I propose to make the following changes. Underlined sentences, with their respective references, are from the current Chemotherapy and Immunotherapy subsection of the Melanoma Wikipedia page.
Small-Molecule Targeted Therapies
Melanoma cells have mutations that allow them to survive and grow indefinitely in the body. [1] Small-molecule targeted therapies work by blocking the genes involved pathways for tumor proliferation and survival. [1] The main treatments are BRAF, C-Kit and NRAS inhibitors. [2] These inhibitors work to inhibit the downstream pathways involved in cell proliferation and tumour development due to specific gene mutations. [3] People can be treated with small-molecule targeted inhibitors if they are positive for the specific mutation. [1] BRAF inhibitors, such as vemurafenib and dabrafenib and a MEK inhibitor trametinib are the most effective, approved treatments for BRAF positive melanoma. [4] [1] Melanoma tumors can develop resistance during therapy which can make therapy no longer effective, but combining the use of BRAF and MEK inhibitors may create a fast and lasting melanoma therapy response. [5]
A number of treatments improve survival over traditional chemotherapy. [1] Biochemotherapy (chemotherapy with cytokines IL-2 and IFN-α) combined with BRAF inhibitors improved survival for people with BRAF positive melanoma. [1] Biochemotherapy alone did not improve overall survival and had higher toxicity than chemotherapy but the toxicity of BRAF inhibitors was not significantly different than chemotherapy. [1]
- ^ a b c d e f g Pasquali, Sandro; Hadjinicolaou, Andreas V; Chiarion Sileni, Vanna; Rossi, Carlo Riccardo; Mocellin, Simone (2018-02-06). "Systemic treatments for metastatic cutaneous melanoma". Cochrane Database of Systematic Reviews. doi: 10.1002/14651858.cd011123.pub2. ISSN 1465-1858.
- ^ Berger, Marina; Richtig, Georg; Kashofer, Karl; Aigelsreiter, Ariane; Richitig, Erika (2018-06). “The window of opportunities for targeted therapy in BRAFwt/NRASwt/KITwt melanoma: biology and clinical implications of fusion proteins and other mutations”. Giornale Italiano di Dermatologia e Venereologia.153 (3): 349-360. doi: 10.23736/S0392-0488.18.05970-9. PMID: 29600692
-
^ Broussard, Lindsey; Howland, Amanda; Ryu, Sunhyo; Song, Kyungsup; Norris, David; Armstrong, Cheryl A.; Song, Peter I. (2018).
"Melanoma Cell Death Mechanisms". Chonnam Medical Journal. 54 (3): 135.
doi:
10.4068/cmj.2018.54.3.135.
ISSN
2233-7385.
PMC
6165917.
PMID
30288368.
{{ cite journal}}: CS1 maint: PMC format ( link) - ^ Maverakis, E; Cornelius, L; Bowen, G; Phan, T; Patel, F; Fitzmaurice, S; He, Y; Burrall, B; Duong, C (2015). "Metastatic Melanoma – A Review of Current and Future Treatment Options". Acta Dermato Venereologica. 95 (5): 516–524. doi: 10.2340/00015555-2035. ISSN 0001-5555.
-
^ Kuske, Marvin; Westphal, Dana; Wehner, Rebekka; Schmitz, Marc; Beissert, Stefan; Praetorius, Christian; Meier, Friedegund (2018-10).
"Immunomodulatory effects of BRAF and MEK inhibitors: Implications for Melanoma therapy". Pharmacological Research. 136: 151–159.
doi:
10.1016/j.phrs.2018.08.019.
ISSN
1043-6618.
{{ cite journal}}: Check date values in:|date=( help)
Thanks for sharing your proposed changes. JenOttawa ( talk) 21:20, 5 November 2018 (UTC)
- I have a few notes to help improve your suggestion.
- We refer to "people" rather than "patients" on Wikipedia.
- Can you add any Wikilinks? Resistance, for example?
- Can you re-word this sentence to improve clarity? Melanoma tumors can develop resistance during therapy so that it is no longer effective, but by combining the use of BRAF and MEK inhibitors, it may create a fast and lasting melanoma therapy response.
Great works so far! JenOttawa ( talk) 17:39, 6 November 2018 (UTC)
I propose to make the following changes. Underlined sentences, with their respective references, are from the current Chemotherapy and Immunotherapy subsection of the Melanoma Wikipedia page.
Small-Molecule Targeted Therapies
Melanoma cells have mutations that allow them to survive and grow indefinitely in the body. [1] Small-molecule targeted therapies work by blocking the genes involved pathways for tumor proliferation and survival. [1] The main treatments are BRAF, C-Kit and NRAS inhibitors. [2] These inhibitors work to inhibit the downstream pathways involved in cell proliferation and tumour development due to specific gene mutations. [3] People can be treated with small-molecule targeted inhibitors if they are positive for the specific mutation. [1] BRAF inhibitors, such as vemurafenib and dabrafenib and a MEK inhibitor trametinib are the most effective, approved treatments for BRAF positive melanoma. [4] [1] Melanoma tumors can develop resistance during therapy which can make therapy no longer effective, but combining the use of BRAF and MEK inhibitors may create a fast and lasting melanoma therapy response. [5]
A number of treatments improve survival over traditional chemotherapy. [1] Biochemotherapy (chemotherapy with cytokines IL-2 and IFN-α) combined with BRAF inhibitors improved survival for people with BRAF positive melanoma. [1] Biochemotherapy alone did not improve overall survival and had higher toxicity than chemotherapy but the toxicity of BRAF inhibitors was not significantly different than chemotherapy. [1]
- ^ a b c d e f g Pasquali, Sandro; Hadjinicolaou, Andreas V; Chiarion Sileni, Vanna; Rossi, Carlo Riccardo; Mocellin, Simone (2018-02-06). "Systemic treatments for metastatic cutaneous melanoma". Cochrane Database of Systematic Reviews. doi: 10.1002/14651858.cd011123.pub2. ISSN 1465-1858.
- ^ Berger, Marina; Richtig, Georg; Kashofer, Karl; Aigelsreiter, Ariane; Richitig, Erika (2018-06). “The window of opportunities for targeted therapy in BRAFwt/NRASwt/KITwt melanoma: biology and clinical implications of fusion proteins and other mutations”. Giornale Italiano di Dermatologia e Venereologia.153 (3): 349-360. doi: 10.23736/S0392-0488.18.05970-9. PMID: 29600692
-
^ Broussard, Lindsey; Howland, Amanda; Ryu, Sunhyo; Song, Kyungsup; Norris, David; Armstrong, Cheryl A.; Song, Peter I. (2018).
"Melanoma Cell Death Mechanisms". Chonnam Medical Journal. 54 (3): 135.
doi:
10.4068/cmj.2018.54.3.135.
ISSN
2233-7385.
PMC
6165917.
PMID
30288368.
{{ cite journal}}: CS1 maint: PMC format ( link) - ^ Maverakis, E; Cornelius, L; Bowen, G; Phan, T; Patel, F; Fitzmaurice, S; He, Y; Burrall, B; Duong, C (2015). "Metastatic Melanoma – A Review of Current and Future Treatment Options". Acta Dermato Venereologica. 95 (5): 516–524. doi: 10.2340/00015555-2035. ISSN 0001-5555.
-
^ Kuske, Marvin; Westphal, Dana; Wehner, Rebekka; Schmitz, Marc; Beissert, Stefan; Praetorius, Christian; Meier, Friedegund (2018-10).
"Immunomodulatory effects of BRAF and MEK inhibitors: Implications for Melanoma therapy". Pharmacological Research. 136: 151–159.
doi:
10.1016/j.phrs.2018.08.019.
ISSN
1043-6618.
{{ cite journal}}: Check date values in:|date=( help)
Thanks for sharing your proposed changes. JenOttawa ( talk) 21:20, 5 November 2018 (UTC)
- I have a few notes to help improve your suggestion.
- We refer to "people" rather than "patients" on Wikipedia.
- Can you add any Wikilinks? Resistance, for example?
- Can you re-word this sentence to improve clarity? Melanoma tumors can develop resistance during therapy so that it is no longer effective, but by combining the use of BRAF and MEK inhibitors, it may create a fast and lasting melanoma therapy response.
Great works so far! JenOttawa ( talk) 17:39, 6 November 2018 (UTC)