Relevant bibliographies by topics / Response to therapies / Journal articles

Journal articles on the topic 'Response to therapies'

To see the other types of publications on this topic, follow the link: Response to therapies.
Author: Grafiati
Published: 7 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Response to therapies.'

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.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Gayan, Chathura. "Evaluate the response of Apoptosis, Angiogenesis and Cancer Therapies." Cancer Research and Cellular Therapeutics 2, no. 1 (March 28, 2018): 01–08. http://dx.doi.org/10.31579/2640-1053/022.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Angiogenesis, the growth of new blood vessels from the existing vasculature, and is maintained in adult tissues by the balanced presence of both angiogenic inducers and inhibitors in the tissue milieu. When inducers predominate, vascular endothelial cells (VECs) become activated and in this activated VECs, distinct cell signaling pathways are initiated providing the specificity of anti-angiogenic therapies to the tumor vasculature. VEC apoptosis has been well documented in regressing vessels, and it has been shown that, in addition to activating the VECs, some inducers such as vascular endothelial growth factor also up-regulate Fas expression, thus sensitizing the cell to apoptotic stimuli. Endogenous angiogenesis inhibitors, such as thrombospondin-1(TSP-1) and pigment epithelium-derived factor (PEDF), stimulate signaling cascades within the VECs and also induce the expression of Fas ligand in activated VECs. Therefore, when inhibitors predominate, the apoptotic cascade is initiated ,thus anti-angiogenic therapies can target the inducer supply or directly target the VECs. Although clinical studies suggest that anti-angiogenic therapies may prove to be most effective when used in combination with traditional therapies
2

Dudekula, Noor, Vikas Arora, Zsuzsanna Callaerts-Vegh, and Richard A. Bond. "The Temporal Hormesis of Drug Therapies." Dose-Response 3, no. 3 (May 1, 2005): dose—response.0. http://dx.doi.org/10.2203/dose-response.003.03.009.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Recent publications in the field of asthma therapeutics and studies performed over the last decade in the treatment of chronic heart failure suggest a phenomenon called ‘temporal hormesis’. This phenomenon can be defined as the beneficial action of drug after chronic administration as opposed to its detrimental acute effects. Temporal hormesis may be related to the classification of the drug molecule as an agonist, antagonist or an inverse agonist. This phenomenon may be a more general principal applicable in the treatment of other diseases apart from asthma and chronic heart failure.
3

Truelove, Edmond, Kimberly Hanson Huggins, Lloyd Mancl, and Samuel F. Dworkin. "NONSPLINT THERAPIES: Authors' response." Journal of the American Dental Association 137, no. 11 (November 2006): 1493–94. http://dx.doi.org/10.14219/jada.archive.2006.0070.

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

Prasad, Vinay, Victoria Kaestner, and Alyson Haslam. "Bridging therapies used in trials testing CAR-T therapies." Journal of Clinical Oncology 42, no. 16_suppl (June 1, 2024): e19011-e19011. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.e19011.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
e19011 Background: Chimeric Antigen Receptor T-cell (CAR-T) therapy can induce durable remission in some patients but requires time for a patient’s own cells to be reengineered to produce CAR proteins that can bind to and destroy cancer cells. During this time, bridging therapy is often used in debulking to reduce treatment toxicities and to control the disease while waiting for the manufacturing of CAR-T cells. Because bridging therapy often involves systemic treatment, the bridging therapies can induce responses, in and of themselves, in clinical trials testing CAR-T therapies. As such, we sought to assess bridging therapies used in CAR-T trials. Methods: Using the FDA labels (labels.fda.gov) to identify the indications and the pivotal clinical trials that led to the approval of each CAR-T cell therapy, we looked at which bridging therapies were used, whether multiple therapies were combined, response rates, and the reported adverse events associated with bridging therapy. We took note of all relevant comments regarding bridging therapy in the main paper and supplemental results. Results: Of the 11 studies testing CAR-T therapies, 10 reported the bridging therapies that were used in the study. Notably, only three of 11 studies provided clear information about which combinations of bridging therapy treatments were used during the trials. Of those that reported the types of bridging therapies (n=10), the most commonly used bridging therapy was dexamethasone, which was used in every study (10/10). The next three most commonly used treatments include rituximab (6/10), gemcitabine (5/10), and etoposide (5/10). Of the trials, 2/11 clearly reported whether patients had a complete response (CR), partial response (PR), or very good partial response (VGPR) to bridging therapy. 5/11 vaguely reported responses, using terminology outside of CR, PR, VGPR. 4/11 trials did not report or mention any response information in regards to bridging therapy. Of all the trials, 1/11 clearly reported adverse events associated with bridging therapy in the supplement, while 10/11 of the trials listed adverse events associated with the treatment groups, without clarifying those associated with bridging. Conclusions: Although patients are often refractory to first-line therapies, which share considerable overlap with the bridging therapies used, these therapies may still induce responses. Despite this possibility, the reporting of bridging therapy combinations and their subsequent response rates and adverse event rates, is highly variable. Of 11 pivotal clinical trials that led to the approval of a CAR-T cell therapy, none clearly reported bridging therapy data that encompassed all three categories (combinations used, response rates, adverse events). What is more, these data were often omitted completely. These findings highlight the need for greater transparency in the reporting of bridging therapy in order to more reliably assess the efficacy of CAR-T therapies.
5

Brown, Barbara G. "Innovative Therapies: Biological Response Modifiers." Journal of the Association of Pediatric Oncology Nurses 5, no. 1-2 (January 1988): 26. http://dx.doi.org/10.1177/104345428800500109.

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

Mattison, Lars, and Paul Iaizzo. "PHRENIC NERVE RESPONSE TO CRYOABLATION THERAPIES." Journal of the American College of Cardiology 65, no. 10 (March 2015): A405. http://dx.doi.org/10.1016/s0735-1097(15)60405-3.

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

Cunningham, Jonathan W., and Peder L. Myhre. "NT-proBNP Response to Heart Failure Therapies." Journal of the American College of Cardiology 78, no. 13 (September 2021): 1333–36. http://dx.doi.org/10.1016/j.jacc.2021.07.045.

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

Gerger, Armin, Melissa LaBonte, and Heinz-Josef Lenz. "Molecular Predictors of Response to Antiangiogenesis Therapies." Cancer Journal 17, no. 2 (March 2011): 134–41. http://dx.doi.org/10.1097/ppo.0b013e318212db3c.

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

Held, Barbara S. "Common dances, uncommon therapies: Response to Ryder." Journal of Family Psychology 1, no. 4 (1988): 476–79. http://dx.doi.org/10.1037/h0084983.

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

Johnston, Stephen R. D., Alexandra Leary, Lesley-Ann Martin, Ian E. Smith, and Mitch Dowsett. "Enhancing endocrine response with novel targeted therapies." Cancer 112, S3 (2008): 710–17. http://dx.doi.org/10.1002/cncr.23190.

Full text
APA, Harvard, Vancouver, ISO, and other styles
11

Yanai, Henit, and Stephen B. Hanauer. "Assessing Response and Loss of Response to Biological Therapies in IBD." American Journal of Gastroenterology 106, no. 4 (April 2011): 685–98. http://dx.doi.org/10.1038/ajg.2011.103.

Full text
APA, Harvard, Vancouver, ISO, and other styles
12

Chupp, Geoffrey Lowell, Ravdeep Kaur, and Anne Mainardi. "New Therapies for Emerging Endotypes of Asthma." Annual Review of Medicine 71, no. 1 (January 27, 2020): 289–302. http://dx.doi.org/10.1146/annurev-med-041818-020630.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
The presentation, pathobiology, and prognosis of asthma are highly heterogeneous and challenging for clinicians to diagnose and treat. In addition to the adaptive immune response that underlies allergic inflammation, innate immune mechanisms are increasingly recognized to be critical mediators of the eosinophilic airway inflammation present in most patients with asthma. Efforts to classify patients by severity and immune response have identified a number of different clinical and immune phenotypes, indicating that the innate and adaptive immune responses are differentially active among patients with the disease. Advances in the detection of these subgroups using clinical characteristics and biomarkers have led to the successful development of targeted biologics. This has moved us to a more personalized approach to managing asthma. Here we review the emerging endotypes of asthma and the biologics that have been developed to treat them.
13

Iacobellis, Gianluca, Alexis Elias Malavazos, Sara Basilico, Silvia Tresoldi, Rocco Francesco Rinaldo, Carola Dubini, Gloria Capitanio, et al. "Epicardial fat inflammation response to COVID‐19 therapies." Obesity 29, no. 9 (August 3, 2021): 1427–33. http://dx.doi.org/10.1002/oby.23232.

Full text
APA, Harvard, Vancouver, ISO, and other styles
14

Harlé, Alexandre, and Jean-Louis Merlin. "Response predictive biomarkers to targeted therapies in oncology." Annales de biologie clinique 71, S1 (November 2013): 89–97. http://dx.doi.org/10.1684/abc.2013.0906.

Full text
APA, Harvard, Vancouver, ISO, and other styles
15

Forshaw, Tom E., Reetta Holmila, Kimberly J. Nelson, Joshua E. Lewis, Melissa L. Kemp, Allen W. Tsang, Leslie B. Poole, W. Todd Lowther, and Cristina M. Furdui. "Peroxiredoxins in Cancer and Response to Radiation Therapies." Antioxidants 8, no. 1 (January 1, 2019): 11. http://dx.doi.org/10.3390/antiox8010011.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Peroxiredoxins have a long-established cellular function as regulators of redox metabolism by catalyzing the reduction of peroxides (e.g., H2O2, lipid peroxides) with high catalytic efficiency. This activity is also critical to the initiation and relay of both phosphorylation and redox signaling in a broad range of pathophysiological contexts. Under normal physiological conditions, peroxiredoxins protect normal cells from oxidative damage that could promote oncogenesis (e.g., environmental stressors). In cancer, higher expression level of peroxiredoxins has been associated with both tumor growth and resistance to radiation therapies. However, this relationship between the expression of peroxiredoxins and the response to radiation is not evident from an analysis of data in The Cancer Genome Atlas (TCGA) or NCI60 panel of cancer cell lines. The focus of this review is to summarize the current experimental knowledge implicating this class of proteins in cancer, and to provide a perspective on the value of targeting peroxiredoxins in the management of cancer. Potential biases in the analysis of the TCGA data with respect to radiation resistance are also highlighted.
16

Shaked, Yuval. "The pro-tumorigenic host response to cancer therapies." Nature Reviews Cancer 19, no. 12 (October 23, 2019): 667–85. http://dx.doi.org/10.1038/s41568-019-0209-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
17

Faycal, Cherine Abou, Sylvie Gazzeri, and Beatrice Eymin. "RNA splicing, cell signaling, and response to therapies." Current Opinion in Oncology 28, no. 1 (January 2016): 58–64. http://dx.doi.org/10.1097/cco.0000000000000254.

Full text
APA, Harvard, Vancouver, ISO, and other styles
18

Dinarello, Charles A. "Anti-Cytokine Therapies in Response to Systemic Infection." Journal of Investigative Dermatology Symposium Proceedings 6, no. 3 (December 2001): 244–50. http://dx.doi.org/10.1046/j.0022-202x.2001.00046.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
19

Stoilova, Bilyana, Rachel Moore, Marlen Metzner, Zhihong Zheng, Marina Konopleva, Courtney DiNardo, and Paresh Vyas. "Mechanisms of Response and Resistance to AML Therapies." Clinical Lymphoma Myeloma and Leukemia 20 (September 2020): S7. http://dx.doi.org/10.1016/s2152-2650(20)30442-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
20

Braun, Theodore P., Christopher A. Eide, and Brian J. Druker. "Response and Resistance to BCR-ABL1-Targeted Therapies." Cancer Cell 37, no. 4 (April 2020): 530–42. http://dx.doi.org/10.1016/j.ccell.2020.03.006.

Full text
APA, Harvard, Vancouver, ISO, and other styles
21

Allen, Matthew R., Janet M. Hock, and David B. Burr. "Periosteum: biology, regulation, and response to osteoporosis therapies." Bone 35, no. 5 (November 2004): 1003–12. http://dx.doi.org/10.1016/j.bone.2004.07.014.

Full text
APA, Harvard, Vancouver, ISO, and other styles
22

Bergeron, Michel G. "Biological Response Modifiers - The Therapies of the Future." Canadian Journal of Infectious Diseases 3, suppl b (1992): 1–2. http://dx.doi.org/10.1155/1992/461649.

Full text
APA, Harvard, Vancouver, ISO, and other styles
23

RIVERA, TANIA L., H. MICHAEL BELMONT, SEEMA MALANI, MELISSA LATORRE, LAURI BENTON, JOSEPH WEISSTUCH, LAURA BARISONI, et al. "Current Therapies for Lupus Nephritis in an Ethnically Heterogeneous Cohort." Journal of Rheumatology 36, no. 2 (February 2009): 298–305. http://dx.doi.org/10.3899/jrheum.080335.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Objective.To evaluate responses to mycophenolate mofetil (MMF) and intravenous cyclophosphamide (CYC) in lupus nephritis in a multiethnic population.Methods.This was a retrospective study of all patients with systemic lupus erythematosus (SLE) that underwent kidney biopsy at New York University Medical Center. Patients with followup of at least 6 months were included. Clinical response was defined as complete (return to ± 10% of normal) or partial (improvement of 50% in abnormal renal measurements).Results.Ninty-nine patients were included in the study: 86% females, 86% non-Caucasian, age 34.2 ± 1.1 years, 62% with proliferative nephritis (PN; ISN/RPS-III and IV), and 32% with membranous nephritis (MN; ISN/RPS-V). Of the 70 patients with PN, 37 were treated with CYC and 33 with MMF. The baseline characteristics of the 2 treatment groups were different in the incidence of ISN/RPS-IV, values of serum creatinine and serum albumin, and type of insurance (p < 0.05). The response rate was greater in the MMF than in the CYC group (70% vs 41%). Responses to MMF were different in Asians (11/11), Caucasians (4/5), African Americans (3/5), and Hispanics (5/11). Responses to CYC had a similar distribution (Asians 6/10, Caucasians 4/5, African Americans 4/9, Hispanics 1/11). In the MN group (N = 23) responses were similar to the PN group (73% MMF and 38% CYC). After adjusting for race, serum creatinine, serum albumin, type of insurance, and class of nephritis, in a logistic regression model, response to MMF was superior to CYC: OR 6.2 (95% CI 1.9–20.2). Hispanics had worse outcome than Caucasians (OR 0.17). Longterm followup suggested no difference in maintenance with MMF or CYC.Conclusion.After controlling for the fact that less severe nephritis is preferentially treated with MMF, we found overall that response to MMF was superior to CYC. In this US population, ethnicity was observed to have an influence on response.
24

Setlai, Botle Precious, Rodney Hull, Meshack Bida, Chrisna Durandt, Thanyani Victor Mulaudzi, Aristotelis Chatziioannou, and Zodwa Dlamini. "Immunosuppressive Signaling Pathways as Targeted Cancer Therapies." Biomedicines 10, no. 3 (March 16, 2022): 682. http://dx.doi.org/10.3390/biomedicines10030682.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Immune response has been shown to play an important role in defining patient prognosis and response to cancer treatment. Tumor-induced immunosuppression encouraged the recent development of new chemotherapeutic agents that assists in the augmentation of immune responses. Molecular mechanisms that tumors use to evade immunosurveillance are attributed to their ability to alter antigen processing/presentation pathways and the tumor microenvironment. Cancer cells take advantage of normal molecular and immunoregulatory machinery to survive and thrive. Cancer cells constantly adjust their genetic makeup using several mechanisms such as nucleotide excision repair as well as microsatellite and chromosomal instability, thus giving rise to new variants with reduced immunogenicity and the ability to continue to grow without restrictions. This review will focus on the central molecular signaling pathways involved in immunosuppressive cells and briefly discuss how cancer cells evade immunosurveillance by manipulating antigen processing cells and related proteins. Secondly, the review will discuss how these pathways can be utilized for the implementation of precision medicine and deciphering drug resistance.
25

Siegel, Jay P. "Clinical Development of Biological Response Modifiers." Canadian Journal of Infectious Diseases 5, suppl a (1994): 5A—8A. http://dx.doi.org/10.1155/1994/583805.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
OBJECTIVE: To present perspectives on selected issues that frequently arise during the clinical development of biological response modifier (BRM) therapies.DATA SOURCES: The perspectives and opinions presented herein were developed over several years of reviewing and consulting on the clinical development of BRM therapies at the United States Food and Drug Administration.CONCLUSIONS: BRM therapies encompass a broad spectrum of products used to treat a wide variety of diseases. Due to this diversity. most principles of clinical trial design and conduct applicable to the majority of BRMS are those that are applicable to all therapies. Nevertheless, the clinical development of BRM therapies often raises specific issues and problems in the areas of selecting animal models, defining the study population, adverse reactions, dosing and defining end-points. Over 10 years’ experience in testing biotechnology derived BRMS in clinical trials has created a database from which we can draw valuable generalizations for guidance in future studies.
26

Asif, Samia, and Benjamin A. Teply. "Biomarkers for Treatment Response in Advanced Prostate Cancer." Cancers 13, no. 22 (November 16, 2021): 5723. http://dx.doi.org/10.3390/cancers13225723.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Multiple treatment options with different mechanisms of action are currently available for the management of metastatic prostate cancer. However, the optimal use of these therapies—specifically, the sequencing of therapies—is not well defined. In order to obtain the best clinical outcomes, patients need to be treated with the therapies that are most likely to provide benefit and avoid toxic therapies that are unlikely to be effective. Ideally, predictive biomarkers that allow for the selection of the therapies most likely to be of benefit would be employed for each treatment decision. In practice, biomarkers including tumor molecular sequencing, circulating tumor DNA, circulating tumor cell enumeration and androgen receptor characteristics, and tumor cell surface expression (PSMA), all may have a role in therapy selection. In this review, we define the established prognostic and predictive biomarkers for therapy in advanced prostate cancer and explore emerging biomarkers.
27

Smolock, Amanda R., and Sarah B. White. "Immune Response to Locoregional Therapy." Digestive Disease Interventions 06, no. 01 (January 4, 2022): 037–40. http://dx.doi.org/10.1055/s-0041-1742102.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
AbstractThe immune response to cancer is an ongoing area of interest and is the focus of newer systemic agents. Liver-directed therapy has been the standard treatment for primary and metastatic disease limited to the liver. It is increasingly being recognized that these therapies may influence a broader systemic response and immune activation. The clinical and translational data supporting this phenomenon are reviewed herein. The findings and potential impact of the immune response to liver-directed therapies are summarized in this article.
28

Audia, Sylvain, and Bernard Bonnotte. "Emerging Therapies in Immune Thrombocytopenia." Journal of Clinical Medicine 10, no. 5 (March 2, 2021): 1004. http://dx.doi.org/10.3390/jcm10051004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Immune thrombocytopenia (ITP) is a rare autoimmune disorder caused by peripheral platelet destruction and inappropriate bone marrow production. The management of ITP is based on the utilization of steroids, intravenous immunoglobulins, rituximab, thrombopoietin receptor agonists (TPO-RAs), immunosuppressants and splenectomy. Recent advances in the understanding of its pathogenesis have opened new fields of therapeutic interventions. The phagocytosis of platelets by splenic macrophages could be inhibited by spleen tyrosine kinase (Syk) or Bruton tyrosine kinase (BTK) inhibitors. The clearance of antiplatelet antibodies could be accelerated by blocking the neonatal Fc receptor (FcRn), while new strategies targeting B cells and/or plasma cells could improve the reduction of pathogenic autoantibodies. The inhibition of the classical complement pathway that participates in platelet destruction also represents a new target. Platelet desialylation has emerged as a new mechanism of platelet destruction in ITP, and the inhibition of neuraminidase could dampen this phenomenon. T cells that support the autoimmune B cell response also represent an interesting target. Beyond the inhibition of the autoimmune response, new TPO-RAs that stimulate platelet production have been developed. The upcoming challenges will be the determination of predictive factors of response to treatments at a patient scale to optimize their management.
29

Garcillán, Beatriz, Miguel Salavert, José R. Regueiro, and Sabela Díaz-Castroverde. "Response to Vaccines in Patients with Immune-Mediated Inflammatory Diseases: A Narrative Review." Vaccines 10, no. 2 (February 15, 2022): 297. http://dx.doi.org/10.3390/vaccines10020297.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Patients with immune-mediated inflammatory diseases (IMIDs), such as rheumatoid arthritis and inflammatory bowel disease, are at increased risk of infection. International guidelines recommend vaccination to limit this risk of infection, although live attenuated vaccines are contraindicated once immunosuppressive therapy has begun. Biologic therapies used to treat IMIDs target the immune system to stop chronic pathogenic process but may also attenuate the protective immune response to vaccines. Here, we review the current knowledge regarding vaccine responses in IMID patients receiving treatment with biologic therapies, with a focus on the interleukin (IL)-12/23 inhibitors. B cell-depleting therapies, such as rituximab, strongly impair vaccines immunogenicity, and tumor necrosis factor (TNF) inhibitors and the cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) fusion protein abatacept are also associated with attenuated antibody responses, which are further diminished in patients taking concomitant immunosuppressants. On the other hand, integrin, IL-6, IL-12/23, IL-17, and B-cell activating factor (BAFF) inhibitors do not appear to affect the immune response to several vaccines evaluated. Importantly, treatment with biologic therapies in IMID patients is not associated with an increased risk of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or developing severe disease. However, the efficacy of SARS-CoV-2 vaccines on IMID patients may be reduced compared with healthy individuals. The impact of biologic therapies on the response to SARS-CoV-2 vaccines seems to replicate what has been described for other vaccines. SARS-CoV-2 vaccination appears to be safe and well tolerated in IMID patients. Attenuated but, in general, still protective responses to SARS-CoV-2 vaccination in the context of certain therapies warrant current recommendations for a third primary dose in IMID patients treated with immunosuppressive drugs.
30

Kolarich, Andrew R., Iakovos Theodoulou, and Christos Georgiades. "Combination Therapies with Ablation: Immunoablation." Digestive Disease Interventions 04, no. 04 (November 19, 2020): 358–64. http://dx.doi.org/10.1055/s-0040-1721453.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
AbstractPercutaneous ablation has been increasingly utilized as an alternative or adjunct to surgical resection of solid tumors. However, high rates of local recurrence and disease progression both with resection and ablation, particularly in patients with primary and metastatic liver malignancies, have limited further extension of overall survival. Systemic oncology treatment has progressed beyond traditional chemotherapeutic agents to immunotherapeutic agents that exert their effect by enhancing the body's immune response against cancer cells. The induction of necrotic cell death and the release of a large number of tumor antigens as a result of ablation have stimulated interest in combination therapy as a potential method of improving response to immunotherapy. This review focuses on the current scientific evidence for combination therapy of immuno-oncologic agents and locoregional ablation techniques.
31

Bhatia, Ankush, Vaios Hatzoglou, Gary Ulaner, Raajit Rampal, David M. Hyman, Omar Abdel-Wahab, Benjamin H. Durham, et al. "Neurologic and oncologic features of Erdheim–Chester disease: a 30-patient series." Neuro-Oncology 22, no. 7 (January 17, 2020): 979–92. http://dx.doi.org/10.1093/neuonc/noaa008.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Abstract Background Erdheim–Chester disease (ECD) is a rare histiocytic neoplasm characterized by recurrent alterations in the MAPK (mitogen-activating protein kinase) pathway. The existing literature about the neuro-oncological spectrum of ECD is limited. Methods We present retrospective clinical, radiographic, pathologic, molecular, and treatment data from 30 patients with ECD neurohistiocytic involvement treated at a tertiary center. Results Median age was 52 years (range, 7–77), and 20 (67%) patients were male. Presenting symptoms included ataxia in 19 patients (63%), dysarthria in 14 (47%), diabetes insipidus in 12 (40%), cognitive impairment in 10 (33%), and bulbar affect in 9 (30%). Neurosurgical biopsy specimens in 8 patients demonstrated varied morphologic findings often uncharacteristic of typical ECD lesions. Molecular analysis revealed mutations in BRAF (18 patients), MAP2K1 (5), RAS isoforms (2), and 2 fusions involving BRAF and ALK. Conventional therapies (corticosteroids, immunosuppressants, interferon-alpha [IFN-α], cytotoxic chemotherapy) led to partial radiographic response in 8/40 patients (20%) by MRI with no complete responses, partial metabolic response in 4/16 (25%), and complete metabolic response in 1/16 (6%) by 18F-fluorodeoxyglucose (FDG)-PET scan. In comparison, targeted (kinase inhibitor) therapies yielded partial radiographic response in 10/27 (37%) and complete radiographic response in 14/27 (52%) by MRI, and partial metabolic response in 6/25 (24%) and complete metabolic response in 17/25 (68%) by FDG-PET scan. Conclusions These data highlight underrecognized symptomatology, heterogeneous neuropathology, and robust responses to targeted therapies across the mutational spectrum in ECD patients with neurological involvement, particularly when conventional therapies have failed.
32

de Mestier, Louis, Clarisse Dromain, Gaspard d'Assignies, Jean-Yves Scoazec, Nathalie Lassau, Rachida Lebtahi, Hedia Brixi, et al. "Evaluating digestive neuroendocrine tumor progression and therapeutic responses in the era of targeted therapies: state of the art." Endocrine-Related Cancer 21, no. 3 (December 18, 2013): R105—R120. http://dx.doi.org/10.1530/erc-13-0365.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Well-differentiated neuroendocrine tumors (NETs) are a group of heterogeneous rare tumors. They are often slow-growing and patients can have very long survival, even at the metastatic stage. The evaluation of tumor progression and therapeutic responses is currently based on Response Evaluation Criteria In Solid Tumors v1.1 (RECIST) criteria. As for other malignancies, RECIST criteria are being reexamined for NETs in the era of targeted therapies because tumor response to targeted therapies is rarely associated with shrinkage, as opposed to prolonged progression-free survival. Therefore, size-based criteria no longer seem to be suitable to the assessment of NET progression and therapeutic responses, especially considering targeted therapies. New imaging criteria, combining morphological and functional techniques, have proven relevant for other malignancies treated with targeted therapies. To date, such studies have rarely been conducted on NETs. Moreover, optimizing the management of NET patients also requires considering clinical, biological, and pathological aspects of tumor evolution. Our objectives herein were to comprehensively review current knowledge on the assessment of tumor progression and early prediction of therapeutic responses and to broaden the outlook on well-differentiated NETs, in the era of targeted therapies.
33

Zawistowski, Jon S., Lee M. Graves, and Gary L. Johnson. "Assessing adaptation of the cancer kinome in response to targeted therapies." Biochemical Society Transactions 42, no. 4 (August 1, 2014): 765–69. http://dx.doi.org/10.1042/bst20130274.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Cancer cells are dependent on protein kinase signalling networks to drive proliferation and to promote survival, and, accordingly, kinases continue to represent a major target class for development of anti-cancer therapeutics. Kinase inhibitors nevertheless have yielded only limited success with many different malignancies due to the inability of single agents to sustain a durable clinical response. Cancer cell kinomes are highly resilient and able to bypass targeted kinase inhibition, leading to tumour resistance. A novel platform has been developed to analyse the activity of the expressed kinome using MIBs (multiplexed inhibitor beads), which consist of Sepharose beads with covalently immobilized inhibitors that preferentially bind activated kinases. Coupling MIB capture with MS (MIB–MS) allows simultaneous determination of the activity of over 75% of the expressed kinome, facilitating high-throughput assessment of adaptive kinase responses resulting from deregulated feedback and feedforward regulatory mechanisms. The adaptive response frequently involves transcriptional up-regulation of specific kinases that allow bypass of the targeted kinase. Understanding how the kinome reprogrammes to targeted kinase inhibition will allow novel therapeutic strategies to be developed for durable clinical responses.
34

Lutfi, Nura, Miguel Alejandro Galindo-Campos, and José Yélamos. "Impact of DNA Damage Response—Targeted Therapies on the Immune Response to Tumours." Cancers 13, no. 23 (November 29, 2021): 6008. http://dx.doi.org/10.3390/cancers13236008.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
The DNA damage response (DDR) maintains the stability of a genome faced with genotoxic insults (exogenous or endogenous), and aberrations of the DDR are a hallmark of cancer cells. These cancer-specific DDR defects present new therapeutic opportunities, and different compounds that inhibit key components of DDR have been approved for clinical use or are in various stages of clinical trials. Although the therapeutic rationale of these DDR-targeted agents initially focused on their action against tumour cells themselves, these agents might also impact the crosstalk between tumour cells and the immune system, which can facilitate or impede tumour progression. In this review, we summarise recent data on how DDR-targeted agents can affect the interactions between tumour cells and the components of the immune system, both by acting directly on the immune cells themselves and by altering the expression of different molecules and pathways in tumour cells that are critical for their relationship with the immune system. Obtaining an in-depth understanding of the mechanisms behind how DDR-targeted therapies affect the immune system, and their crosstalk with tumour cells, may provide invaluable clues for the rational development of new therapeutic strategies in cancer.
35

Klineova, Sylvia, Rebecca Straus Farber, Tracy DeAngelis, Tungming Leung, Tyler Smith, Richard Blanck, Lana Zhovtis-Ryerson, and Asaff Harel. "Vaccine-breakthrough SARS-CoV-2 infections in people with multiple sclerosis and related conditions: An observational study by the New York COVID-19 Neuro-Immunology Consortium (NYCNIC-2)." Multiple Sclerosis Journal 29, no. 8 (July 2023): 990–1000. http://dx.doi.org/10.1177/13524585231185246.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Background: People with MS (PwMS) and related conditions treated with anti-CD20 and S1P modulating therapies exhibit attenuated immune responses to SARS-CoV-2 vaccines. It remains unclear whether humoral/T-cell responses are valid surrogates for postvaccine immunity. Objective: To characterize COVID-19 vaccine-breakthrough infections in this population. Methods: We conducted a prospective multicenter cohort study of PwMS and related CNS autoimmune conditions with confirmed breakthrough infections. Postvaccination antibody response, disease-modifying therapies (DMTs) at the time of vaccination, and DMT at the time of infection were assessed. Results: Two hundred nine patients had 211 breakthrough infections. Use of anti-CD20 agents at time of infection was associated with increased infection severity ( p = 0.0474, odds ratio (OR) = 5.923) for infections during the Omicron surge and demonstrated a trend among the total cohort ( p = 0.0533). However, neither use of anti-CD20 agents at the time of vaccination nor postvaccination antibody response was associated with hospitalization risk. Anti-CD20 therapies were relatively overrepresented compared to a similar prevaccination-era COVID-19 cohort. Conclusion: Use of anti-CD20 therapies during vaccine breakthrough COVID-19 infection is associated with higher severity. However, the attenuated postvaccination humoral response associated with anti-CD20 therapy use during vaccination may not drive increased infection severity. Further studies are necessary to determine if this attenuated vaccine response may be associated with an increased likelihood of breakthrough infection.
36

Stewart, A. Keith. "Novel therapies for relapsed myeloma." Hematology 2009, no. 1 (January 1, 2009): 578–86. http://dx.doi.org/10.1182/asheducation-2009.1.578.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
AbstractTreatment of myeloma relapse needs to be individualized to reflect the effectiveness and toxicities of prior therapies, with consideration given to pragmatic issues such as the tempo of relapse, age of the patient, access to drugs and patient preference. In general, combination therapies have been associated with higher response rates and improved progression-free survival and may be preferable when a rapid response is required. Nevertheless, in a slower-tempo relapse it is unclear at this juncture whether sequencing of drugs or multi-agent combinations offer superior overall survival results. Fortunately, active novel agents that offer further possibilities for some myeloma patients have become available in clinical trials. In this review we will describe the various classes of novel drugs being tested and the pros and cons of preclinical testing, and will particularly focus on two agents with single-agent activity in myeloma: carfilzomib, a proteasome inhibitor, and pomalidomide, a member of the immunomodulatory class of drugs.
37

Blair, Edward D., Martina Kaufmann, and Mieke Keppens. "Prediction of response to targeted and immune checkpoint therapies." Personalized Medicine 15, no. 1 (January 2018): 45–56. http://dx.doi.org/10.2217/pme-2017-0051.

Full text
APA, Harvard, Vancouver, ISO, and other styles
38

Ghali, Jalal K., and JoAnn Lindenfeld. "Sex differences in response to chronic heart failure therapies." Expert Review of Cardiovascular Therapy 6, no. 4 (April 2008): 555–65. http://dx.doi.org/10.1586/14779072.6.4.555.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Vaquero, Javier, Allan Pavy, Ester Gonzalez-Sanchez, Mark Meredith, Ander Arbelaiz, and Laura Fouassier. "Genetic alterations shaping tumor response to anti-EGFR therapies." Drug Resistance Updates 64 (September 2022): 100863. http://dx.doi.org/10.1016/j.drup.2022.100863.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Lim, Kok Haw Jonathan, Evangelos Giampazolias, Oliver Schulz, Neil C. Rogers, Anna Wilkins, Erik Sahai, Jessica Strid, and Caetano Reis e Sousa. "Loss of secreted gelsolin enhances response to anticancer therapies." Journal for ImmunoTherapy of Cancer 10, no. 9 (September 2022): e005245. http://dx.doi.org/10.1136/jitc-2022-005245.

Full text
APA, Harvard, Vancouver, ISO, and other styles
Abstract:
Type 1 conventional dendritic cells (cDC1) play a critical role in priming anticancer cytotoxic CD8+ T cells. DNGR-1 (a.k.a. CLEC9A) is a cDC1 receptor that binds to F-actin exposed on necrotic cancer and normal cells. DNGR-1 signaling enhances cross-presentation of dead-cell associated antigens, including tumor antigens. We have recently shown that secreted gelsolin (sGSN), a plasma protein, competes with DNGR-1 for binding to dead cell-exposed F-actin and dampens anticancer immunity. Here, we investigated the effects of loss of sGSN on various anticancer therapies that are thought to induce cell death and provoke an immune response to cancer. We compared WT (wildtype) with Rag1–/–, Batf3–/–, Clec9agfp/gfp, sGsn–/– or sGsn–/– Clec9agfp/gfp mice implanted with transplantable tumor cell lines, including MCA-205 fibrosarcoma, 5555 BrafV600E melanoma and B16-F10 LifeAct (LA)-ovalbumin (OVA)-mCherry melanoma. Tumor-bearing mice were treated with (1) doxorubicin (intratumoral) chemotherapy for MCA-205, (2) BRAF-inhibitor PLX4720 (oral gavage) targeted therapy for 5555 BrafV600E, and (3) X-ray radiotherapy for B16 LA-OVA-mCherry. We confirmed that efficient tumor control following each therapy requires an immunocompetent host as efficacy was markedly reduced in Rag1–/– compared with WT mice. Notably, across all the therapeutic modalities, loss of sGSN significantly enhanced tumor control compared with treated WT controls. This was an on-target effect as mice deficient in both sGSN and DNGR-1 behaved no differently from WT mice following therapy. In sum, we find that mice deficient in sGsn display enhanced DNGR-1-dependent responsiveness to chemotherapy, targeted therapy and radiotherapy. Our findings are consistent with the notion some cancer therapies induce immunogenic cell death (ICD), which mobilizes anticancer T cells. Our results point to cDC1 and DNGR-1 as decoders of ICD and to sGSN as a negative regulator of such decoding, highlighting sGSN as a possible target in cancer treatment. Further prospective studies are warranted to identify patients who may benefit most from inhibition of sGSN function.
41

Galons, Jean Philippe, David L. Morse, Dominique R. Jennings, and Robert J. Gillies. "Diffusion-Weighted MRI and Response to Anti-Cancer Therapies." Israel Journal of Chemistry 43, no. 1-2 (November 2003): 91–101. http://dx.doi.org/10.1560/gj5m-pp8r-ghub-vuup.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Chan, Happy, and Prabha Ranganathan. "Will Pharmacogenetics Predict Response to Therapies in Rheumatoid Arthritis?" Current Pharmacogenomics 4, no. 4 (December 1, 2006): 307–19. http://dx.doi.org/10.2174/157016006778992750.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Leader, Darian. "RESPONSE TO ‘THE FUTURE OF THE TRANSFERENCE-BASED THERAPIES’." British Journal of Psychotherapy 25, no. 3 (August 2009): 349–51. http://dx.doi.org/10.1111/j.1752-0118.2009.01128.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

Lepper, Georgia. "RESPONSE TO ‘THE FUTURE OF THE TRANSFERENCE-BASED THERAPIES’." British Journal of Psychotherapy 25, no. 3 (August 2009): 352–56. http://dx.doi.org/10.1111/j.1752-0118.2009.01129.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Stroehl, Yasmin W., Brian S. Letzen, Johanna M. M. van Breugel, Jean-Francois Geschwind, and Julius Chapiro. "Intra-arterial therapies for liver cancer: assessing tumor response." Expert Review of Anticancer Therapy 17, no. 2 (December 27, 2016): 119–27. http://dx.doi.org/10.1080/14737140.2017.1273775.

Full text
APA, Harvard, Vancouver, ISO, and other styles
46

Smith, Kevin R. "Anomalous Therapies and Public Health: A Utilitarian Bioethical Response." Public Health Nursing 25, no. 3 (May 2008): 269–77. http://dx.doi.org/10.1111/j.1525-1446.2008.00704.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

Reider, Bruce. "PRP Therapies—Is It Time for Potency Assays? Response." American Journal of Sports Medicine 44, no. 11 (October 31, 2016): NP64. http://dx.doi.org/10.1177/0363546516676456.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

Amoaku, W. M., U. Chakravarthy, R. Gale, M. Gavin, F. Ghanchi, J. Gibson, S. Harding, et al. "Defining response to anti-VEGF therapies in neovascular AMD." Eye 29, no. 6 (April 17, 2015): 721–31. http://dx.doi.org/10.1038/eye.2015.48.

Full text
APA, Harvard, Vancouver, ISO, and other styles
49

Teicher, Beverly A. "Role of angiogenesis in the response to anticancer therapies." Drug Resistance Updates 1, no. 1 (March 1998): 59–61. http://dx.doi.org/10.1016/s1368-7646(98)80215-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
50

Bignami, M., I. Casorelli, and P. Karran. "Mismatch repair and response to DNA-damaging antitumour therapies." European Journal of Cancer 39, no. 15 (October 2003): 2142–49. http://dx.doi.org/10.1016/s0959-8049(03)00569-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Response to therapies' for other source types:
Dissertations / Theses Books

To the bibliography