http://hdl.handle.net/10059/3120.

Full text
Abstract:
Breast cancer is the most commonly occurring cancer in women, with incidence rates approaching 1.38 million cases per year worldwide. Over the last few decades, there have been numerous attempts to develop, synthesise and advance into the clinic novel and selective breast cancer therapies. Research work has shown that bisnaphthalimidopropyl diaminodicyclohexylmethane (BNIPDaCHM) exerts potent in vitro anti-cancer activities and strong DNA binding properties. The aim of this thesis was to synthetise novel bisnaphthalimidopropyl derivatives (BNIPs) and investigate their subsequent modes of action within two human metastatic breast cancer cell lines, MDA-MB-231 and SKBR-3. A series of novel BNIPs, bisnaphthalimidopropyl-piperidylpropane (BNIPPiProp), bisnaphthalimidopropyl- ethylenedipiperidine (BNIPPiEth) and (trans(trans))-4,4’-methylenebis-cyclohexylamine (trans,trans-BNIPDaCHM) were synthesised, characterised and studied in comparison to BNIPDaCHM for their DNA binding and anti-cancer activities against MDA-MB-231 and SKBR-3 cells. Thermal denaturation studies have shown that BNIPs can intercalate and stabilize the double helix of Calf Thymus, each BNIP can competitively displace EtBr from DNA in a dose dependent manner and by UV binding studies, high affinity was found for the three novel BNIPs. After 24 hours treatment, all novel BNIPs, exhibited strong cytotoxicity with IC50 values ranging from 1.4 μM to 3.3 μM in MDA-MB-231 cells and 0.2 - 0.7 μM in SKBR-3 cells, confirming the importance of bisnaphthalimidopropyl functionality. BNIPs were also found to increase intracellular ROS levels after 8 hours treatment and induce a significant increase in DNA strand breaks compared to endogenous levels, after 24 hour treatment in both cell lines. After cell synchronisation, cell cycle distribution was studied, revealing that trans,trans-BNIPDaCHM induces sub-G1 cell population arrest in MDA-MB-231 and SKBR-3 cells, after 24 hours treatment. In addition, BNIPs induced apoptotic phosphatidylserine exposure, after 0.5 hours treatment, inhibited Caspase-3 activity and increased autophagy, after 24 hour treatment in MDA-MB-231 and SKBR-3 cells. Moreover, BNIPs inhibited histone deacetylases (HDAC) activity after 24 hours treatment in MDA-MB-231 and SKBR-3 cells and BNIPDaCHM was identified as a potential SIRT2 inhibitor, in SKBR-3 cells. According to Proteome Profiler Arrays, BNIPDaCHM and BNIPPiEth altered the expression of cell stress-related proteins in a cell dependent manner and bioinformatic analysis revealed two novel, putative pathways for BNIP-induced oxidative stress-mediated cell death in MDA-MB-231 and SKBR-3 cells. The above findings indicate that BNIPs represent promising candidates for future breast cancer studies and cancer treatment.
APA, Harvard, Vancouver, ISO, and other styles
8

Karihtala, P. (Peeter). "Oxidative damage and counteracting mechanisms in breast carcinoma." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514279530.

Full text
Abstract:
Abstract Breast cancer is the leading cause of death from cancer among Finnish women, but the ultimate causation of carcinogenesis still remains unclear. Reactive oxygen species (ROS) is a collective term for several types of reactive oxygen metabolites that are continuously generated in human cells mainly as by-products of aerobic respiration. ROS, including nitric oxide and its derivatives, play highly important roles in cell physiology. If ROS production exceeds the capacity of detoxification systems, principally antioxidant enzymes, oxidative stress is said to occur. This state is known to contribute to all stages of carcinogenesis. To explore the widely unstudied role of ROS and cell redox state modulating enzymes in breast carcinomas, the extent of ROS-derived macromolecule damage and the expression of the vast majority of known antioxidant enzymes were assessed in a large series of breast carcinomas, and the results were compared to the patients' clinicopathological parameters. The results were also compared to angiogenesis, DNA repair enzymes, cell proliferation, NF-κB, p53 expression, and survival. Immunohistochemistry was the main method applied, but western blotting and immunoelectron microscopy were also used. There is extensive oxidative damage in breast carcinomas, which seems to associate with tumor development. Oxidative macromolecule damage is notable even in stage I tumors. Cell redox state regulating enzymes, such as peroxiredoxin V, thioredoxin, thioredoxin reductase, and glutamate-cysteine ligase, associate with more aggressive phenotypes of tumors, including larger primary tumors, growth of metastases, increased cell proliferation, and poor differentiation. This indirectly suggests that cell redox state modulating enzymes may be inductive of tumor promotion in an oxidated environment. The results of this thesis support the importance of ROS in all stages of carcinogenesis. These observations are largely in line with the previous studies on different carcinomas, but there seem to be certain carcinoma type specific differences in the expression of these enzymes. Since the expression of given cell redox state modulating enzymes distinctly associates with clinicopathological parameters, these enzymes may be useful as prognostic indicators and facilitate the choice of appropriate treatment in the future.
APA, Harvard, Vancouver, ISO, and other styles
9

Abdullah, Ammara. "Inhibitors of cytochrome P450 enzymes CYP17 and 17β-HSD3 : their role in the treatment of hormone-dependent prostate and breast cancer." Thesis, Kingston University, 2012. http://eprints.kingston.ac.uk/25093/.

Full text
Abstract:
Androgens play an important part in the initiation and progression of hormone-dependent prostate and breast cancer. These types of cancers can be treated by androgen ablation therapy. However, androgen ablation is associated with short (2-3 years) remission of the disease. Therefore therapies that inhibit the systemic biosynthesis of androgens, by targeting the P450 enzymes (CYP17 and 17-[beta]HSD type 3) which catalyse androgen biosynthesis, may represent a rational approach in the treatment of androgen-dependent cancer. Inhibitors of the enzyme CYP17: ketoconazole and liarozole, have been shown to decrease tumour cell adhesion to the endothelium and expression of adhesion molecules. The adhesion of cancer cells to the endothelium is an important preliminary event that underlies cancer matastasis. Within the this study, the development of assays for the enzymes; CYP17 and 17[beta]-HSD3 and the evaluation of a series of compounds which were designed to inhibit these enzymes have been considered. The preliminary screening of the compounds showed good inhibition of 17[alpha]=OHase and 17, 20 lyase components of the CYP17 enzyme in comparison to the reference drug, ketoconazole (KTZ). The IC[sub]50 of compounds 31, 34, 38, 41, 48 and 51 and KTZ was calculated as 14.40 [Mu]M, 5.82 [Mu]M, 0.18 [Mu]M, 1.35[Mu]M, 1.21[Mu]M, 0.50[Mu]M and 5.65[Mu]M respectively. However, only a few of the compounds designed to inhibit 17[beta]-HSD3 showed ap potent inhibitory activity. Compound 132 showed the highest percentage inhibition (40.51 [plus or minus] 0.14%) of 17[beta]- HSD3 activity when compared to the reference drugs, 7-hydroxy flavone (12.90 [plus or minus] 0.31%) and biacalein (13.66 [plus or minus] 0.31%). CYP17 inhibitors did not have any cytoxic effect on human cancerous and non-cancerous cell lines. The adhesion of DU145, PC3 and MCF7 to a non-stimulated HUVEC monolayers was decreased from 100 [plus or minus] 0.01% cell adhesion to 60.93 [plus or minus] 3.95%, 65.79 [plus or minus] 9.39% and 65.12 [plus or minus] 4.04% by compounds 38. 48 and 51 respectively in the absence of tumour necrosis factor alpha (THF-[alpha]). Similarly, compounds 38, 48 and 51 showed the highest anti-adhesion effect of DU145 on stimulated HUVEC monolayers (69.85 [plus or minus] 2.51%) cells respectively. Flow cytometry and immunostaining of intracellular adhesion molecules showed that CYP17 inhibitors did not have any effect on the expression of ICAM-1. In conclusion, the synthesised compounds were found to be good indicators of the CYP17 enzyme with no cytoxic and better anti-adhesion effects when compared to KTZ. Thus, these compounds can be further investigated as a therapeutic strategy against hormone-dependent prostate and breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
10

Lam, Maria Shuk Mun. "Genetic polymorphisms in AH receptor and cytochrome P450 drug-metabolizing enzymes in relation to estradiol metabolism and breast cancer susceptibility." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0021/MQ54164.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Enzymes; Breast cancer"

1

Lam, Maria Shuk Mun. Genetic polymorphisms in AH receptor and cytochrome P450 drug-metabolizing enzymes in relation to estradiol metabolism and breast cancer susceptibility. Ottawa: National Library of Canada, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Molecular therapy of breast cancer: Classicism meets modernity. Hauppauge (NY), USA: Nova Publishers, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

John, Kelly. Three on the edge: The stories of ordinary American families in search of a medical miracle. New York: Bantam Books, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Obesity And Breast Cancer The Role Of Dysregulated Estrogen Metabolism. Springer-Verlag New York Inc., 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

R, Lamonte Jean, ed. Aromatase inhibitors: Types, mode of action, and indications. Hauppauge, N.Y: Nova Science Publishers, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

R, Lamonte Jean, ed. Aromatase inhibitors: Types, mode of action and indications. New York: Nova Biomedical Books, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

R, Lamonte Jean, ed. Aromatase inhibitors: Types, mode of action, and indications. Hauppauge, N.Y: Nova Science Publishers, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Aromatase Inhibition. Parthenon Publishing Group, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

M, Dowsett, ed. Aromatase inhibition: Then, now, and tomorrow. London: Parthenon Pub. Group, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Enzymes; Breast cancer"

1

Salhab, Mohamed, and Kefah Mokbel. "The role of aromatase and other oestrogen producing enzymes in mammary carcinogenesis." In Metastasis of Breast Cancer, 151–70. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-5867-7_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Gulyaeva, Lyudmila F., Olga N. Mikhailova, Vladimir O. PustyInyak, Inessa V. Kim, Alexei V. Gerasimov, Sergey E. Krasilnikov, Maxim L. Filipenko, and Eugene V. Pechkovsky. "Comparative Analysis of SNP in Estrogen-metabolizing Enzymes for Ovarian, Endometrial, and Breast Cancers in Novosibirsk, Russia." In Hormonal Carcinogenesis V, 359–66. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ravichandiran, Nerethika, Muneesh Kumar Barman, Sai Tejaswi Lavuri, Manjita Srivastava, Shalini Sakthivel, Meenakshi Singh, Kailash Chand, Subash C. Sonkar, and Prudhvilal Bhukya. "Precision Medicine in Cancer." In Handbook of Research on Advancements in Cancer Therapeutics, 433–66. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-6530-8.ch015.

Full text
Abstract:
Cancer is the one of the deadliest diseases and takes the lives of millions of people every year across the world. Due to disease heterogeneity and multi-factorial reasons, traditional treatment such as radiation therapy, immunotherapy, or chemotherapy are effective only among a small population of the patients. Tumors can have different fundamental genetic causes and protein expressions that differ from one patient to another. This variability among individual lends itself to the field of precision and personalized medicine. Following the completion of human genome sequencing, significant progress has been observed in the characterization of human epigenome, proteome, and metabolome. Pharmacogenetics and pharmacogenomics use this sequence to study the genetic causes of individual variations in drug response and the simultaneous impact of change in genome that decide the patient's response to drug respectively. On summation, identify the subpopulation of patient and provide them tailored therapy thus increasing the effectiveness of treatment. All these evolved the field of precision or personalized medicine that plays a crucial role in cancer prevention, prognosis, diagnosis, and therapeutics. These tailored therapies are characterized by increased efficiency and reduced toxicity. Not all cancers have genetic variability; some are also influenced by polymorphism of gene encoding enzymes that play an important role in pharmacokinetics of drug. The discoveries of cancer predisposition genes allow diagnosis of a patient at risk of cancer development and let them make the decision on précised individual risk modification characteristic. The use of CYP2D6 genotyping for breast cancer, mutation in KRAS in colorectal cancer, genomic variation in EGFR in small lung cancer, melanoma are some of the examples of importance of cancer predisposition genes. In recent times, distinct molecular subtypes of cancers have been identified with requirement of different treatment for each subtype. Precision medicine shifts the trend from reaction to prevention and forestalls disease progression.
APA, Harvard, Vancouver, ISO, and other styles
4

Philippe, Becuwe. "Antioxidant Enzymes as New Biomarkers for Prediction of Tumor Progression in Breast Cancer." In Breast Cancer - Recent Advances in Biology, Imaging and Therapeutics. InTech, 2011. http://dx.doi.org/10.5772/23004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Chetrite, Gérard. "The Selective Estrogen Enzyme Modulators (SEEM) in Breast Cancer." In Breast Cancer, 187–249. CRC Press, 2002. http://dx.doi.org/10.1201/b14039-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

"The Selective Estrogen Enzyme Modulators (SEEM) in Breast Cancer." In Breast Cancer, 209–72. CRC Press, 2002. http://dx.doi.org/10.3109/9780203909249-10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Jayaraman, Hariharan, Praveen Kumar Posa Krishnamoorthy, Lakshmi Suresh, Mahalakshmi Varadan, Aparna Madan, and Balu Ranganathan. "Enzyme Inhibitors for Breast Cancer Therapy." In Frontiers in Enzyme Inhibition, 204–27. BENTHAM SCIENCE PUBLISHERS, 2020. http://dx.doi.org/10.2174/9789811460821120010013.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

"Sodium Bisulfite Conversion of Human Genome for DNA Methylation Studies." In Protocols used in Molecular Biology, edited by Aastha Mishra and Qadar Pasha, 89–96. BENTHAM SCIENCE PUBLISHERS, 2020. http://dx.doi.org/10.2174/9789811439315120010012.

Full text
Abstract:
The regulation of transcription and translation of a gene under a given environment is dependent on several factors and epigenetics is one such factor, responsible for the differential expression of several genes in health and in various diseases. DNA methylation, an important epigenetics mechanism has been shown to play a vital role in numerous cellular processes, and the abnormal patterns of methylation have been linked to the number of human diseases. CpG islands, a short stretch of DNA enriched with CpG sites in the 5’ end of a gene, although remains unmethylated but tends to methylate aberrantly upon certain environmental exposures. The methylation of the promoter region bearing transcriptional start sites of those genes that encodes tumor suppressors such as tumor protein p53, retinoblastoma-associated protein 1, tumor protein p16, breast cancer 1 and many more result in the reduced expression of these genes and have been implicated in a large number of cancers like retinoblastoma, colon, lung and ovarian. A growing number of human diseases have been found to be associated with the aberrant DNA methylation. Hence, a deep insight into the individual’s epigenetic profile is the need of the hour. Several approaches have been developed to map DNA methylation patterns genome-wide. Some of these approaches include enzymatic digestion with methylation-sensitive restriction enzymes, the capture of 5-mC by methylated DNA-binding proteins followed by nextgeneration sequencing and methyl-DNA immunoprecipitation followed by sequencing of precipitated fragments. However, this chapter is going to describe the most recommended method for studying DNA methylation pattern, the method based on bisulfite sequencing. The bisulfite treatment of DNA converts unmethylated cytosine(s) to uracil(s), which are subsequently amplified as Ts by PCR. Hence, the bisulfitetreated DNA has mutations specifically at unmethylated Cs that can be mapped by Next-Generation sequencing.
APA, Harvard, Vancouver, ISO, and other styles
9

"Melatonin and Breast Cancer: Selective Estrogen Enzyme Modulator Actions." In Advances in Cancer Drug Targets, edited by Samuel Cos, Alicia Gonzalez, Virginia Alvarez-Garcia, Carolina Alonso-Gonzalez, and Carlos Martinez-Campa, 207–37. BENTHAM SCIENCE PUBLISHERS, 2013. http://dx.doi.org/10.2174/9781608054749113010009.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Aiyengar, Tupurani Mohini, Padala Chiranjeevi, and Hanumanth Surekha Rani. "Role of Endothelial Nitric Oxide Synthase in Breast Cancer." In Nitric Oxide Synthase - Simple Enzyme-Complex Roles. InTech, 2017. http://dx.doi.org/10.5772/67493.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Enzymes; Breast cancer"

1

Ruckhäberle, E., A. Rody, R. Gaetje, K. Engels, U. Holtrich, T. Karn, and M. Kaufmann. "Prognostic and predictive value of enzymes of the sphingolipid metabolism in breast cancer." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6014.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Evtimov, Vera, and Tracey Brown. "Abstract 3023: The characterisation of hyaluronan-related enzymes in breast cancer cell subpopulations." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3023.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Денисова, Дарья Андреевна. "CYCLIN-DEPENDENT KINASES CDK8 / 19 AND THEIR INFLUENCE ON THE ORIGIN AND DEVELOPMENT OF TUMOR PROCESSES." In Наука. Исследования. Практика: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Апрель 2020). Crossref, 2020. http://dx.doi.org/10.37539/srp290.2020.80.21.015.

Full text
Abstract:
Циклин-зависимая киназа CDK8 и её паралог, CDK19, являются ферментами, задействованными в развитии таких онкологических заболеваний, как рак молочной железы, колоректальный рак, рак простаты, острый миелоидный лейкоз и другие. The cyclin-dependent kinase CDK8 and its paralogue, CDK19, are enzymes involved in the development of oncological diseases such as breast cancer, colorectal cancer, prostate cancer, acute myeloid leukemia and others.
APA, Harvard, Vancouver, ISO, and other styles
4

McNamara, KM, F. Guestini, T. Sauer, JC Lindstrøm, H. Sasano, and J. Geisler. "Abstract P3-05-08: Steroid receptors and steroidogenic enzymes in human breast cancer: Associations with breast cancer subtypes and clinical outcome." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p3-05-08.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Feng, I. Jung, and Tomas Radivoyevitch. "SNP-SNP Interactions between dNTP Supply Enzymes and Mismatch DNA Repair in Breast Cancer." In 2009 Ohio Collaborative Conference on Bioinformatics (OCCBIO). IEEE, 2009. http://dx.doi.org/10.1109/occbio.2009.25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Salvador, F., JM Cejalvo, M. Guiu, E. Fernández, L. Paré, A. Prat, and RR Gomis. "PO-184 Role of ubiquitin-conjugating enzymes in chromosome instability and breast cancer metastasis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.223.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Thill, M., D. Fischer, S. Becker, C. Tim, K. Diedrich, and M. Friedrich. "Expression of prostaglandin metabolizing enzymes in correlation with vitamin D receptor in benign and malignant breast cell lines and breast tissue and regulation of prostaglandin metabolism by calcitriol." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6028.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Lee, Min-Ho, and Mi-Ock Lee. "Abstract 2400: Identification of histone modifying enzymes associated with tamoxifen resistance in MCF7 breast cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2400.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Saeki, T., M. Suzuki, T. Nakata, Y. Shiotsu, H. Ishida, S. Akinaga, K. Aogi, T. Utsumi, and N. Harada. "Expression Levels of Enzymes Related to In Situ Estrogen Synthesis and Clinicopathological Parameters in Breast Cancer Patients." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4155.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Thomas, T. J., Hui-Chen Hsu, Mervi Hyvonen, and Tuomo Keinanen. "Abstract 5511: Endoxifen inhibits polyamine biosynthetic enzyme activity and up-regulates metabolizing enzymes, spermine oxidase (SMO) and acetyl spermine oxidase (APAO)in breast cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5511.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Enzymes; Breast cancer"

1

Nawaz, Zafar. Ubiquitin Pathway Enzymes: Coactivators of Nuclear Hormone Receptors and Their Role in the Development of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada397349.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Nawaz, Zafar. Ubiquitin Pathway Enzymes: Coactivators of Nuclear Hormone Receptors and Their Role in the Development of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408069.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Harris, Reuben S. Enzyme-Catalyzed Mutation in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada613711.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

McIntire, William S. A Polyamine Oxidizing Enzyme as a Drug to Treat Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada532320.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

McIntire, William S. A Polyamine Oxidizing Enzyme as a Drug to Treat Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada521388.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Cooper, David L. Chimeric Enzyme/Prodrug Therapy as Novel Gene Therapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1997. http://dx.doi.org/10.21236/ada338689.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Sweeney, Carol, and Kristin E. Anderson. Metabolizing Enzyme 1 Polymorphisms and Prognosis Among Women Treated with Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada431327.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Sweeney, Carol. Metabolizing Enzyme 1 Polymorphisms and Prognosis Among Women Treated with Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada422722.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Hamstra, Daniel, and Alnawaz Rehemtulla. Development of a Novel Enzyme/Prodrug Strategy for Gene Therapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada394306.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Nephew, Kenneth P., Meiyun Fan, Teresa Craft, and Annie Park. Role of the Neddylation Enzyme Uba3, A New Estrogen Receptor Corepressor, in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada438888.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Enzymes; Breast cancer' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography