Talk:Breast cancer management
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Text and/or other creative content from this version of Breast cancer was copied or moved into Breast cancer management with this edit on 05:36, 13 October 2007. The former page's history now serves to provide attribution for that content in the latter page, and it must not be deleted as long as the latter page exists. |
Possibly copyright violation
[edit]I just barely split article out from main Breast cancer page. I will scan the article and try to rewrite/paraphrase where possible to avoid copy violation. Consider this a hang on tag for a couple hours until I can do this. Optigan13 05:51, 13 October 2007 (UTC)
- You don't have to rewrite it, since the source is Wikipedia. You just have to attribute the parent article for GFDL compliance reasons. I'll do it below and on the article page. -- But|seriously|folks 05:53, 13 October 2007 (UTC)
LN as indication for XRT
[edit]I changed the XRT section from "4 or more LNs" (paraphrasing here) as an indication for post-mastectomy XRT (PMRT) to "substantial involvement" as an indication. The 4 or more recommendation is predominantly based on subset analysis from the randomized Danish PMRT studies. Similar subset analyses demonstrate that the 1-3 positive LN patients have the same relative survival benefit as those with greater numbers of LNs, even with 8 or more nodes removed (median in the study was 7 LN removed, and this has formed the basis for the argument that fewer LNs involved probably do not require PMRT if "adequate" surgery (10 or more nodes) is performed). Three randomized studies have shown a survival benefit for PMRT in node positive patients, while one has not. Thus, the NCCN advocates PMRT for all women with 4 or more nodes involved and "strong consideration" for women with 1-3 nodes involved. I feel the new wording is more permissive in allowing consideration of PMRT in all node positive patients (micromets or IHC excluded, hence the "substantial" wording) rather than just in those women with 4 or more positive nodes. Schwartzenator (talk) 04:47, 20 May 2008 (UTC)
Immuno Therapy
[edit]This section is a copy/paste of its source.--Mandor (talk) 14:12, 2 March 2009 (UTC)
No mention of Abraxane/Paclitaxel
[edit]Article doesn't seem to mention Abraxane (a formulation of Paclitaxel) which was approved by the FDA in 2005 for treatment of refractory breast cancer. Rod57 (talk) 19:51, 12 June 2010 (UTC)
Lymphedema section looks like a huge copy from somewhere
[edit]Includes lots of references at the end. No wikilinks. Is it worth editing or should it just refer to Lymphedema ? - Rod57 (talk) 21:53, 15 December 2015 (UTC)
External links modified
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pipeline
[edit]The table and "preclinical" sections below were an ambitious effort by somebody to track the pipeline of drug candidates for breast cancer. Content is mostly unsourced or based on primary sources and outdated. Questionable whether this sort of detail belongs in WP per WP:NOTNEWS as well
Other types of targeted therapies that are being researched to fight cancer include:
- Angiogenesis inhibitors. These antibodies prevent the growth of new blood vessels, cutting off the supply of oxygen and nutrients to cancer cells.
- Signal transduction inhibitors. These antibodies block signals inside the cancer cell that helps the cells divide, stopping the cancer from growing.
- Antibodies/antagonists for other hormones/receptors such as androgen receptors and prolactin receptors, which are present in a high proportion of breast cancers.
Target | Drug | Type | Efficacy Trial |
---|---|---|---|
ER |
|
Aromatase inhibitor | [1][unreliable medical source?] |
|
Other | ||
AR in ER+ cancers |
|
androgen agonist | |
AR in ER- cancers | androgen receptor antagonist | Phase II MBC testing underway[2] | |
HER2 receptor protein |
|
Monoclonal antibody | |
Kinase inhibitor | |||
PRLR | selective dopamine D2 and serotonin agonist reducing prolactin levels | very good results in pretreated MBC in combination with docetaxel[6] | |
Vaccine | NeuVax is a HER2/neu peptide-based T-cell immunotherapy aimed at preventing disease recurrence and prolonging survival in cancer patients that have tumors expressing the HER2/neu oncoprotein. To date, clinical study results have demonstrated that NeuVax significantly reduces the rate of cancer recurrence while showing minimal side effects[7] | ||
|
Other | ||
HER1/ EGFR |
|
tyrosine kinase inhibitor | However, clinical studies did not find most EGFR inhibitors effective against breast cancer for a large enough proportion of patients. Some oncologists believe it may be possible to select a fraction of patients, either through genetics or the characteristics of their tumors, who have a better chance of having the drugs work[11][unreliable medical source?] |
insulin-like growth factor-1 receptor (IGF-1R) | Monoclonal antibody | ||
insulin-like growth factor-1 receptor (IGF-1R) and insulin receptor (IR) |
|
Dual kinase inhibitor | |
PI3K/AKT/mTOR cell survival pathway | Kinase inhibitor | ||
VEGF receptor protein (involved
in forming tumor blood vessels) |
|
Monoclonal antibody | |
Kinase inhibitor | |||
Other | |||
P53 |
|
Vaccine | |
Gene therapy | |||
|
Other | ||
PARP protein inhibitor |
|
DNA repair blocker - kills cancer cells with a faulty BRCA1 or BRCA2 gene by preventing the repair of DNA. A cell with a BRCA fault relies on a protein called PARP to keep its DNA healthy. Olaparib, known as a 'PARP-inhibitor', blocks PARP, which causes the cancer cells to die. |
Olaparib - In the initial findings, Over 40% of tumours in the higher dose group reduced significantly in size, and tumours were prevented from progressing for an average of six months, while one patient's tumour disappeared completely in a heavily pre-treated set of patiens in an ongoning trail.[15][unreliable medical source?] BSI-201 - Among other investigational PARP inhibitors in the industry, BSI-201 is the furthest along in clinical development in metastatic TNBC. BSI-201 is currently being evaluated for its potential to enhance the effect of chemotherapy-induced DNA damage. The clinical development of BSI-201 is supported by well documented safety profile based on studies of more than 200 patients.[16][unreliable medical source?] |
ATGR1 (ERBB2) |
|
AGTR1 is seen in 10 percent to 20 percent of breast tumors. Specifically, overexpressed only in tumors that are HER2-negative and ER-positive. AGTR1 was found to be as much as 100-fold overexpressed in some tumors. | [17][unreliable medical source?] |
eIF4E gene |
|
eIF4E gene is dysregulated in 30 percent of cancers including breast, prostate, head and neck, colon and stomach cancer. | The trial studied patients with M4/M5 acute myeloid leukemia who had undergone several other treatments that had previously failed. They had striking clinical improvements with even partial and complete remissions.[18][unreliable medical source?] |
Other Targets |
|
Kinase inhibitor | Drug already used to treat CML is a possible cure for a subset of breast cancer population who test positive for alpha-v beta-3.[19][unreliable medical source?] |
|
Kinase inhibitor | Combining Herceptin and saracatinib to treat resistant tumors in mice reduced tumor volume by 90 percent in 25 days. Herceptin alone kept tumor volume about the same during the same period, while control and saracatinib alone permitted growth of more than 200 percent.[20][unreliable medical source?] | |
|
multi-kinase inhibitor | ||
|
Vaccine - Stimuvax | ||
|
Other |
- Preclinical
- Protein tyrosine phosphatase 1B (PTP1B)
In the March 2007, edition of the scientific journal, Nature Genetics, researchers from Canada's McGill University reported that they had developed a potential drug target for treating up to 40 percent of breast cancers by blocking an enzyme called protein tyrosine phosphatase 1B (PTP1B), which has been implicated in the onset of breast cancer in mouse models of the disease.[24] Elevated levels of PTP1B have also been found in diabetes and obesity. A drug to block the activity of PTP1B is under development by Merck, and was found to delay the development of breast tumors and prevent lung cancer up to two months from the administration of the drug. The researchers hope to continue further research in mouse models which are also HER-2 positive (responsive to Herceptin) so that the drug could benefit a significant population of women.[25]
- Cholesterol drug - Ro 48-8071
It is possible that one mechanism utilized by PRIMA-1 to kill cancer cells may include shutting down cholesterol synthesis. What is now known is that Ro 48-8071 stops cholesterol synthesis, and it has been proved to be just as effective in destroying cancer cells as PRIMA-1, without harming other normal breast cells.[26][unreliable medical source?]
- Antidiabetic
In experiments led by postdoctoral fellows Heather Hirsch and Dimitrios Iliopoulos, the combination of metformin and the cancer drug doxorubicin killed human cancer stem cells and non-stem cancer cells in culture. The researchers used four genetically distinct breast cancer cell lines.
In mice, pretreatment with the diabetes drug prevented the otherwise dramatic ability of human breast cancer stem cells to form tumors. In other mice where tumors were allowed to take hold for 10 days, the dual therapy also reduced tumor mass more quickly and prevented relapse for longer than doxorubicin alone. In the two months between the end of treatment and the end of the experiment, tumors regrew in mice treated with chemotherapy alone, but not in mice that had received both drugs. By itself, metformin was ineffective in treating tumors.[27][28]
- Thermochemotherapy
Modern advancements in hyperthermia biology have led to refinements for individualised thermochemotherapy approaches to treatments as well as interesting potential for exploiting hyperthermia in conjunction with cancer vaccines.[citation needed] MR imaging is playing an increasing role for measuring patient response to hyperthermia.[citation needed]
Interest in hyperthermia as a treatment for breast cancer has led to significant advances and research activity which, in turn, has had a significant impact on treatment protocol.[citation needed] The National Comprehensive Cancer Network (NCCN) now includes hyperthermia in their Breast Cancer Guidelines as a treatment for recurrent cancer.
Erasmus Medical Centre in the Netherlands is one of Europe's largest hyperthermia centres.
ThermoDox is a proprietary heat-activated liposomal encapsulation of doxorubicin, an approved and frequently used oncology drug for the treatment of a wide range of cancers including breast cancer. ThermoDox, which is administered intravenously and in combination with local hyperthermia, has the potential to provide local tumor control and improve quality of life. Localized mild hyperthermia (39.5-42 degrees Celsius) releases the entrapped doxorubicin from the liposome. This delivery technology enables high concentrations of doxorubicin to be deposited preferentially in a targeted tumor.[citation needed]
- Flax
Testing of flaxseed (the highest source of mammalian lignans) on rats led to reduction and regression of tumours. This led to a formal randomized, placebo-controlled, double-blind study involving 32 postmenopausal patients confirming that 25g flaxseed daily intake significantly reduced cell proliferation, increased apoptosis and reduced c-erbB2 expression of human breast cancer cells.[29] The preliminary research into flax seeds indicates that flax can significantly change breast cancer growth and metastasis, and enhance the inhibitory effect of tamoxifen on estrogen-dependent tumors.[29][30][31][32]
[{reflist-talk}}
-- Jytdog (talk) 15:43, 10 October 2016 (UTC)
References
- ^ "Meta Analyses Of Global Trials Finds In Favor Of Aromatase Inhibitors". Medical News Today. 12 December 2008. Retrieved 24 October 2013.
- ^ http://www.asco.org/ascov2/Meetings/Abstracts?&vmview=abst_detail_view&confID=102& abstractID=80446 [dead link]
- ^ "Herceptin (trastuzumab)". MediLexicon. Retrieved 24 October 2013.
- ^ "In Trastuzumab-Resistant Metastatic Breast Cancer, Small Molecule Inhibitor Shows Promise". Medical News Today. 29 May 2009. Retrieved 24 October 2013.
- ^ "Tykerb (lapatinib)". MediLexicon. Retrieved 24 October 2013.
- ^ Frontini, L.; Lissoni, P.; Vaghi, M.; Perego, M. S.; Pescia, S.; Ardizzoia, A.; Gardani, G. (2004). "Enhancement of the efficacy of weekly low-dose taxotere by the long acting anti-prolactinemic drug cabergoline in pretreated metastatic breast cancer". Anticancer research. 24 (6): 4223–4226. PMID 15736476.
- ^ "NeuVax™ (nelipepimut-S)". Galena Biopharma Pipeline. Galena Biopharma. Retrieved 24 October 2013.
- ^ "Promising Targeted Therapy For Her2-Positive Metastatic Breast Cancer". Medical News Today. 9 October 2010. Retrieved 24 October 2013.
- ^ Stephan, Pam (16 June 2008). "Iressa (Gefitinib) – Targeted Therapy Drug for Breast Cancer". About.com. Retrieved 24 October 2013.
- ^ "Triple-Negative Breast Cancer Responds Well To Cetuximab Addition To Chemotherapy". Medical News Today. 12 October 2010. Retrieved 24 October 2013.
- ^ "Curbing Hormones' Effects In Obese Patients Could Aid Against Breast Cancer". Medical News Today. 2 December 2008. Retrieved 24 October 2013.
- ^ a b "New Phase III Study Of Avastin In Advanced Breast Cancer Meets Its Primary Endpoint Of Increasing The Time Patients Live". Medical News Today. 28 November 2008. Retrieved 24 October 2013.
- ^ "Tigris Pharmaceuticals Presents Results Of Breast Cancer Research At AACR Annual Meeting". Medical News Today. 1 May 2009. Retrieved 24 October 2013.
- ^ "Iniparib Extends Overall Survival In Metastatic Triple-Negative Breast Cancer". Medical News Today. 13 October 2010. Retrieved 24 October 2013.
- ^ "Breakthrough Breast Cancer Research Centre Pioneering Work Leads To Patient Trial Of New Generation Cancer Drug". Medical News Today. 26 June 2009. Retrieved 24 October 2013.
- ^ "Investigational Cancer Drug BSI-201 Showed Clinical Benefit In 62% Of Patients With Triple-Negative Metastatic Breast Cancer". Medical News Today. 7 June 2009. Retrieved 24 October 2013.
- ^ "Discovery Of Breast Cancer Gene That's Blocked By Blood Pressure Drug". Medical News Today. 2 June 2009. Retrieved 24 October 2013.
- ^ "Novel Therapy May Prove Effective In Treatment Of 30 Percent Of Cancers". Medical News Today. 14 May 2009. Retrieved 24 October 2013.
- ^ "Malignant Signature Identifies Possible Response To Therapy". Medical News Today. 8 September 2009. Retrieved 24 October 2013.
- ^ "Combination Overcomes Breast Cancer Resistance To Herceptin". Medical News Today. 14 March 2011. Retrieved 24 October 2013.
- ^ "The Length Of Time Before Breast Cancer Worsens Significantly Improved By Sorafenib". Medical News Today. 24 September 2009. Retrieved 24 October 2013.
- ^ "Antisoma Starts Phase II Trial Of AS1402 In Breast Cancer". Medical News Today. 30 September 2008. Retrieved 24 October 2013.
- ^ "Peregrine Pharmaceuticals Reports Positive Data In Second Phase II Bavituximab Breast Cancer Trial". Medical News Today. 28 April 2009. Retrieved 24 October 2013.
- ^ Julien, S. G.; Dubé, N.; Read, M.; Penney, J.; Paquet, M.; Han, Y.; Kennedy, B. P.; Muller, W. J.; Tremblay, M. L. (2007). "Protein tyrosine phosphatase 1B deficiency or inhibition delays ErbB2-induced mammary tumorigenesis and protects from lung metastasis". Nature Genetics. 39 (3): 338–346. doi:10.1038/ng1963. PMID 17259984.
- ^ "Breast tumour drug target found". BBC News. 12 May 2007. Retrieved 24 October 2013.
- ^ "Compound Used To Block Cholesterol Could Also Kill Breast Cancer, MU Researcher Finds". Medical News Today. 24 February 2011. Retrieved 23 October 2013.
- ^ "In Combination Treatment In Mice, Diabetes Drug Kills Cancer Stem Cells". Medical News Today. 15 September 2009. Retrieved 24 October 2013.
- ^ "New Test Identifies Cancer Patients To Benefit From 10p-A-Day Diabetes Drug". Medical News Today. 14 April 2011. Retrieved 24 October 2013.
- ^ a b Thompson, L. U.; Chen, J. M.; Li, T.; Strasser-Weippl, K.; Goss, P. E. (2005). "Dietary Flaxseed Alters Tumor Biological Markers in Postmenopausal Breast Cancer". Clinical Cancer Research. 11 (10): 3828–3835. doi:10.1158/1078-0432.CCR-04-2326. PMID 15897583.
- ^ Wang, L.; Chen, J.; Thompson, L. U. (2005). "The inhibitory effect of flaxseed on the growth and metastasisof estrogen receptor negative human breast cancer xenograftsis attributed to both its lignan and oil components". International Journal of Cancer. 116 (5): 793–798. doi:10.1002/ijc.21067. PMID 15849746.
- ^ Chen, J.; Hui, E.; Ip, T.; Thompson, L. U. (2004). "Dietary Flaxseed Enhances the Inhibitory Effect of Tamoxifen on the Growth of Estrogen-Dependent Human Breast Cancer (MCF-7) in Nude Mice". Clinical Cancer Research. 10 (22): 7703–7711. doi:10.1158/1078-0432.CCR-04-1130. PMID 15570004.
- ^ Chen, J.; Stavro, P. M.; Thompson, L. U. (2002). "Dietary Flaxseed Inhibits Human Breast Cancer Growth and Metastasis and Downregulates Expression of Insulin-Like Growth Factor and Epidermal Growth Factor Receptor". Nutrition and Cancer. 43 (2): 187–192. doi:10.1207/S15327914NC432_9. PMID 12588699.
External links modified
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