Relevant bibliographies by topics / Immune check point inhibitor

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Immune check point inhibitor'

Author: Grafiati
Published: 25 May 2024

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 'Immune check point inhibitor.'

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 "Immune check point inhibitor"

1

Jaswani, Tamika S., Meeta Desai, Douglas Grider, and Jonathan M. Bern. "Immune Check Point Inhibitor-induced Colitis." American Journal of Gastroenterology 112 (October 2017): S858—S860. http://dx.doi.org/10.14309/00000434-201710001-01575.

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

Bobart, Shane A., Itunu Owoyemi, Joseph Grande, Nelson Leung, and Sandra M. Herrmann. "Immune Check Point Inhibitor–Associated Endothelialitis." Kidney International Reports 5, no. 8 (August 2020): 1371–74. http://dx.doi.org/10.1016/j.ekir.2020.05.027.

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

Ashour, Tarek, Georges Nakhoul, Pradnya Patil, Pauline Funchain, and Leal Herlitz. "Immune Check Point Inhibitor–Associated Glomerulonephritis." Kidney International Reports 4, no. 2 (February 2019): 355–59. http://dx.doi.org/10.1016/j.ekir.2018.10.017.

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

Kumar, Aswini, Maximilian Lee, and Talhat Azemi. "IMMUNE CHECK POINT INHIBITOR MYOCARDITIS MIMICKING ACS." Journal of the American College of Cardiology 73, no. 9 (March 2019): 2681. http://dx.doi.org/10.1016/s0735-1097(19)33287-5.

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

Nilajgi, Shalini, Nicholas Kasmeridis, and Kichendasse Ganessan. "A Case Of Immune Check Point Inhibitor - Induced Hypophysitis." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A560. http://dx.doi.org/10.1210/jendso/bvab048.1142.

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

Suchý, David. "Immune-related adverse events associated with immune check-point inhibitors." Klinická farmakologie a farmacie 33, no. 3 (October 28, 2019): 20–24. http://dx.doi.org/10.36290/far.2019.019.

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

Marthey, Lysiane, Raef Abdallah, Christophe Bellanger, Clément Bresteau, Antoine Meyer, Aurélien Amiot, and Franck Carbonnel. "Immune check-point inhibitors related enterocolitis." Hépato-Gastro & Oncologie Digestive 30, no. 8 (October 2023): 826–32. http://dx.doi.org/10.1684/hpg.2023.2641.

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

Johncilla, Melanie, Shilpa Grover, Xuchen Zhang, Dhanpat Jain, and Amitabh Srivastava. "Morphological spectrum of immune check‐point inhibitor therapy‐associated gastritis." Histopathology 76, no. 4 (February 18, 2020): 531–39. http://dx.doi.org/10.1111/his.14029.

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

Kim, Jin Young, Chi Heum Cho, and Hong Suk Song. "Targeted therapy of ovarian cancer including immune check point inhibitor." Korean Journal of Internal Medicine 32, no. 5 (September 1, 2017): 798–804. http://dx.doi.org/10.3904/kjim.2017.008.

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

Vergne-Santiago, Norma, Ernesto Jos E. Sola Sanchez, and Michelle Marie Mangual Garcia. "Immune Check Point Inhibitors Triggering Non Autoimmune Polyendocrinopathy." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A136—A137. http://dx.doi.org/10.1210/jendso/bvab048.275.

Full text
Abstract:
Abstract The superlative therapeutic response of cancer immunotherapy is activation of the immune system against cancer cells. Currently, one of the most considered immune system enhancer are the immunomodulatory antibodies well known as checkpoint inhibitor therapy. Among this type of treatment, programed cell death-1 receptor blocker, is one of the most sought-after therapies on demand now a day. Notwithstanding the important clinical benefits of this therapeutic modality, serial autoimmune adverse effects and variety of atypical presentations of life-threatening endocrinopathies are expected to occur. We present a case of a 78-year-old man with dyslipidemia and lung CA who was referred to our clinic after developing electrolyte disturbances with associated dizziness and fatigue one month after Pembrolizumab therapy initiation. Physical exam was unremarkable. Laboratory data was consistent with mild hyponatremia, hyperkalemia and adequate fasting blood sugar levels. Aldosterone levels were extremely low, ACTH levels were extremely high with inappropriate low total cortisol response and negative 21-Hydroxylase antibodies. Diagnosis of primary adrenal insufficiency was established and Fludrocortisone 0.05 mg PO daily therapy was started with further resolution of hyponatremia and initial symptoms. In addition, concurrent primary hyperthyroidism along with thyroid RAIU-Scan results were consistent with thyroiditis, but TSI and TPO’s antibody levels were unexpectedly negative. Eventually, a suspicious thyroid nodule was identified requiring biopsy. Initial FNA results showed a follicular lesion of undetermined significance followed by a benign finding when repeated after six months. During follow up, patient’s primary hyperthyroidism converted to severe primary hypothyroidism without any intervention for her prior hyperthyroidism. Patient’s TPO’s levels remain undetectable and his current status is post-thyroiditis with residual primary hypothyroidism. Primary adrenal insufficiency also persist and its antibodies have not yet been identified either. It is known that autoimmunity can predispose to the development of primary adrenal and thyroid disorders in patients undergoing PD-1 receptor blockers therapy against cancer. Both disorders are increasingly recognized and reported as one of the most common adverse effects presenting in patients treated with these agents. However, to our knowledge, cases of non-immune related adverse effects are barely documented. This case of uncommon endocrine manifestations related to checkpoint inhibitors therapy is meritorious of being reported since it should raise awareness in the medical community for prompt identification of signs and symptoms, as well as to offer adequate management, accurate treatment and provide a better standard of care.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Immune check point inhibitor"

1

Dréan, Raphaelle. "Développement de nano-anticorps antagonistes du point de contrôle immunitaire ILT4 pour une application en immunothérapie antitumorale." Electronic Thesis or Diss., Sorbonne université, 2022. http://www.theses.fr/2022SORUS446.

Full text
Abstract:
Le récepteur ILT4 est un point de contrôle immunitaire, principalement exprimé par les cellules myéloïdes du système immunitaire. Dans le contexte cancéreux, ILT4 participe au développement tumoral en maintenant un microenvironnement immunitaire protumoral et en activant directement la prolifération tumorale. L’activation d’ILT4 par la molécule du complexe majeur d’histocompatibilité (CMH) de classe I non-classique HLA-G induit des cellules myéloïdes tolérogènes. De plus, l’expression ectopique d’ILT4 a été rapportée dans plusieurs types de cancers. L’interaction entre l’angiopoiétine-like2 (ANGPTL2) et l’ILT4 promeut la prolifération de cellules de cancer du poumon non à petites cellules et inhibe leur apoptose. Cibler ce nouveau point de contrôle immunitaire par des anticorps bloquants est donc une approche prometteuse en immunothérapie. A la lumière de certaines limitations des anticorps conventionnels bloquants en thérapies des tumeurs solides, nous avons investigué le potentiel d’inhibiteurs basés sur des VHH. Ce petit format d’anticorps, dérivé des anticorps homodimériques de camélidés, allie les propriétés de spécificité des anticorps à celles des petites molécules. Grâce au criblage par phage-display d’une banque immunologique obtenue par immunisation d’un alpaga, nous avons sélectionné un VHH hautement affin et spécifique pour ILT4, qui inhibe l’interaction entre le récepteur et ses deux ligands. Nous avons démontré l’effet biologique antagoniste du VHH in vitro sur des modèles de cellules tumorales et de macrophages de type M2 protumoraux issus de monocytes. Ces premiers résultats de caractérisation supportent le développement futur de ce nouveau format d’anticorps VHH bloquant ILT4 en immunothérapie antitumorale
ILT4 (Immunoglobulin-Like Transcript 4) is an immune checkpoint receptor mainly expressed by myeloid immune cells. In cancer context, ILT4 participates in tumor development by maintaining a protumoral immuno-microenvironment and directly promoting tumor cell proliferation. ILT4 interaction with the non-classical MCH class I molecule HLA-G induces an immunosuppressive microenvironment by promoting tolerogenic myeloid cells. Moreover, the ectopic expression of ILT4 has been reported in several solid tumors. The activation of ILT4 by Angiopoietin-like-2 (ANGPTL2) promotes non-small cell lung tumor cell proliferation and inhibits cell apoptosis. Targeting this new immune checkpoint with blocking antibodies is therefore a promising cancer immunotherapy approach. In light of several drawbacks of classical IgG blocking antibodies in solid cancer, we investigated the potential of VHH-based inhibitors. This small monoclonal antibody format, derived from camelid homodimeric antibodies, combine the binding capacities of antibodies to the properties of small molecules. After immunization of an alpaca and phage-display screening, we selected a VHH with high affinity and specificity to ILT4 that inhibits the interaction of the receptor with both ligands. We validated the VHH’s biological antagonist activity on tumor cells and monocyte-derived pro-tumoral M2 like macrophages in vitro. These results support the potential of this new VHH-based antibody targeting ILT4 in cancer immunotherapy
APA, Harvard, Vancouver, ISO, and other styles
2

Fournel, Ludovic. "Influence Du Cisplatine sur l'expression du Check-Point Immunitaire PD-1/PD-L1 Dans Le Cancer Broncho-Pulmonaire Non A Petites Cellules Cisplatin Increases PD-L1 Expression and Optimizes Immune Check-Point Blockade in Non-Small Cell Lung Cancer Modulation of Lung Cancer Cell Plasticity and Heterogeneity with the Restoration of Cisplatin Sensitivity by Neurotensin Antibody." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASS077.

Full text
Abstract:
Malgré les nombreux progrés réalisés ces dernières années dans la prise en charge thérapeutique du cancer broncho-pulmonaire, cette pathologie reste la première cause de décès lié au cancer dans le monde. L’enjeu majeur pour cette maladie est donc de développer de nouveaux traitements et d’optimiser l’utilisation des drogues existantes, en particulier les sels de platine. Les protocoles combinant des inhibiteurs de points de contrôle immunitaire avec des sels de platine est actuellement en plein essor malgré un certain manque en études précliniques. Dans ce travail, j’ai cherché à évaluer l'impact du cisplatine sur l'expression de PD-L1 en analysant des patients ayant reçu une chimiothérapie néo-adjuvante à base de cisplatine. Le traitement d'induction augmentait considérablement le marquage PD-L1 des cellules tumorales et immunitaires du microenvironnement. Vingt-deux patients présentaient une variation positive du pourcentage de cellules tumorales PD-L1+ après chimiothérapie néoadjuvante; dont 9 (23,1%) passant de <50% à ≥50% des cellules tumorales marquées. Nous avons également confirmé la régulation positive de PD-L1 par le cisplatine, tant au niveau de l'ARNm qu’au niveau protéique, in-vitro et in-vivo sur des souris nude et des souris immunocompétentes greffées par des tumeurs expérimentales issues de lignées cellulaires de cancer du poumon A549, LNM-R ou LLC1. L’up-régulation de PD-L1 par le cisplatine fait intervenir la voie de signalisation PI3K/AKT. De plus, l'administration combinée d'anticorps anti-PD-L1 (3 mg / kg) et de cisplatine (1 mg / kg) à des souris portant un carcinome pulmonaire réduisait significativement la croissance tumorale par rapport aux traitements en monothérapie et par rapport aux contrôles. Le cisplatine augmente donc précocément et durablement l'expression de PD-L1 et pourrait donc agir de manière synergique avec un blocage de PD-1 / PD-L1 pour améliorer la réponse tumorale aux traitements. En parallèle, nous avons pu développer une thérapie ciblée anti-neurotensine permettant de bloquer ses effets paracrines stimulants la prolifération, la croissance, et les capacités d’invasion des cellules de tumeurs pulmonaires. Les anticorps anti-neurotensine amélioraient également la sensibilité au cisplatine de tumeurs préalablement résistantes par des mécanismes qui impliquent probablement l’augmentation de l’influx et la diminution de l’efflux de platine au niveau de sa cible intra-nucléaire qu’est l’ADN. L’ensemble de ces résultats apportent du rationnel à la réalisation d’essais cliniques impliquant le cisplatine et visant par différents biais à améliorer l’efficacité de traitements systémiques de cancers broncho-pulmonaires non à petites cellules
Despite many advances in the recent years in the therapeutic management of bronchopulmonary cancer, it remains the leading cause of death linked to cancer in the world. The major challenge for this disease is therefore to develop new treatments and optimize the use of existing drugs, in particular platinum salts. The number of clinical protocols testing combined therapies including immune check-point inhibitors and platinum salts is currently increasing in lung cancer treatment, however preclinical studies and rationale are often lacking. Here, we evaluated the impact of cisplatin treatment on PD-L1 expression analyzing the clinicopathological characteristics of patients who received cisplatin-based neoadjuvant chemotherapy followed by surgery and showed that cisplatin-based induction treatment significantly increased PD-L1 staining in both tumor and immune cells from the microenvironment. Twenty-two patients exhibited positive PD-L1 staining variation after neoadjuvant chemotherapy; including 9 (23.1%) patients switching from <50% to ≥50% of stained tumor-cells. We also confirmed the up-regulation of PD-L1 by cisplatin, at both RNA and protein levels, in nude and immunocompetent mice bearing tumors grafted with A549, LNM-R, or LLC1 lung cancer cell lines. Up-regulation of PD-L1 by cisplatin involved the PI3K / AKT signaling pathway.The combined administration of anti-PD-L1 antibodies (3mg/kg) and cisplatin (1mg/kg) to mice harboring lung carcinoma significantly reduced tumor growth compared to single agent treatments and controls. Overall, these results suggest that cisplatin treatment could synergize with PD-1/PD-L1 blockade to increase the clinical response, in particular through early and sustainable enhancement of PD-L1 expression. Simultaneously, we were able to develop a targeted anti-neurotensin therapy to block its paracrine effects which stimulate proliferation, growth, and metastatic potential of lung tumor cells. Anti-neurotensin antibodies also improved the sensitivity to cisplatin of previously resistant tumors by mechanisms which probably involve increased influx and decreased efflux of platinum at the intra-nuclear level where resides its target DNA. All of these results provide a rationale for carrying out clinical trials involving cisplatin and aiming, by various ways, to improve the effectiveness of systemic treatments for non-small cell broncho-pulmonary cancers
APA, Harvard, Vancouver, ISO, and other styles
3

Grosjean, Iris. "SQSTM1, une protéine de plateforme à la croisée de la réponse aux dommages à l’ADN et de la réponse à l’immunothérapie dans le cancer : rôles des rétrovirus endogènes." Electronic Thesis or Diss., Université Côte d'Azur, 2020. http://www.theses.fr/2020COAZ6037.

Full text
Abstract:
Le cancer du poumon non à petites cellules (CPNPC) est le cancer le plus mortel au monde, en partie en raison de résistance acquises chez des patients qui initialement répondaient aux thérapies anti-cancéreuses comme les chimiothérapies génotoxiques et la radiothérapie (agents endommageant l'ADN, nommés ci-après DDA) et aux thérapies ciblées. L’immunothérapie (dont les inhibiteurs des points de contrôle immunitaires (ICI)) est une véritable révolution dans la prise en charge des patients. Cette stratégie a en effet eu un impact positif rendant des cancers avancés n’ayant pas de cibles « actionnables » que l’on considérait incurables, traitables. La survie à 5 ans est passée de seulement 5% avec un traitement conventionnel à 20% avec les immunothérapies et jusqu’à 50% - 60% pour le mélanome et le cancer du poumon par l’utilisation de combinaisons thérapeutiques incluant les ICI et les DDA. Le défi actuel des essais cliniques est de développer des stratégies thérapeutiques combinées qui augmentent l’efficacité des différents traitements tout en limitant les résistances. Elucider les mécanismes de résistance est essentiel pour proposer de nouveaux biomarqueurs prédictifs robustes et de nouvelles approches thérapeutiques pour améliorer l'efficacité des ICI.Nous avons émis l'hypothèse que la résistance aux DDA et aux ICI est en partie médiée par des mécanismes tumoraux intrinsèques, dont certains peuvent être partagés. Ainsi, nous avons étudié l'action des DDA et leurs conséquences moléculaires pouvant conduire à une évasion immunitaire. Grâce à trois approches complémentaires (in silico, in vivo sur des cohortes de patients et in vitro), nous identifions que la protéine d'échafaudage p62/SQSTM1 est un médiateur moléculaire clé capable de prédire et de contrôler la sensibilité aux DDA et ICI. Nous soulignons pour la première fois que SQSTM1 est à l’origine d’un profil tumoral immunitaire « CHAUD », tout en régulant à la baisse les mécanismes de réparation de l'ADN. De plus SQSTM1 est essentiel pour la réactivation induite par les DDA des rétrovirus endogènes humains (hERV). En aval, les hERV induisent une réponse antivirale innée, entraînant l'expression d'interférons, MHC-I et PD-L1, conduisant à une évasion immunitaire tumorale.En conclusion, i) nous proposons SQSTM1 comme biomarqueur prédictif pour sélectionner les patients pouvant bénéficier des stratégies de combinaison ICI + DDA, et ii) nous montrons une justification biologique de l'efficacité de telles stratégies dans le cancer du poumon réfractaire, visant à promouvoir leur utilisation et améliorant ainsi le pronostic du CBPNPC
Non-small cell lung cancer (NSCLC) is the deadliest cancer in the world, due to acquired resistance to genotoxic chemotherapy and radiotherapy (DNA-damaging agents, named DDAs hereafter) and targeted therapies. Immunotherapy (including immune checkpoint inhibitors (ICIs)) is a real revolution in patient care. This strategy has indeed had a positive impact, turning into treatable advanced cancers without "actionable" targets that were considered incurable. Survival at 5-year has increased from 5% with conventional treatment to 20% with immunotherapies and up to 50/60% for melanoma and lung cancer with therapies combining ICIs and DDAs. The current challenge in clinical trials is to develop combined therapeutic strategies that increase efficacy while limiting resistance to different treatments. Elucidating resistance mechanisms is essential to propose new robust predictive biomarkers and new therapeutic approaches to improve the efficacy of ICIs.We have hypothesized that resistance to DDAs and ICIs is mediated by intrinsic tumor mechanisms, some of which may be shared. Thus, we have studied the action of DDAs and their molecular consequences that lead to immune evasion. Through three complementary approaches (in silico, in vivo on patient cohorts and in vitro), we identify the p62/SQSTM1 scaffold protein as a key molecular mediator capable of predicting and controlling sensibility to DDAs and ICIs. We report for the first time that SQSTM1 causes a "HOT" tumor immune profile, while downregulating DNA repair mechanisms. In addition, SQSTM1 is essential for the DDAs-induced reactivation of human endogenous retroviruses (hERVs). Downstream, hERVs induce an innate antiviral response, resulting in the expression of interferons, MHC-I and PD-L1, leading to tumor immune evasion.In conclusion, i) we propose SQSTM1 as a predictive biomarker for selecting patients who may benefit from ICI plus DDA combination strategies, and ii) we highlight a biological rationale for the efficacy of such strategies in refractory lung cancer, aimed at promoting their use and thus improving the prognosis of NSCLC
APA, Harvard, Vancouver, ISO, and other styles
4

Munivenkata, Swamy Preethi. "Combined CTLA-4 and PD-1 inhibition a single institute in-depth analysis of toxicity and efficacy in patients treated at the Dana-Farber Cancer Institute." Thesis, 2017. https://hdl.handle.net/2144/26950.

Full text
Abstract:
PURPOSE: The purpose of this study was to compare the rate of grade 3-4 immune related adverse events (irAEs) in patients with advanced metastatic melanoma treated with the combined anti-CTLA-4 and anti-PD-immune-therapy at the Dana Farber Cancer Institute(DFCI), to that of the published rate of grade 3-4 irAEs among patients treated with the same combination of check-point therapy in the pivotal phase II and phase III trials that led to the FDA approval of the combination regimen. This study also measures the tumor response with the Ipi-Nivo combination therapy and overall-survival of patients in the study cohort at DFCI. METHODS/PROCEDURES: This is a retrospective cohort study conducted at DFCI during 2014 to 2016 among stage III/IV melanoma patients treated outside of the clinical trials with the Ipi-Nivo combination therapy. Chart review of the electronic medical record(EMR) was conducted to abstract the data for this study. irAEs were graded and classified as per the NCI-CTCAE v.4.0 guidelines. The comparison of the rate of grade 3 4 toxicity in the clinical settings at DFCI and the clinical trials was performed using a one sample proportion hypothesis test. For efficacy assessment of tumor response, RECIST1.1 criterion was used to ascertain the best clinical response. RESULTS: During an overall follow-up period of 600 days, 52 patients were treated on expanded access protocol (EAP) and commercial Ipi-Nivo combination therapy at DFCI. The rate of grade 3-4 immune mediated toxicity for this cohort of patients treated outside of clinical trials was 32.6%. The average rate of grade 3-4 irAEs reported in phase II/III clinical trials was approximately 55%. The results from the one-proportion hypothesis test [(P-value: 0.002) (95% C.I: 19.14-46.23)], prove that patients in the “real world” clinical settings have a different safety profile than patients treated in the clinical trials. The rate of grade 3-4 irAEs was found to be lower (19.14% to 46.23%) in the population treated with Ipi/Nivo combination therapy at the DFCI, compared to the check-mate clinical trials (approximately 55%) CONCLUSION: The results from the study indicate a lower rate of grade 3-4 irAEs in patients treated at DFCI, in comparison with the patients treated in the clinical trials for the Ipi-Nivo combination group. The results support the need for preemptive safety signal detection of symptoms of irAEs to improve patient’s safety. However, larger database studies are required for the generalizability of this results to a wider patient population treated outside of DFCI.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Immune check point inhibitor"

1

Patel, Anush, Haisam Abid, and Amrat Kumar. "The Endocrinological Side Effects of Immunotherapies." In Advances in Precision Medicine Oncology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96491.

Full text
Abstract:
The use of immunotherapies is gaining importance in the treatment of advanced malignancies. There are many checkpoints in the immune system which prevents T-cells from attacking one’s own body cells. The cancer cells can camouflage from the T-cells and the immune system is unable to mount an effective anti-tumor response. The immunotherapies, mainly monoclonal antibodies anti-cytotoxic T-lymphocyte antigen 4 (CTLA-4), anti-programmed cell death protein-1 (PD-1) and anti-PD-1 ligand molecules (PD-L1 and L2) reactivate the immune system to act against cancerous cells but they can also cause T-cells to attack healthy cells causing various autoimmune diseases, which are known as immune related adverse events (irAEs). Current clinical data shows increased incidence of pituitary disorders with CTLA4 inhibitors and thyroid dysfunction in patients with PD-1/PD L-1 1 blockade. There have also been association of type 1 diabetes mellitus and primary adrenal insufficiency in patients with immune check point inhibitors. In this chapter we will discuss the incidence, characteristic findings, diagnosis and management of various endocrinological side effects due to targeted immunotherapies used in various malignancies.
APA, Harvard, Vancouver, ISO, and other styles
2

Thompson, John F., Richard A. Scolyer, and Richard F. Kefford. "Skin cancer: melanoma." In Oxford Textbook of Oncology, 674–89. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199656103.003.0049.

Full text
Abstract:
The development of cutaneous melanoma is attributed mainly to UV-induced DNA damage producing genetic mutations that make melanocytes capable of invasion and metastasis. Early diagnosis and surgical excision are the key to successful treatment. Breslow thickness, ulceration and mitotic rate are the most important prognostic factors. Histological examination of the ‘sentinel’ lymph node indicates prognosis with even greater accuracy, and is now routinely recommended for patients with melanomas ≥1.0 mm in Breslow thickness. Early complete regional node clearance in sentinel node-positive patients may improve melanoma-specific survival. Clinically involved nodes are best treated by surgery, as are isolated systemic metastases. However, new systemic therapies are achieving good short- to-medium term systemic disease control; these include BRAF and MEK inhibitors and immune check-point regulators (e.g. CTLA-4 inhibitors and agents targeting PD-1 and PDL-1). Radiotherapy, regional chemotherapy, topical therapies and intralesional therapies may also be effective in patients with metastatic melanoma.
APA, Harvard, Vancouver, ISO, and other styles
3

Yadav, Hemang, Alastair C. Carr, and Philippe R. Bauer. "Oncological Aspects of Respiratory Critical Care." In Oxford Textbook of Respiratory Critical Care, 437–44. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/med/9780198766438.003.0049.

Full text
Abstract:
Abstract Summary Acute respiratory failure (ARF) is the most common cause for intensive care unit admission in patients with cancer and is associated with high morbidity and mortality. Airway disorders such as central airway occlusion can occur from intrinsic or extrinsic compression by tumours. Bronchoscopic interventions can be vital in maintaining airway patency and permitting effective ventilation. Parenchymal lung disease can arise from both infectious and non-infectious causes. Many patients with cancer will experience periods of immunosuppression when they will be at increased risk of infections including from opportunistic pathogens. Pleural disease with malignant effusions and empyema can occur and may need repeated drainage or other interventional procedures. Pulmonary vascular disorders can also contribute to ARF in cancer patients. As new cancer therapies emerge so to can respiratory complications. Whilst therapies such as Chimeric antigen receptor T-cells (CAR-T) cells and immune check-point inhibitors have shown benefits in several advanced cancers, and are now extending their indications for use, they bring with them risks of respiratory side effects which may necessitate management in the ICU. Care planning and decisions around intensity of therapy are important in the management of patients with cancer, and where possible this should be done with the patient when they are well enough to be involved in the decisions. In this chapter, we outline the different causes of ARF in cancer patients as well as principles for diagnostic evaluation and management.
APA, Harvard, Vancouver, ISO, and other styles
4

Zekeridou, Anastasia. "“Restlessness” After Cancer Diagnosis and Treatment." In Mayo Clinic Cases in Neuroimmunology, edited by Andrew McKeon, B. Mark Keegan, and W. Oliver Tobin, 157–59. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0051.

Full text
Abstract:
A 76-year-old woman sought care for unintentional weight loss, hematuria, and fatigue. She was diagnosed with plurimetastatic renal cell carcinoma. After resection of the primary tumor and metastases, she was treated with pembrolizumab, an immune checkpoint inhibitor. The patient experienced involuntary tongue and face movements with dysphagia and weight loss. She was also described as “restless.” At that point, the patient was in cancer remission with ongoing immune checkpoint inhibitor treatment. Blood testing was unremarkable. Brain magnetic resonance imaging showed basal ganglia T2/fluid-attenuated inversion recovery hyperintensities without gadolinium enhancement. Cerebrospinal fluid testing showed slightly increased protein concentration and 8 cerebrospinal fluid-restricted oligoclonal bands. Serum and cerebrospinal fluid testing for neural autoantibodies showed immunoglobulin G immunoreactivity in a mouse tissue indirect immunofluorescence assay, predominantly staining the basal ganglia. The immunoglobulin G was subsequently identified to bind to phosphodiesterase 10A. The patient was diagnosed with paraneoplastic phosphodiesterase 10A-immunoglobulin G autoimmunity manifesting as hyperkinetic movement disorder triggered by immune checkpoint inhibitor treatment. Given the patient’s cancer remission, the immune checkpoint inhibitor treatment was discontinued. She was treated with high-dose intravenous corticosteroids, with improvement of her hyperkinetic movement disorder but persistence of some dystonic movements. Further treatment with oral prednisone did not produce further improvement. The patient was treated symptomatically with onabotulinumtoxinA injections and tetrabenazine, which ameliorated her dystonic movements. Three years after her cancer diagnosis, she was alive and in cancer remission with minimal residual movements. Immune checkpoint inhibitors are monoclonal antibodies targeting “stop signs” of the immune response, which lead to enhanced endogenous responses, including those against cancer. Autoimmune complications are consequences of the enhanced immunity and can affect all organs, including the nervous system.
APA, Harvard, Vancouver, ISO, and other styles
5

T. Silveira, Fernando, Marliane B. Campos, Silvia F. Müller, Patrícia K. Ramos, Luciana V. Lima, Thiago V. dos Santos, Claudia Maria Gomes, Márcia D. Laurenti, Vania Lucia da Matta, and Carlos Eduardo Corbett. "From Biology to Disease: Importance of Species-Specific Leishmania Antigens from the Subgenera Viannia (L. braziliensis) and Leishmania (L. amazonensis) in the Pathogenesis of American Cutaneous Leishmaniasis." In Leishmania Parasites [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.108967.

Full text
Abstract:
American cutaneous leishmaniasis (ACL) is one of the most complex parasitic diseases from a clinical-immunopathological point of view due to the great heterogeneity of Leishmania species responsible for the disease. Currently, fifteen Leishmania species of the subgenera Leishmania, Viannia and Mundinia may give rise to ACL in Latin America. In Brazil, seven species are associated to the disease, but L. (V.) braziliensis and L. (L.) amazonensis stand out for producing the broadest clinical-immunopathological spectrum: localized cutaneous leishmaniasis [LCL: DTH+/++], borderline disseminated cutaneous leishmaniasis [BDCL: DTH+/−], mucocutaneous or mucosal leishmaniasis [MCL/ML: DTH++++], and anergic diffuse cutaneous leishmaniasis [ADCL: DTH−]. Although human genetic profile plays important factor in the immunopathogenesis of ACL, it deserves to be highlighted the crucial role of species-specific antigens of L. (V.) braziliensis and L. (L.) amazonensis [lipophosphoglycans, phosphatidylserine, proteophosphoglycans, glycoprotein-63 and CD200 – a macrophage activation inhibitor molecule] in the modulation of T-cell immune response (CD4+/CD8+) that will define the infection evolution.
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Immune check point inhibitor"

1

Lai, K., V. R. Shannon, D. Balachandran, A. Sheshadri, L. Bashoura, and S. A. Faiz. "Role of Infliximab in Immune Check Point Inhibitor Induced Pneumonitis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4736.

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

Ibraheim, Hajir, Lavinia Spain, Amit Samani, Sophie Papa, Nadia Yousaf, Martin Gore, James Larkin, Samra Turajlic, and Nick Powell. "PWE-025 Microscopic colonic inflammation in immune check point inhibitor-induced diarrhoea/colitis." In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.157.

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

Alexander, S. A., V. Mathew Thomas, M. Singh, and P. Premkumar. "A Fatal Case of Multisystem Organ Dysfunction Secondary to Immune Check Point Inhibitor Use." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1714.

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

Hutmacher-Berndt, Cornelia Deborah, and Dario Neri. "Abstract 3811: Targeted Interleukin 2 and synergy with immune check-point inhibitors." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3811.

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

Spain, Lavinia, Amit Samani, Hajir Ibraheim, Lewis Au, Zayd Tippu, Shuai Zhang, Sophie Merrick, et al. "PTU-006 Incidence of immune check point inhibitor induced diarrhoea/colitis- experience from a multi-centre cohort." In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.128.

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

Sasikumar, Pottayil G., Leena K. Satyam, Rajeev Shrimali, Raghuveer Ramachandra, Ketha A. Reddy, Adurthi Sreenivas, Amit Dhudashia, Dodderi S. Samiulla, and Murali Ramachandra. "Abstract 1231: Equipotent antagonism, transient immune activation and excellent antitumor efficacy with a peptide inhibitor of PD-1 immune check point pathway." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1231.

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

Mitra, D. K., P. Kaur, G. Mehta, A. Mohan, and M. Basil. "Immune Check Point Inhibitors in TB Patients: Impact on In-vitro Bacillary Clearance." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4870.

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

Wong, Chi Wah, Susan E. Yost, Jin Sun Lee, Sarah K. Highlander, and Yuan Yuan. "Abstract 336: Gut microbiome predicts response to CDK4/6 inhibitor and immune check point inhibitor combination in patients with hormone receptor positive metastatic breast cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-336.

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

Miron Elorriaga, G., Y. Viseda Torrellas, M. Palacios Filardo, M. Cardenas Sierra, FJ Goikolea Ugarte, A. Martin Torrente, L. Torio Alvarez, et al. "5PSQ-112 Relationship between effectiveness and immune-mediated toxicity of immune check-point inhibitors in advanced non-small-cell lung cancer." In 27th EAHP Congress, Lisbon, Portugal, 22-23-24 March 2023. British Medical Journal Publishing Group, 2023. http://dx.doi.org/10.1136/ejhpharm-2023-eahp.454.

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

McKenzie, Andrew, Nektaria Papadopoulou, Simon Jiang, Jane Wrigley, Kelly Jones, Russell Garland, Neil Williams, and Rajendra Kumari. "Abstract A140: Check point inhibitor modulation of tumor microenvironment at orthotopic and metastatic sites using bioluminescent syngeneic cell line models in immune competent mice." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a140.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Immune check point inhibitor' for particular source types:
Journal articles
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