Breast cancer future or investigational therapies: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 2: | Line 2: | ||
{{Breast cancer}} | {{Breast cancer}} | ||
{{CMG}} {{AE}}{{Soroush}} | {{CMG}} {{AE}}{{Soroush}} | ||
==Immunotherapeutic interventions== | |||
Generally, cancer immunotherapy refers to immune checkpoint inhibitors and cytokines, adoptive cell therapy, and cancer vaccines. | |||
===Immune checkpoint inhibitors=== | |||
====Programmed cell death protein 1 (PD-1)==== | |||
*Programmed cell death protein 1 (PD-1) is an inhibitory immune checkpoint inhibitor that limits T-cell effector function within tissues, and it is expressed on the surfaces of immune effector cells (T-cells, B cells, NK cells, DCs, and many TILs)and has two known ligands, namely, PD-L1 and PD-L2. | |||
:*Anti-PD-1 antibodies (Pembrolizumab, JS001, PDR001, and Nivolumab) | |||
:*Anti-PD-L1 antibodies (Atezolizumab and Durvalumab) | |||
====Anti-CTLA-4 antibodies (Ipilimumab and Tremelimumab)==== | |||
*Cytotoxic T lymphocyte-associated protein 4 (CTLA-4) is a T-cell inhibitory receptor that is expressed on activated CD8+ T cells and CD4+ regulatory T cells that express CD25 and Foxp3. <ref name="pmid8596936">Leach DR, Krummel MF, Allison JP (1996) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=8596936 Enhancement of antitumor immunity by CTLA-4 blockade.] ''Science'' 271 (5256):1734-6. PMID: [https://pubmed.gov/8596936 8596936]</ref> | |||
*Immune checkpoint inhibitors might be combined with targeted therapy (i.e Vascular endothelial growth factor (VEGF) and EGFR (epidermal growth factor receptor) inhibitors) | |||
===Adoptive cell therapy=== | |||
*Adoptive cell therapy is defined as the induction of anti-tumor immune responses via the isolation of highly active and tumor-specific lymphocytes, such as TILs, cytotoxic T lymphocytes (CTLs), Th cells, NK and DC cells.<ref name="pmid17549249">June CH (2007) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=17549249 Adoptive T cell therapy for cancer in the clinic.] ''J Clin Invest'' 117 (6):1466-76. [http://dx.doi.org/10.1172/JCI32446 DOI:10.1172/JCI32446] PMID: [https://pubmed.gov/17549249 17549249]</ref> | |||
:*Chimeric antigen receptors T-cell-based therapy | |||
:*T cell receptors (TCRs)—engineered T cells | |||
===Cancer vaccines=== | |||
*Cancer-testis antigens (CTA) as a vaccine target<ref name="pmid29088794">Mirandola L, Pedretti E, Figueroa JA, Chiaramonte R, Colombo M, Chapman C et al. (2017) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=29088794 Cancer testis antigen Sperm Protein 17 as a new target for triple negative breast cancer immunotherapy.] ''Oncotarget'' 8 (43):74378-74390. [http://dx.doi.org/10.18632/oncotarget.20102 DOI:10.18632/oncotarget.20102] PMID: [https://pubmed.gov/29088794 29088794]</ref> | |||
*Personalized peptide vaccination (PPV)<ref name="pmid24992895">Takahashi R, Toh U, Iwakuma N, Takenaka M, Otsuka H, Furukawa M et al. (2014) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=24992895 Feasibility study of personalized peptide vaccination for metastatic recurrent triple-negative breast cancer patients.] ''Breast Cancer Res'' 16 (4):R70. [http://dx.doi.org/10.1186/bcr3685 DOI:10.1186/bcr3685] PMID: [https://pubmed.gov/24992895 24992895]</ref> | |||
*Antigen-presenting cell (APC) and DC-based tumor vaccination<ref name="pmid25036145">Zhang P, Yi S, Li X, Liu R, Jiang H, Huang Z et al. (2014) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=25036145 Preparation of triple-negative breast cancer vaccine through electrofusion with day-3 dendritic cells.] ''PLoS One'' 9 (7):e102197. [http://dx.doi.org/10.1371/journal.pone.0102197 DOI:10.1371/journal.pone.0102197] PMID: [https://pubmed.gov/25036145 25036145]</ref> | |||
===Antibody–drug conjugates (ADC)=== | |||
*Utilization of monoclonal antibodies that recognize TAAs/TSAs and preferably internalizes when bound to the tumour cells to deliver highly potent cytotoxic agents.<ref name="pmid24423619">Panowski S, Bhakta S, Raab H, Polakis P, Junutula JR (2014) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=24423619 Site-specific antibody drug conjugates for cancer therapy.] ''MAbs'' 6 (1):34-45. [http://dx.doi.org/10.4161/mabs.27022 DOI:10.4161/mabs.27022] PMID: [https://pubmed.gov/24423619 24423619]</ref> | |||
===Exosomes=== | |||
*Exosomes are mall 30–100 nm sized extracellular vesicles | |||
*They are are present in many eukaryotic fluids (normal and malignant) | |||
*Particles that encapsulate contents, such as microRNAs. | |||
*Exosome messaging contributes to:<ref name="pmid29137633">Dioufa N, Clark AM, Ma B, Beckwitt CH, Wells A (2017) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=29137633 Bi-directional exosome-driven intercommunication between the hepatic niche and cancer cells.] ''Mol Cancer'' 16 (1):172. [http://dx.doi.org/10.1186/s12943-017-0740-6 DOI:10.1186/s12943-017-0740-6] PMID: [https://pubmed.gov/29137633 29137633]</ref> | |||
:*TME interactions, including: | |||
::*Immune suppression and immune escape, | |||
::*Invasive growth, adhesion, angiogenesis, | |||
::*Radiation resistance, chemo-resistance | |||
::*Genetic intercellular exchange, | |||
::*May manipulate tumor progression and metastatic cascade | |||
==Endoxifen== | |||
==Personalized medicine and I-SPY 2 clinical trial== | |||
==Immunotherapeutic interventions== | ==Immunotherapeutic interventions== | ||
Revision as of 19:45, 26 April 2019
|
Breast Cancer Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Breast cancer future or investigational therapies On the Web |
|
American Roentgen Ray Society Images of Breast cancer future or investigational therapies |
|
Breast cancer future or investigational therapies in the news |
|
Risk calculators and risk factors for Breast cancer future or investigational therapies |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]
Immunotherapeutic interventions
Generally, cancer immunotherapy refers to immune checkpoint inhibitors and cytokines, adoptive cell therapy, and cancer vaccines.
Immune checkpoint inhibitors
Programmed cell death protein 1 (PD-1)
- Programmed cell death protein 1 (PD-1) is an inhibitory immune checkpoint inhibitor that limits T-cell effector function within tissues, and it is expressed on the surfaces of immune effector cells (T-cells, B cells, NK cells, DCs, and many TILs)and has two known ligands, namely, PD-L1 and PD-L2.
- Anti-PD-1 antibodies (Pembrolizumab, JS001, PDR001, and Nivolumab)
- Anti-PD-L1 antibodies (Atezolizumab and Durvalumab)
Anti-CTLA-4 antibodies (Ipilimumab and Tremelimumab)
- Cytotoxic T lymphocyte-associated protein 4 (CTLA-4) is a T-cell inhibitory receptor that is expressed on activated CD8+ T cells and CD4+ regulatory T cells that express CD25 and Foxp3. [1]
- Immune checkpoint inhibitors might be combined with targeted therapy (i.e Vascular endothelial growth factor (VEGF) and EGFR (epidermal growth factor receptor) inhibitors)
Adoptive cell therapy
- Adoptive cell therapy is defined as the induction of anti-tumor immune responses via the isolation of highly active and tumor-specific lymphocytes, such as TILs, cytotoxic T lymphocytes (CTLs), Th cells, NK and DC cells.[2]
- Chimeric antigen receptors T-cell-based therapy
- T cell receptors (TCRs)—engineered T cells
Cancer vaccines
- Cancer-testis antigens (CTA) as a vaccine target[3]
- Personalized peptide vaccination (PPV)[4]
- Antigen-presenting cell (APC) and DC-based tumor vaccination[5]
Antibody–drug conjugates (ADC)
- Utilization of monoclonal antibodies that recognize TAAs/TSAs and preferably internalizes when bound to the tumour cells to deliver highly potent cytotoxic agents.[6]
Exosomes
- Exosomes are mall 30–100 nm sized extracellular vesicles
- They are are present in many eukaryotic fluids (normal and malignant)
- Particles that encapsulate contents, such as microRNAs.
- Exosome messaging contributes to:[7]
- TME interactions, including:
- Immune suppression and immune escape,
- Invasive growth, adhesion, angiogenesis,
- Radiation resistance, chemo-resistance
- Genetic intercellular exchange,
- May manipulate tumor progression and metastatic cascade
Endoxifen
Personalized medicine and I-SPY 2 clinical trial
Immunotherapeutic interventions
Generally, cancer immunotherapy refers to immune checkpoint inhibitors and cytokines, adoptive cell therapy, and cancer vaccines.
Immune checkpoint inhibitors
Programmed cell death protein 1 (PD-1)
- Programmed cell death protein 1 (PD-1) is an inhibitory immune checkpoint inhibitor that limits T-cell effector function within tissues, and it is expressed on the surfaces of immune effector cells (T-cells, B cells, NK cells, DCs, and many TILs)and has two known ligands, namely, PD-L1 and PD-L2.
- Anti-PD-1 antibodies (Pembrolizumab, JS001, PDR001, and Nivolumab)
- Anti-PD-L1 antibodies (Atezolizumab and Durvalumab)
Anti-CTLA-4 antibodies (Ipilimumab and Tremelimumab)
- Cytotoxic T lymphocyte-associated protein 4 (CTLA-4) is a T-cell inhibitory receptor that is expressed on activated CD8+ T cells and CD4+ regulatory T cells that express CD25 and Foxp3.
- Immune checkpoint inhibitors might be combined with targeted therapy (i.e Vascular endothelial growth factor (VEGF) and EGFR (epidermal growth factor receptor) inhibitors)
Adoptive cell therapy
- Adoptive cell therapy is defined as the induction of anti-tumor immune responses via the isolation of highly active and tumor-specific lymphocytes, such as TILs, cytotoxic T lymphocytes (CTLs), Th cells, NK and DC cells.
- Chimeric antigen receptors T-cell-based therapy
- T cell receptors (TCRs)—engineered T cells
Cancer vaccines
- Cancer-testis antigens (CTA) as a vaccine target
- Personalized peptide vaccination (PPV)
- Antigen-presenting cell (APC) and DC-based tumor vaccination
Antibody–drug conjugates (ADC)
- Utilization of monoclonal antibodies that recognize TAAs/TSAs and preferably internalizes when bound to the tumour cells to deliver highly potent cytotoxic agents.
Exosomes
- Exosomes are mall 30–100 nm sized extracellular vesicles
- They are are present in many eukaryotic fluids (normal and malignant)
- Particles that encapsulate contents, such as microRNAs.
- Exosome messaging contributes to:
- TME interactions, including:
- Immune suppression and immune escape,
- Invasive growth, adhesion, angiogenesis,
- Radiation resistance, chemo-resistance
- Genetic intercellular exchange,
- May manipulate tumor progression and metastatic cascade
Endoxifen
- Endoxifen is a nonsteroidal selective estrogen receptor modulator (SERM) of the triphenylethylene group. It is an active metabolite of tamoxifen and has been found to be effective in patients that have failed previous hormonal therapies (tamoxifen, aromatase inhibitors, and fulvestrant).[8]
Personalized medicine and I-SPY 2 clinical trial
References
- ↑ Leach DR, Krummel MF, Allison JP (1996) Enhancement of antitumor immunity by CTLA-4 blockade. Science 271 (5256):1734-6. PMID: 8596936
- ↑ June CH (2007) Adoptive T cell therapy for cancer in the clinic. J Clin Invest 117 (6):1466-76. DOI:10.1172/JCI32446 PMID: 17549249
- ↑ Mirandola L, Pedretti E, Figueroa JA, Chiaramonte R, Colombo M, Chapman C et al. (2017) Cancer testis antigen Sperm Protein 17 as a new target for triple negative breast cancer immunotherapy. Oncotarget 8 (43):74378-74390. DOI:10.18632/oncotarget.20102 PMID: 29088794
- ↑ Takahashi R, Toh U, Iwakuma N, Takenaka M, Otsuka H, Furukawa M et al. (2014) Feasibility study of personalized peptide vaccination for metastatic recurrent triple-negative breast cancer patients. Breast Cancer Res 16 (4):R70. DOI:10.1186/bcr3685 PMID: 24992895
- ↑ Zhang P, Yi S, Li X, Liu R, Jiang H, Huang Z et al. (2014) Preparation of triple-negative breast cancer vaccine through electrofusion with day-3 dendritic cells. PLoS One 9 (7):e102197. DOI:10.1371/journal.pone.0102197 PMID: 25036145
- ↑ Panowski S, Bhakta S, Raab H, Polakis P, Junutula JR (2014) Site-specific antibody drug conjugates for cancer therapy. MAbs 6 (1):34-45. DOI:10.4161/mabs.27022 PMID: 24423619
- ↑ Dioufa N, Clark AM, Ma B, Beckwitt CH, Wells A (2017) Bi-directional exosome-driven intercommunication between the hepatic niche and cancer cells. Mol Cancer 16 (1):172. DOI:10.1186/s12943-017-0740-6 PMID: 29137633
- ↑ Hawse JR, Subramaniam M, Cicek M, Wu X, Gingery A, Grygo SB et al. (2013) Endoxifen's molecular mechanisms of action are concentration dependent and different than that of other anti-estrogens. PLoS One 8 (1):e54613. DOI:10.1371/journal.pone.0054613 PMID: 23382923
- ↑ Wu X, Hawse JR, Subramaniam M, Goetz MP, Ingle JN, Spelsberg TC (2009) The tamoxifen metabolite, endoxifen, is a potent antiestrogen that targets estrogen receptor alpha for degradation in breast cancer cells. Cancer Res 69 (5):1722-7. DOI:10.1158/0008-5472.CAN-08-3933 PMID: 19244106
- ↑ Gingery A, Subramaniam M, Pitel KS, Reese JM, Cicek M, Lindenmaier LB et al. (2014) The effects of a novel hormonal breast cancer therapy, endoxifen, on the mouse skeleton. PLoS One 9 (5):e98219. DOI:10.1371/journal.pone.0098219 PMID: 24853369