scispace - formally typeset
Search or ask a question

Are patients on immunotherapy immunocompromised? 

Answers from top 6 papers

More filters
Papers (6)Insight
Patients ≥65 y can benefit more from immunotherapy than younger patients.
Dedicated clinicians play a crucial role in AS programs involving immunocompromised patients.
Clinical judgment remains important when discussing the benefits and safety profile with immunocompromised patients.
Some patients could respond to immunotherapy.
All 249 patients undergoing immunotherapy completed the survey.
These findings indicate that it might be possible to select patients who are likely to benefit from prolonged immunotherapy.

See what other people are reading

Why do tils need il2?
5 answers
Tumor-infiltrating lymphocytes (TILs) require IL-2 for their expansion and activation. IL-2 plays a crucial role in the ex vivo expansion of TILs, which is essential for effective adoptive transfer immunotherapy in cancer treatment. Studies have shown that IL-2, along with IL-15 and IL-21, promotes the expansion of TILs with a central memory phenotype, enhancing their reactivity against tumor cells. Additionally, IL-2 administration is associated with the depletion of regulatory T cells, further boosting the efficacy of TILs in targeting tumors. Therefore, IL-2 is a key component in the process of growing and activating TILs, making it essential for the success of adoptive T cell therapy in cancer patients.
Is 120 mbq of 177-lu-psma safe in mouse model for prostate cancer?
5 answers
In preclinical studies, the safety and efficacy of [177Lu]Lu-PSMA in mouse models of prostate cancer have been evaluated. Various doses of [177Lu]Lu-PSMA have been tested, including 60 MBq and 80 MBq, showing promising results in terms of tumor growth inhibition and immune response induction. Additionally, studies have investigated different 177Lu-labeled ligands, such as [177Lu]Lu-PSMA-Q and [177Lu]Lu-Ibu-DAB-PSMA, demonstrating significant anti-tumor effects and therapeutic potential with doses up to 10 MBq per mouse. Furthermore, a novel therapeutic radioligand, [177Lu]Lu-1h, showed high tumor uptake and extended blood circulation, leading to improved survival rates in mice treated with 4-6 MBq doses. Therefore, based on these preclinical findings, a dose of 120 MBq of [177Lu]Lu-PSMA may not be considered safe in mouse models due to potential toxicity concerns.
How much 177-lu-psma activity is needed for sufficient immune activation?
5 answers
The immune activation induced by [177Lu]Lu-PSMA therapy is dose-dependent, with significant effects observed at 60 MBq in terms of immunogenic cell death (ICD) markers like cell surface CRT, HMGB1 release, and ATP release. Additionally, [177Lu]Lu-PSMA treatment resulted in delayed tumor growth and prevented tumor growth in approximately 50% of cases upon rechallenge, indicating immune activation. Furthermore, the combination of 177Lu-PSMA-617 with pembrolizumab showed promising immune activation with a PSA50-RR of 76% in metastatic castration-resistant prostate cancer patients. Therefore, a sufficient immune activation response can be achieved with an activity of 60 MBq of [177Lu]Lu-PSMA, as evidenced by the observed immunogenic cell death and tumor growth inhibition in preclinical and clinical studies.
How does IL-34 contribute to angiogenesis of prostate cancer?
4 answers
IL-34 plays a significant role in promoting angiogenesis in prostate cancer (PCA) by influencing the tumor microenvironment. Endothelial cells, which express CD31 and CD34, are increased in PCA and contribute to metastasis by enhancing cancer cell invasion. IL-34, secreted by various cells including tumor cells, has been implicated in promoting cancer growth and metastasis in various cancers. Additionally, IL-34 is involved in regulating immune cells, particularly macrophages, in the tumor microenvironment, which can lead to immune suppression and cancer progression. The combination of IL-34 inhibition with immune checkpoint inhibitors (ICIs) has been proposed as a potential strategy to overcome resistance to ICIs and improve cancer treatment efficacy. Therefore, targeting IL-34 may offer a promising approach to hinder angiogenesis and enhance therapeutic outcomes in prostate cancer.
What is the difference between cryoablation in solid organs and cryoablation in the lung?
5 answers
Cryoablation in solid organs and cryoablation in the lung differ in their applications and outcomes. Solid organ cryoablation, such as for tumors, has shown better tumor response and faster recovery over time, especially when combined with immunotherapy. In contrast, lung cryoablation, particularly for metastatic lung cancers, has been conducted using liquid nitrogen and has demonstrated efficacy in treating tumors <2.2 cm, with varying local control rates based on tumor size and histological type. Additionally, cryoablation in the lung can lead to complications like pneumothorax. Both types of cryoablation aim to induce tumor necrosis and stimulate the immune system, but the specific techniques and outcomes vary based on the organ being treated.
Where is ACE2 expressed?
5 answers
ACE2 is expressed in various locations within the human body. In Alzheimer's disease, ACE2 is mainly found on the surface of brain endothelial cells. Human spermatozoa express ACE2 uniformly on the sperm head and flagellum, with the short-ACE2 isoform concentrated in the post-acrosomal region and midpiece. Additionally, ACE2 is present in different tissues, with unique regulation and expression levels in mice and humans, influencing susceptibility to SARS-CoV-2 infection and the subsequent host response. The expression of ACE2 in spermatozoa and its potential role in male reproduction warrant further investigation to understand its implications fully.
What are the most common biomarkers used for the diagnosis and monitoring of colorectal cancer?
4 answers
The diagnosis and monitoring of colorectal cancer (CRC) have significantly advanced with the identification and application of various biomarkers, which are crucial for early detection, prognosis, and monitoring therapeutic responses. Among the most common biomarkers, genetic and epigenetic alterations, including mutations in APC, TP53, KRAS, BRAF, and PIK3CA genes, are widely recognized for their roles in CRC pathogenesis and as diagnostic tools. Additionally, DNA methylation patterns, such as those in SEPT9, HLTF, NEUROG1, MLH1, ALX4, and LINE-1, serve as epigenomic biomarkers, offering insights into CRC's epigenetic landscape. Transcriptomic markers, particularly microRNAs (miRNAs) like miR-21, miR-92a, miR-103a-3p, and miR-127-3p, have emerged as valuable tools for CRC diagnosis due to their altered expression levels in CRC tissues compared to normal tissues. Furthermore, the role of non-coding RNAs, including long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and PIWI-interacting RNAs (piRNAs), is being explored for their diagnostic and prognostic potential in CRC. Proteomic markers, such as CEA, NDKA, calprotectin (S100A8/A9), CLU, TIMP1, and ECM1, have shown promise in CRC detection and monitoring, benefiting from advancements in mass spectrometry and other proteomic technologies. Liquid biopsy, analyzing circulating tumor DNA (ctDNA), circulating tumor cells (CTCs), and other components like extracellular vesicles, offers a non-invasive approach for CRC diagnosis, prognosis, and treatment monitoring, reflecting tumor heterogeneity and dynamics. Fecal biomarkers, including DNA, RNA, protein biomarkers, gut microbes, and volatile organic compounds, have also been identified for CRC screening and early diagnosis, providing a non-invasive, cost-effective method suitable for large-scale population screening. In summary, the landscape of CRC biomarkers encompasses a wide array of molecular signatures from genetic, epigenetic, transcriptomic, proteomic, and fecal biomarkers to liquid biopsy components, each contributing to the comprehensive understanding and management of CRC.
How does inflammation contribute to the development and progression of stroke?
5 answers
Inflammation plays a crucial role in the development and progression of stroke by impacting both the brain and peripheral organs. The acute inflammatory response post-stroke exacerbates brain injury, while systemic inflammation from peripheral organs like the spleen, lymph nodes, and gastrointestinal system also significantly contributes to secondary cell death in stroke. Moreover, infectious diseases and systemic inflammation increase the risk of stroke by interacting with hemostasis disturbances, endothelial damage, and cytotoxic lymphocytes activation. Atherothrombotic stroke, a common subtype, is driven by an inflammatory process in the vascular wall, leading to atherosclerosis and acute vascular events. Understanding these inflammatory mechanisms is crucial for developing effective therapeutic strategies to mitigate stroke pathology.
What are the administration routes of chemotherapeutics with nanocarriers in the treatment of colorectal cancer?
7 answers
In the treatment of colorectal cancer (CRC), nanocarriers have revolutionized the administration routes of chemotherapeutics, offering targeted and efficient delivery methods that aim to minimize side effects and enhance therapeutic efficacy. The primary administration routes for these nanocarrier-based chemotherapeutics include oral administration and targeted delivery systems, each with its unique mechanisms and advantages. Oral administration is highlighted as an attractive approach for CRC therapy due to its potential to improve the efficacy of local drug delivery while reducing systemic toxicity. This route faces challenges such as poor drug solubility, stability, and permeability, but nanotechnology offers solutions to overcome these barriers. Chitosan-based nanocarriers, for example, have been developed to enhance stability, targeting, and bioavailability of anti-CRC agents, providing a promising strategy for oral drug delivery. The unique physicochemical properties of nanoparticles assist in overcoming oral delivery challenges, including protection against gastrointestinal degradation. Targeted delivery systems, on the other hand, utilize nanocarriers functionalized with monoclonal antibodies or other targeting agents to actively direct chemotherapeutics to CRC cells. This approach leverages the enhanced permeability and retention (EPR) effect and specific molecular markers over-expressed on CRC cells to increase tumor accumulation and reduce adverse effects on healthy tissues. Surface-engineered nanocarriers can facilitate receptor-mediated deliveries, targeting overexpressed receptors in the CRC microenvironment for precise drug delivery. Additionally, magneto-fluorescent nanoparticles modified with targeting agents have shown potential for targeted nanotherapy, indicating the versatility of nanocarriers in delivering drugs directly to tumor sites. These administration routes, oral and targeted delivery, represent the forefront of nanocarrier-based chemotherapeutic delivery in CRC treatment. They exemplify the ongoing efforts to enhance the specificity, efficacy, and safety of cancer therapies through advanced nanotechnology.
In which organs or cells is ACE2 expressed?
5 answers
ACE2 is expressed in various organs and cells throughout the body. It is found in oral mucosal cells, including keratinocytes and fibroblasts, where it plays a role in infection and inflammation following SARS-CoV-2 invasion. Additionally, ACE2 is present in tissues such as the liver, kidney, alveolar tissue, pancreas, colon, and salivary gland. In human spermatozoa, ACE2 is uniformly expressed on the sperm head and flagellum, with a concentration in the post-acrosomal region and midpiece. Furthermore, ACE2 expression is observed in pericytes in the central nervous system, heart, and pancreas, as well as in bronchial epithelium and alveolar type II cells in the lung. The expression of ACE2 in diverse organs and cells underscores its significance as the receptor for SARS-CoV-2 and its potential implications in COVID-19 pathogenesis.
How does clinic policy in regards to late show or no-show policies affect patient behaviors?
5 answers
Clinic policies regarding late show or no-show policies significantly impact patient behaviors. Patients with a history of missed appointments or frequent rescheduling are more likely to no-show. Implementing predictive models can help identify high-risk patients, such as those with past no-shows, lack of private insurance, or inactive communication channels. No-shows not only waste clinic resources but also reduce educational opportunities for healthcare trainees. Reframing policies through a diversity, equity, and inclusion (DEI) lens can enhance patient care, prevent alienation of patient populations, and improve clinical efficiency. By combining population-based and individual-based behavior prediction techniques, clinics can minimize no-shows by detecting potential non-attendance and finding suitable replacements.