Иммунотерапия раковых опухолей: взгляд со стороны системной биологии. Максим Артемов
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This document summarizes recent advances in cancer immunotherapy from the perspective of systems biology. It discusses how checkpoint blockade immunotherapy works by addressing the second co-inhibitory checkpoint signal needed for T cell activation. Computational methods are now able to identify tumor-specific neoantigens that can be targeted by immunotherapy. Mouse model studies showed that certain tumors are naturally rejected due to expression of a mutant antigen recognized by T cells, and that antigen-specific T cells are present before immunotherapy treatment. The high mutational load in melanoma makes it particularly responsive to checkpoint blockade. Early work in the 19th century by William Coley observed tumor regression following bacterial infection, which led to development of a toxin mixture that resembled modern vaccine formulations. Members of
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Here you will get PowerPoint presentation about Monoclonal antibodies. To more update like share and follow slide share account
KarineHerveCV2015-
This document summarizes the professional experience and skills of an individual. It includes:
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2) Previous roles developing antibody expression systems at Glycart Biotechnology and identifying novel asthma drug targets at Novartis.
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View the video:
https://youtu.be/-a7DfHT8dU8
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Follow CCSN on social media:
Twitter - https://twitter.com/survivornetca
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Instagram: https://www.instagram.com/survivornet...
Pinterest - https://www.pinterest.com/survivornet...
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tumor immunology.pptx
- Cancer remains a leading cause of death globally, with an estimated 12.7 million cases expected to increase to 21 million by 2030.
- Tumors can be detected through abnormal cell proliferation caused by genetic mutations or loss of growth control.
- The immune system responds to tumor antigens expressed by cancer cells and tumor-associated antigens shared between tumors induced by the same virus.
- However, tumors have developed multiple mechanisms to evade immune surveillance such as low immunogenicity, antigen modulation, immune suppression, and inducing lymphocyte apoptosis.
Cancer immunology
Tumor immunotherapy activates a patient's immune system to fight cancer. There are two main types of immunotherapy - antigen-specific therapies which directly transfer immune cells or induce immune responses to specific antigens, and non-specific therapies which stimulate immune function regardless of antigen specificity. Adoptive transfer directly transfers immune cells while vaccination administers antigens to induce immune responses. Non-specific therapies were once tested on their own but are now used alongside antigen-specific therapies to enhance communication between immune cells.
Tumor immunology by nidhi
What is immunology?
What is Tumor?
Types of tumor
Classification of Malignant tumors
Malignant transformation of cells
General features of Tumor immunity
Tumor antigens
Tumor specific antigen
Tumor associated antigens
Immune response to tumor
Evasion of immune response by tumor
Cancer Immunosurveillance versus Immunoediting
Immunotechniques
RIA
ELISA
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This document outlines the history and mechanisms of the indoleamine-2,3-dioxygenase (IDO) pathway and its role in cancer immunotherapy. It discusses key findings such as:
1) Munn's 1999 discovery that IDO suppresses T-cell mediated rejection of tumors and fetal allografts by depleting tryptophan.
2) Mechanistic studies showing IDO induces T-cell arrest and inhibits proliferation through tryptophan depletion and kynurenine production, leading to Treg differentiation and CTL inhibition.
3) Preclinical studies combining IDO inhibitors with chemotherapy or vaccines, showing enhanced anti-tumor effects.
4) Ongoing clinical
Tumour immunology
1) The document discusses cancer and the immune system, covering topics like tumor antigens, immune responses to tumors, and tumor escape mechanisms.
2) It provides an overview of tumor immunology, including how tumors evade the immune system through mechanisms like down-regulating class I MHC expression and antigen modulation.
3) The document also summarizes different immunotherapy approaches, such as treatments using cytokines, monoclonal antibodies, and vaccination strategies using isolated tumor peptides or transfected tumor cells.
contagious cancer
While cancer itself is not contagious, some cancers can be transmitted between animals in rare cases. Three known examples are Tasmanian devil facial tumor disease, canine transmissible venereal tumor, and transmissible leukemia in clams. These cancers become contagious due to low variability in the animals' immune systems, which allows the cancer cells to evade detection between hosts. In humans, our highly variable immune systems provide strong protection against contagious cancers, except in rare circumstances when the immune system is compromised, such as during organ transplants or pregnancy.
Mariano Barbacid-El cáncer como consecuencia del envejecimiento
This document discusses five key developments in oncology since 2000:
1. The rise of targeted therapies that selectively inhibit molecular cancer drivers
2. Tumor stratification based on driver mutations and molecular profiles to select targeted treatments
3. Emergence of resistance to targeted therapies due to secondary mutations or activation of alternative pathways
4. Cancer genome sequencing revealing high mutation burdens and heterogeneity within tumors
5. Discovery of tumor heterogeneity with subclones evolving over time, challenging targeted treatment approaches
Ijsrp p10758
Cancer is one of the most challenging diseases and up until now. One of the most challenging things about cancer treatment is not the cure itself but the differentiation between the tumor cells and the normal cells. Most of the medical treatments of the cancer today cannot differentiate between the cancer cells and the normal one as well as it damages the hall tissue and it is still considered as a low-effect treatment to be applied in cancer. One of the most popular treatments of this kind is chemotherapy which is known for damaging the hall cells, cancer, and normal ones. Our research is focusing on generating a new therapy that can target the cancer cell itself so it will give us more efficiency ratio to stop cancer and will keep the other cells without any damage. We will use an antibody body for the protein antigen ErbB-2 which is located rabidly in the lung cancer cells' membrane surface. These antibodies will be produced by the immune system so it will target the tumor cells especially and stop the cell growth and damage it in some cases.
Cancer biology.pdf
Cancer arises from mutations in genes that control cell growth. These include proto-oncogenes, which promote growth, and tumor suppressor genes, which slow growth. Cancer develops in stages - initiation causes DNA damage, promotion involves continued cell division, and progression leads to uncontrolled growth. Cancer cells evade programmed cell death, self-stimulate growth, and invade other tissues. Doctors use tumor markers in blood and tissues to detect and monitor cancer.
Immunosurveillance
The document discusses immunosurveillance, which is the concept that the immune system prevents tumour development by detecting and eliminating abnormal cells. It provides a history of the theory and describes the mechanisms by which the immune system responds to tumour antigens through cellular and humoral responses. However, tumours can evade the immune system through mechanisms like antigen loss or suppression of immune cells. While the immune system plays a role in controlling cancer, its theory is imperfect as tumours still develop, requiring updated concepts like cancer immunoediting.
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Иммунотерапия раковых опухолей: взгляд со стороны системной биологии. Максим Артемов
- 1. Иммунотерапия раковых опухолей с точки зрения системной биологии Максим Артёмов 25 мая 2015
- 2. T cell activation requires 2 signals
- 3. CTLA4 and PD-1 are checkpoint regulatory molecules
- 4. Immunotherapy addresses second checkpoint
- 5. Huge success both in clinics and in academia 2011 - ipilimumab approved by FDA for melanoma 2013 - breakthrough of the year
- 7. Mouse model of tumor rejection – panel of sarcomas Some mouse sarcomas are naturally rejected while others grow out Matsushita et al, Nature 2012
- 8. Mouse model of tumor rejection – panel of sarcomas Hypothesis: Tumor neoantigen is responsible for rejecion Matsushita et al, Nature 2012 compare mutational landscape of regressor vs progressor tumors
- 9. Only regressor tumors express spnb2 mutant! Matsushita et al, Nature 2012
- 10. Only regressor tumors express spnb2 mutant! Spnb2 mutant is also computationally strong binder to MHC! Matsushita et al, Nature 2012
- 11. Computational filtering allows to go identify neoantigens
- 12. Computational filtering allows to go identify neoantigens
- 13. Computational filtering allows to go identify neoantigens
- 14. Computational filtering allows to go identify neoantigens
- 15. Checkpoint blockade works in progressor tumors aCTLA4/aPD1 treatments “cure” the mice Gubin et al, Nature 2014
- 16. Potential Antigens identified for T3 tumor
- 17. Antigen-specific T-cells are present in tumor even before treatment!
- 18. Theraputic vaccination saves the mouse!
- 19. Theraputic vaccination saves the mouse!
- 20. Independent validation in two additional tumors
- 21. Mutational load is predictive of immunotherapy response Rizvi et al, Science 2015
- 22. This is why first successes of checkpoint blockade are in melanoma!!
- 23. It all started in 19th century Worked in New York Cancer Hospital (later became a part of Memorial Sloan Kettering Cancer Center) • Noticed that infection with erysipelas often leads to spontaneous regression of sarcomas • Started therapeutically infection patients with inoperable sarcomas
- 24. It all started in 19th century Worked in New York Cancer Hospital (later became a part of Memorial Sloan Kettering Cancer Center) • Noticed that infection with erysipelas often leads to spontaneous regression of sarcomas • Started therapeutically infection patients with inoperable sarcomas
- 25. It turns out that Streptococci alone is not enough! What we refer to as Coley’s toxins is combination of two components: • Streptococci – gram-positive bacterial infection (no endotoxins) • Serratia – gram-negative bacteria (endotoxins)
- 26. It turns out that Streptococci alone is not enough! Note resemblance to classical vaccine formulation: Adjuvant + Adaptive Immunity Target What we refer to as Coley’s toxins is combination of two components: • Streptococci – gram-positive bacterial infection (no endotoxins) • Serratia – gram-negative bacteria (endotoxins)
- 27. Streptococci action is sarcoma specific! Survival
- 28. Sarcomas have characteristic genomic landscape
- 29. Fusion neoantigens are similar to Streptococci native protein epitopes!
- 30. Artyomov Lab members (and associated members) Alex Predeus Katya Loginicheva Alexey Sergushichev Vicky Lampropoulou Mike Orzel Anton Alexandrov Pavel Zakharov Many thanks to lab members and collaborators Bob Schreiber Matt Gubin Jeff Ward (WashU) Ben Zeskind Fadi Towfic (Immuneering)