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Academic literature on the topic 'CDKIs'

Author: Grafiati

Published: 1 April 2023

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Journal articles on the topic "CDKIs"

1

Campbell, Grace Jean, Emma Langdale Hands, and Mathew Van de Pette. "The Role of CDKs and CDKIs in Murine Development." International Journal of Molecular Sciences 21, no. 15 (July 28, 2020): 5343. http://dx.doi.org/10.3390/ijms21155343.

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Cyclin-dependent kinases (CDKs) and their inhibitors (CDKIs) play pivotal roles in the regulation of the cell cycle. As a result of these functions, it may be extrapolated that they are essential for appropriate embryonic development. The twenty known mouse CDKs and eight CDKIs have been studied to varying degrees in the developing mouse, but only a handful of CDKs and a single CDKI have been shown to be absolutely required for murine embryonic development. What has become apparent, as more studies have shone light on these family members, is that in addition to their primary functional role in regulating the cell cycle, many of these genes are also controlling specific cell fates by directing differentiation in various tissues. Here we review the extensive mouse models that have been generated to study the functions of CDKs and CDKIs, and discuss their varying roles in murine embryonic development, with a particular focus on the brain, pancreas and fertility.

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2

Giannone, Gaia, Valentina Tuninetti, Eleonora Ghisoni, Sofia Genta, Giulia Scotto, Gloria Mittica, and Giorgio Valabrega. "Role of Cyclin-Dependent Kinase Inhibitors in Endometrial Cancer." International Journal of Molecular Sciences 20, no. 9 (May 12, 2019): 2353. http://dx.doi.org/10.3390/ijms20092353.

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Endometrial Cancer (EC) is an important cause of death in women worldwide. Despite early diagnosis and optimal treatment of localized disease, relapsed patients have few therapeutic options because after first line therapy, currently no standard of care exists. On the basis of endocrine positivity of most endometrioid ECs, Endocrine Therapy (ET) is a reasonable and widely accepted option. Better knowledge of molecular mechanisms involved in cancer highlighted the deregulated activity of Cyclin-Dependent Kinases (CDKs) in the cell cycle as a hallmark of carcinogenesis supporting the development of a new class of drugs: CDK inhibitors (CDKis). The aim of this review is to give an overview on CDKis preclinical, early clinical activity and future development in EC. Use of CDKis has a strong preclinical rationale but we have poor clinical data. Similar to breast cancer, most ongoing trials are investigating synergistic associations between CDKis and ET. These trials will probably help in defining the best clinical setting of CDKis in ECs, which are the best partner drugs, and how to manage CDKis toxicities with a focus on potential biomarkers of response.

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3

Phuong, Lisa, Janki Patel, Nadia Baka, Jessica Goldman, Michael Lyudmer, Stephanie Shamir, Junwen Deng, Alvaro Alvarez Soto, and Jesus Del Santo Anampa Mesias. "Effect of cyclin-dependent kinase 4 and 6 inhibitors (CDKIs) on body composition (BC) in patients (pts) with hormone receptor-positive, HER2-negative (HR+/HER2-) metastatic breast cancer (MBC)." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e13033-e13033. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e13033.

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e13033 Background: CDKIs with endocrine therapy (ET) is first-line treatment in HR+/HER2- MBC. Mouse models have shown that CDKIs prevent pRB phosphorylation in the mediobasal hypothalamus, a pathway hyper-activated in diet-induced obesity; and CDKIs lead to fat mass decrease without significant effect on lean mass. We aimed to assess the impact of CDKIs on weight (wt) and BC in pts with HR+/HER2- MBC. Methods: We identified pts with HR+/HER2- MBC who received CDKIs and ET from 2015-2018. To isolate the effect of CDKIs on BC, we identified another cohort of pts who only received ET. Body mass index (BMI), wt, and computed tomography (CT) records were reviewed. BC was analyzed at L3 on CT scans using Tomovision’s SliceOmatic v5.0 and included skeletal muscle area (SMA), skeletal muscle density (SMD), subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), and muscle adiposity (MA). Total adipose tissue (TAT) was defined as SAT+VAT+MA. BC changes at 3 and 6 months of therapy were evaluated using paired t-tests. Results: There were 107 pts who received CDKI plus ET - 43% were Black, and 41% were Hispanic. CDKIs used were palbociclib (85%), abemaciclib (9%), and ribociclib (6%). ETs used were letrozole (47%), fulvestrant (39%), anastrozole (12%), and exemestane (2%). Median number of prior chemo and ET lines was 0 (range 0-5). 63 pts received ET alone. There was no difference in age (63 vs. 65 years, p = 0.26), BMI (28.80 vs. 28.12kg/m2, p = 0.48), and visceral disease (69% vs. 65%, p = 0.64) between CDKI plus ET and ET alone group. At month 3 of CDKI plus ET, there was a significant decrease in wt (-0.30kg, Interquartile range [IQR] -2.55-0.95, p = 0.02), BMI (-0.12kg/m2, IQR -1.06-0.46, p = 0.02), SAT (-8.05cm2, IQR -32.58-14.74, p = 0.01), and TAT (-8.51cm2, IQR -50.42-17.84, p < 0.01), with similar results at month 6. These findings were not seen in pts on ET only at 3 months (wt: 0.00kg, IQR -2.65-2.38, p = 0.98; BMI: 0.00kg/m2, IQR -1.07-0.91, p = 0.93; SAT: -2.97cm2, IQR -26.10-25.15, p = 0.60; TAT: -0.58cm2, IQR -44.39-27.43, p = 0.18), or at 6 months. There were no significant changes in VAT, SMA, SMD, or MA in both groups at 3 or 6 months. In the CDKI plus ET group, baseline wt (74.64 vs. 72.72kg, p = 0.60), BMI (29.21 vs. 27.88kg/m2, p = 0.31), and SAT (280.29 vs. 252.75cm2, p = 0.31) were not significantly different for those who did or did not develop grade 3/4 toxicities. We obtained similar results when stratifying toxicities into hematological- and GI-related events. Conclusions: CDKIs are associated with decrease in BMI and SAT with no significant effect on VAT, SMA, or SMD. Given the known effect of obesity on breast cancer prognosis, CDKIs may have an additional effect on breast cancer prognosis by modulating body fat. Further studies are required to determine if decrease in SAT is associated with breast cancer outcomes or toxicities in pts on CDKIs.

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4

Chao, Sheng-Hao, John R. Walker, Sumit K. Chanda, Nathanael S. Gray, and Jeremy S. Caldwell. "Identification of Homeodomain Proteins, PBX1 and PREP1, Involved in the Transcription of Murine Leukemia Virus." Molecular and Cellular Biology 23, no. 3 (February 1, 2003): 831–41. http://dx.doi.org/10.1128/mcb.23.3.831-841.2003.

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ABSTRACT Cyclin-dependent kinase inhibitors (CDKIs) have been shown to block human immunodeficiency virus and herpes simplex virus. It is hypothesized that CDKIs block viral replication by inhibiting transcription of specific cellular genes. Here we find that three CDKIs, flavopiridol, purvalanol A, and methoxy-roscovitine, block Moloney murine leukemia virus (MLV) transcription events. Using gene expression microarray technology to examine the inhibitory effects of CDKIs, we observed a cellular gene, the pre-B-cell leukemia transcription factor 1 (Pbx1) gene, down-regulated by CDKI treatment. The PBX consensus element (PCE), TGATTGAC, is conserved in the long terminal repeats of several murine retroviruses, including Moloney MLV. Mutations in the PCE completely inhibited viral transcription whereas overexpression of PBX1 and a PBX1-associated protein, PREP1, enhanced viral transcription. The interaction between the PCE and PBX1-PREP1 proteins was confirmed by gel shift experiments. Blocking PBX1 protein synthesis resulted in a significant decrease in viral transcription. Collectively, our results represent the first work demonstrating that the homeodomain proteins PBX1 and PREP1 are cellular factors involved in Moloney MLV transcription regulation.

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Dao, Mo A., and Catherine M. Verfaillie. "STI571 Suppresses Proliferation by Restoring Nuclear Cyclin Dependent Kinase Inhibitors (CDKIs) while STI571+TRAIL Promotes Cell Death by Decreasing Cytoplasmic CDKIs." Blood 104, no. 11 (November 16, 2004): 1992. http://dx.doi.org/10.1182/blood.v104.11.1992.1992.

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Abstract Cyclin dependent kinase inhibitors (CDKIs), p27Kip1 and p21Cip1, function as cell cycle inhibitors when located in the nucleus. When localized to the cytoplasm, these CDKIs can function as anti-apoptotic molecules by sequestering/preventing the activation of pro-apoptotic proteins such as ASK1 and procaspase-3. Our lab has reported elevated cytoplasmic CDKIs and decreased nuclear CDKIs in hematopoietic cells expressing BCR/ABL, the oncogene found in more than 90% of cases of chronic myeloid leukemia. Within the past decade, STI571 has been shown highly promising for CML treatment. However, there is increasing evidence suggesting that the drug might function more as a suppressor of proliferation and less as a promoter of cell death. In the current studies, we differentiate the effect of STI571 on proliferation vs. survival by tracking the subcellular increase/decrease in CDKIs using MO7e cells engineered to express BCR/ABL. To determine if a correlation exists between STI571 resistance and levels of cytoplasmic anti-apoptotic CDKIs, we also investigated changes in levels of nuclear vs. cytoplasmic CDKIs in LAMA84 -S (sensitive to STI571) vs. LAMA84-R (resistant to STI571). And lastly, we tested whether activation of TRAIL would enhance cell death in STI571-resistant cells. STI571 treatment increases nuclear CDKIs, correlating directly with a decrease in proliferation of MO7e/p210 cells. However, the high levels of cytoplasmic CDKIs in MO7e/p210bcr/abl was not modulated following STI571 treatment and cell death was not prominent, unless growth factors were removed. Moreover, cytoplasmic p21Cip co-immunoprecipitated with ASK1 and procaspase 3. When compared with LAMA-S cells, LAMA-R cells expressed even higher levels of cytoplasmic CDKIs. Treatment with STI571 decreased cytoplasmic CDKIs in LAMA84-S cells and resulted in cell death. As hypothesized, LAMA84-R cells did not show reduction in cytoplasmic CDKIs and did not enter apoptosis. However, when treated with STI571 and TRAIL, LAMA84-R cells showed a decrease in cytoplasmic CDKIs, and increase in apoptosis. Based on these observations, we conclude that: 1. BCR/ABL expression reduces nuclear CDKIs but increases cytoplasmic CDKIs. 2. STI571 treatment restores nuclear CDKIs and reduces cell proliferation of BCR/ABL expressing cells under physiological conditions. 3. Treatment of STI571+TRAIL reduces cytoplasmic CDKIs and increases cell death of BCR/ABL expressing cells, most notably, the STI571-resistant cells. In conclusion, we show that the imbalance between nuclear (cell cycle inhibitor) and cytoplasmic (cell survival enhancer) CDKIs exist in BCR/ABL-hematopoietic cells.

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Abdelmalak, Mary, Rajanbir Singh, Mohammed Anwer, Pavel Ivanchenko, Amritdeep Randhawa, Myra Ahmed, Anthony W. Ashton, Yanming Du, Xuanmao Jiao, and Richard Pestell. "The Renaissance of CDK Inhibitors in Breast Cancer Therapy: An Update on Clinical Trials and Therapy Resistance." Cancers 14, no. 21 (November 1, 2022): 5388. http://dx.doi.org/10.3390/cancers14215388.

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Cyclin-dependent kinases (CDKs) govern cell-cycle checkpoint transitions necessary for cancer cell proliferation. Recent developments have illustrated nuanced important differences between mono CDK inhibitor (CDKI) treatment and the combination therapies of breast cancers. The CDKIs that are currently FDA-approved for breast cancer therapy are oral agents that selectively inhibit CDK4 and CDK6, include palbociclib (Ibrance), ribociclib (Kisqali), and abemaciclib (Verzenio). CDKI therapy is effective in hormone receptor positive (HR+), and human epidermal growth factor receptor two negative (HER2−) advanced breast cancers (ABC) malignancies, but remains susceptible due to estrogen and progesterone receptor overexpression. Adding a CDK4/6I to endocrine therapy increases efficacy and delays disease progression. Given the side effects of CDKI, identifying potential new treatments to enhance CDKI effectiveness is essential. Recent long-term studies with Palbociclib, including the PALLAS and PENELOPE B, which failed to meet their primary endpoints of influencing progression-free survival, suggest a deeper mechanistic understanding of cyclin/CDK functions is required. The impact of CDKI on the anti-tumor immune response represents an area of great promise. CDKI therapy resistance that arises provides the opportunity for specific types of new therapies currently in clinical trials.

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Gervaso, Lorenzo, Alberto J. Montero, Xuefei Jia, and Alok A. Khorana. "Venous thromboembolism in breast cancer patients receiving cyclin-dependent kinase inhibitors." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e18184-e18184. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e18184.

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e18184 Background: Venous thromboembolism (VTE) complicates several anti-cancer regimens including chemotherapy and anti-angiogenic agents. Cyclin-dependent kinase 4/6 inhibitors (CDKIs) are a new approach for hormone receptor positive (HR+) metastatic breast cancer (mBC). Reported VTE rates in randomized trials range from 0.6% for ribociclib (MONALEESA-2) to 2% for palbociclib (PALOMA-3) and 5% for abemaciclib (MONARCH-3) but these may underestimate actual rates compared to patients in clinical practice who are generally older and have greater comorbidities. Little is known about real world incidence or prevalence of VTE with CDKIs in mBC. The aim of this study was to evaluate rates of VTE in clinical practice and association with outcomes in mBC patients on CDKIs. Methods: We conducted a retrospective cohort study at Cleveland Clinic Taussig Cancer Institute, approved by the institutional review board. We identified consecutive mBC patients who received any of three FDA-approved CDKIs (palbociclib, ribociclib, abemaciclib) from 1/2015 through 12/2017. VTE including deep venous thrombosis (DVT) and pulmonary embolism (PE) were identified by electronic medical record review. Overall survival (OS), progression free survival (PFS) and time to VTE were estimated by the Kaplan-Meier method and evaluated for association with VTE using Cox proportional hazard regression. Results: The study population included 424 patients, with a median age at diagnosis of 54.76 yrs, (range 27 -85). Palbociclib was the most commonly used CDKI (n = 390, 91.8%); 27 patients (6.3%) received more than one drug. VTE during CDKI therapy occurred in 9% of patients (n = 38), including DVT in 52.6% (n = 20), PE in 18.5% (n = 7) and visceral vein thrombosis (VVT) in 15.8% (n = 6). Median time to VTE was 314 days, and 6-months rate was 4.1%. VTE was associated with numerically worse PFS and OS, but this was not statistically significant (PFS [HR 1.25, 95% CI 0.73 – 2.14, p = 0.42], OS [HR 1.60, 95% CI 0.89 – 2.87, p = 0.12]). Conclusions: VTE affected nearly 10% of breast cancer patients receiving CDKIs, 2- to 5-fold greater than reported in registration trials. Further work is necessary to identify pathophysiology, risk factors and benefit of thromboprophylaxis.

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Zeki, K., I. Morimoto, T. Arao, S. Eto, and U. Yamashita. "Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA." Journal of Endocrinology 160, no. 1 (January 1, 1999): 67–73. http://dx.doi.org/10.1677/joe.0.1600067.

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This study provides the first report that the same cytokine (interleukin-1 (IL-1)) can induce opposite effects on cyclin-dependent kinases (Cdks) and Cdk inhibitors (Cdkis) in the G1 phase even in the same type of cancer cells (papillary thyroid carcinoma cells). Cell cycle analysis revealed an increase in NIM1 cells and a decrease in NPA cells in the S and G2+M phases after treatment with IL-1alpha. The addition of IL-1alpha to NIM1 cells reduced the expression of p16 and p21 protein and induced the expression of Cdk2 and Cdk4 protein, which leads to the phosphorylation of retinoblastoma protein. The addition of IL-1alpha to NPA cells induced the expression of p27 protein and reduced the expression of Cdk2 protein, which leads to induction of p107 protein expression. It is of interest that p21 protein expression was not observed in NPA cells. These results suggest that several Cdks and Cdkis play a regulatory role in the G1 cell cycle progression and arrest induced by IL-1alpha in thyroid carcinoma cell lines.

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Buckley, S., B. Driscoll, K. D. Anderson, and D. Warburton. "Cell cycle in alveolar epithelial type II cells: integration of Matrigel and KGF." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 3 (September 1, 1997): L572—L580. http://dx.doi.org/10.1152/ajplung.1997.273.3.l572.

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The regulation of cell cycle control in alveolar epithelial type II cells (AEC2) in response to peptide growth factors and extracellular matrix signals is not well understood. Herein, we have determined that, in adult rat AEC2 in primary culture on Engelbreth-Holm-Swarm biomatrix (Matrigel) in the presence of keratinocyte growth factor, the expression of key cell cycle control elements, including cyclins A and D and cyclin-dependent kinases (cdk) 1 and 4, is increased and that retinoblastoma protein (pRb) phosphorylation is also increased, with a corresponding decrease in the expression of p53 and the cdk inhibitors (cdkis) p21WAF1/CIP1 and p27KIP-1 compared with cells cultured on plastic. The Matrigel biomatrix-KGF culture conditions were also associated with an enhanced proliferative response, as measured by fluorescent-activated cell sorter analysis, thymidine incorporation into DNA, and proliferating cell nuclear antigen expression. This enhanced proliferation occurred with neither a soluble extract of Matrigel biomatrix nor with other simple biological matrices. We conclude that coordinated induction of key cyclins and cdks, with the concomitant suppression of key negative cell cycle regulators, occurs in AEC2 on Matrigel biomatrix in the presence of KGF. We speculate that the balance between cyclin and cdk activation and cdki suppression in AEC2 serves to integrate the combined influences of biomatrix and KGF signaling on pRb phosphorylation, thereby controlling transit through S phase of the cell cycle. Conversely, AEC2 express high levels of cdkis and p53 at rest in G1 phase. The latter finding may explain the quiescent state of normal adult AEC2 in vivo.

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Bencivenga, Debora, Emanuela Stampone, Angela Vastante, Myassar Barahmeh, Fulvio Della Ragione, and Adriana Borriello. "An Unanticipated Modulation of Cyclin-Dependent Kinase Inhibitors: The Role of Long Non-Coding RNAs." Cells 11, no. 8 (April 14, 2022): 1346. http://dx.doi.org/10.3390/cells11081346.

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It is now definitively established that a large part of the human genome is transcribed. However, only a scarce percentage of the transcriptome (about 1.2%) consists of RNAs that are translated into proteins, while the large majority of transcripts include a variety of RNA families with different dimensions and functions. Within this heterogeneous RNA world, a significant fraction consists of sequences with a length of more than 200 bases that form the so-called long non-coding RNA family. The functions of long non-coding RNAs range from the regulation of gene transcription to the changes in DNA topology and nucleosome modification and structural organization, to paraspeckle formation and cellular organelles maturation. This review is focused on the role of long non-coding RNAs as regulators of cyclin-dependent kinase inhibitors’ (CDKIs) levels and activities. Cyclin-dependent kinases are enzymes necessary for the tuned progression of the cell division cycle. The control of their activity takes place at various levels. Among these, interaction with CDKIs is a vital mechanism. Through CDKI modulation, long non-coding RNAs implement control over cellular physiology and are associated with numerous pathologies. However, although there are robust data in the literature, the role of long non-coding RNAs in the modulation of CDKIs appears to still be underestimated, as well as their importance in cell proliferation control.

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Dissertations / Theses on the topic "CDKIs"

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Henderson, Andrew. "Isosteres of sulfonamide inhibitors of cyclin-dependent kinases (CDKs)." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512187.

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Marchetti, Francesco. "Structure-activity relationships for alkoxypirimidine inhibitors of cyclin-dependent kinases (CDK’s)." Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.556141.

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Cyclin-dependent kinases (CDKs) are a family of serine/threonine protein kinases that play a fundamental role in the regulation of eukaryotic cell-cycle progression, particularly at cell- cycle checkpoints. Cell-cycle alterations result in a loss of checkpoint function, which correlates with increased or aberrant CDK activity in human tumours. CDK inhibitors are therefore recognised to have potential therapeutic effects in the treatment of cancer and other proliferative diseases. This research project centres on the medicinal chemistry of a new class of CDK inhibitors, based on the 2,6-diamino-4-alkoxy- 5-nitrosopyrimidine pharmacophore (77). Previous studies, employing a structure-based inhibitor design approach, have resulted in the identification of 2-arylamino-06- alkylguanines exhibiting potent inhibitory activity against CDK2, and exemplified by NU6102 (31; IC50 = 5 nM). Structure-activity relationship studies revealed that the purine pharmacophore is not a prerequisite for CDK-inhibitory activity. Thus, comparable activity resides in the corresponding pyrimidines, where an intramolecular hydrogen bond between a 5-nitroso substituent and a 6-amino group confers a 'purine-mimetic' structure (164; CDK2/A, IC50 = 1 nM). Guided by results obtained previously for the corresponding 06-alkylguanines, systematic structural modifications have been made at the pyrimidine 2-, 4- and 5- positions, via the development and optimisation of efficient synthetic pathways Replacement of the 5-nitroso substituent of the parent inhibitors (77, 164) by groups that are more acceptable from a toxicological standpoint has been a prominent target of this work. Formyl, ketone and oxime functionalities have been successfully introduced at the pyrimidine 5-position, while different alkoxy and arylamino substituents were introduced at the pyrimidine 4-position and 2-position, respectively, to probe additional potential interactions within the ATP ribose-binding domain and CDK2 specificity pocket. The synthesis and structure-activity relationships for this new series of CDK inhibitors have been investigated, as exemplified by (220) (CDK2/A, IC50 = 49 nM), (239) (CDK2/A, IC50 = 7.4 nM) and (109) (CDK2/A, IC50 = 23.3 μM). These studies have resulted in the identification of novel compounds, such as (225), exhibiting improved potency against CDKs, with sub-nanomolar inhibitory activity versus CDK2/A (IC5o = 0.77 nM) and good cell growth inhibition properties (G150 = 0.57 μM).

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Lolli, Graziano. "Cdks at the interface of cell cycle and and transcription regulation." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426389.

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Chiurato, Matteo. "Synthèse de tétrahydropyrido-[isoindolones/isoquinolones/indolizinones] pour l'élaboration d'inhibiteurs de CDks." Orléans, 2007. http://www.theses.fr/2007ORLE2069.

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Cette thèse est divisée en cinq parties. La première partie traite de la chimie des ions iminiums. Après une brève introduction sur leur découverte, sont présentées leurs préparations et leurs applications dans divers champs de la chimie, en particulier dans la synthèse de produits naturels. En suite nous traiterons des ions N-acyl iminiums, en évoquant les mécanismes de leur formation, les diverses applications et leurs particularités. La première partie se termine par la présentation des différentes voies d'accès à des structures du type isoindoquinolinonique obtenues notamment par formation d’ions d'acyl iminiums. La seconde partie de la thèse concerne une étude méthodologique de la réaction de cyclisation présentée par le groupe du Prof. Y. Troin. Cette réaction, basée sur un intermédiaire N-acyl iminium, permet la synthèse d'un système de type isoquinolone. La réaction est une cycloaddition intermoléculaire d’une cétone protégée, et le carboxy benzaldéhyde. entre une amine primaire en Nous avons repris ces premiers travaux et avons étendu la méthode à toute une série de noyaux comme des systèmes benzéniques différemment substitués (avec des groupes -OMe en différentes positions du cycle), des systèmes polyaromatiques (naphtalène) et des hétérocycles (pyridine, quinoléine etc. . . ). La différence de réactivité des différents systèmes est discutée, et une méthode alternative de hydroxy lactames est proposée. synthèse passant par des Dans la troisième partie l’application de nos recherches à la problématique de la chimiothérapie anticancéreuse est abordée. Après avoir rappelé les principales causes, les mécanismes et quelques notions sur le cycle cellulaire et sur quelques médicaments utilisables à ce jour, nous évoquerons le rationnel permettant l’utilisation de la 10-amino-1,3,4,10b-tétrahydro-2H-pyrido[2,1-a]isoindol-6-one pour arriver à une série de diarylurées, inhibiteurs potentiels de kinases dépendantes des cyclines. La quatrième partie traite donc du chemin synthétique utilisé pour atteindre ces objectifs, et se termine par les résultats des tests biologiques et l’étude des premières relations entre structure et activité. Enfin, des perspectives de travail sont évoquées et une conclusion générale est proposée.

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Delmas, Christelle. "Modes de régulation de l'inhibiteur de CDKs, p27kip1, par les MAPKsp42/p44." Toulouse 3, 2003. http://www.theses.fr/2003TOU30006.

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Bettayeb, Karima. "Optimisation et caractérisation de nouveaux inhibiteurs pharmacologiques de kinases cycline-dépendantes (CDKs)." Rennes 1, 2008. http://www.theses.fr/2008REN1S025.

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Les kinases cycline-dépendantes (CDKs) sont des régulateurs essentiels du cycle de division cellulaire (CDK1, 2, 3, 4, 6, 7), de l’apoptose (CDK1, 5), et de la transcription (CDK7, 9). Les inhibiteurs pharmacologiques de CDKs constituent une nouvelle famille de produits anti-cancéreux potentiels : dix sont actuellement en clinique, dont la roscovitine issue de notre laboratoire. Ma thèse a porté sur l’identification, l’optimisation et la caractérisation détaillée des effets biochimiques et cellulaires de trois nouvelles classes d’inhibiteurs de kinases : indirubines-7-bromées (7BIO), meriolines et nouveaux analogues de la roscovitine (N&N1 et C&R8). Le 7BIO induit une mort cellulaire non-apoptotique par un mécanisme encore inconnu (pas de relargage de cytochrome C, pas d’activation de caspases). En revanche les meriolines et les roscovitine de seconde génération induisent une mort apoptotique classique suite à l’inhibition de CDK9. Qui conduit à une disparition d’un facteur de survie cellulaire essentiel, Mcl-1. Ces trois familles chimiques ont des effets anti-prolifératifs et tumoraux prometteurs
Cyclin-dependent kinases (CDKs) are key regulators of cell division cycle (CDK1, 2, 3, 4, 6, 7), apoptosis (CDK1, 5), and transcription (CDK7, 9). Pharmacological inhibitors of CDKs constitute a new family of potential antitumor agents: ten are under clinical trials, among which roscovitine, was discovered in our laboratory. My thesis is about identification, optimisation and characterization of biochemical and cellular effects of three new kinase inhibitory classes: 7-bromo-indirubins (7BIO), meriolin and new analogs of roscovitine (N&N1 and C&R8). 7BIO induces non-apoptotic cell death through an unknown mechanism (no release of cytochrome C, nor caspase activation). On the other hand, meriolins and second generation roscovitine analogs induce a classical apoptosis due to CDK9 inhibition, thus leading to disappearance of the cell survival factor, Mcl-1. These three classes of chemicals display promising anti-proliferative and antitumor properties

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7

Wołowiec, Dariusz. "Étude des CDKS et des cyclines dans le tissu lymphoïde normal et pathologique." Lyon 1, 1995. http://www.theses.fr/1995LYO1T147.

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Appleyard, Lindsey Jemma. "Overcoming financial exclusion : Community Development Finance Institutions (CDFIs) and the balancing of financial and social objectives." Thesis, University of Birmingham, 2008. http://etheses.bham.ac.uk//id/eprint/386/.

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This thesis explores Community Development Finance Institutions (CDFI) as an alternative vehicle for the supply of debt finance to financially excluded enterprises. CDFIs are part of a broader approach to addressing financial exclusion that is experienced by commercial and social enterprises in the US and UK. The thesis explores US and UK CDFI lending processes to develop an understanding of how financial and social objectives are balanced in the lending process and the ways in which CDFIs become embedded in local financial and business support networks. The analysis is based upon detailed comparative research of CDFIs located in the US and the UK; interviews were undertaken with CDFIs, their clients and a quantitative analysis of a CDFIs loan portfolio was undertaken. The research concludes that CDFIs are complex dynamic organizations as they have to balance a double or triple bottom line which has the potential to undermine the firm’s long term survival or mission. The danger is that over time a CDFI will reduce its exposure to risk and become more like a mainstream bank. The tensions with the CDFI business model implies that they will only ever provide a partial solution to the enterprise finance gap.

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9

Baïdi, Feriel. "Simplicity and complexity in cell cycle control." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B021.

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Mes travaux de recherche portent sur le contrôle du cycle cellulaire chez la levure de fission, Schizosaccharomyces pombe. Chez S. pombe, cette régulation est assurée principalement par une protéine kinase cycline-dépendante (CDK), nommée Cdc2. Au cours du cycle cellulaire, cette enzyme s’associe avec différentes cyclines (Cig1, Cig2, Puc1 et Cdc13), formant ainsi une variété de complexes CDK-cycline qui confèrent des activités spécifiques à chaque phase du cycle. Cependant, il a été montré que ce réseau complexe peut être simplifié et remplacé par un système minimal, qui consiste en la fusion des deux gènes cdc2 et cdc13, indépendant d’un grand nombre de régulations endogènes. Cette découverte a ainsi permis d'établir un nouveau modèle pour le contrôle du cycle cellulaire eucaryote. Dans ce travail nous avons d’une part, voulu comprendre pourquoi la régulation du cycle cellulaire s’est complexifiée au cours de l’évolution, étant donné qu’une grande partie du circuit endogène semble dispensable. Dans ce but, j’ai investigué les limites du système minimal, quand les cellules sont exposées à différents stress. De manière surprenante, nous avons découvert que la simplification du réseau des CDKs confère aux cellules une résistance au stress réplicative. Nous avons montré que ce phénotype était indépendant de la régulation de l’inhibiteur Rum1 et des points de contrôles. Il résulte plutôt du fait que le cycle cellulaire soit régulé uniquement par Cdc13. Nous avons trouvé que le programme de réplication était inchangé dans les minimale qui présentaient moins de dommage à l’ADN comparé aux cellules sauvages. Nos data suggèrent que l’activité des CDKs associée au cyclines de phase G1/S, représente un moyen alternatif de moduler la réponse au stress. D’autre part, en utilisant le même système dans lequel l’activité des CDKs peut être finement modulée par l’inhibiteur. Nous avons démontré que la transcription périodique des gènes dépendait d’une régulation quantitative par les CDKs. Par conséquence nous proposons le model, l’opposé de ce qui a été suggéré chez la S. cerevisiea. Dans notre model, la progression du cycle cellulaire ainsi que la transcription périodique des gènes sont toutes les deux sous le contrôle de l’activité des CDKs
The cyclin-dependent protein kinases (CDKs) are at the core of cell cycle control. In fission yeast, cell proliferation is regulated by CDK1/Cdc2 in association with the four cyclins Cdc13, Cig1, Cig2 and Puc1 at different stages of the cell cycle. However, this complex endogenous system can be replaced by a minimal module consisting of a fusion between Cdc2 and Cdc13 in the absence of G1/S cyclins. Surprisingly, this minimal CDK network drives the entire cell cycle in a wild type manner. Since a number of aspects of cell cycle control in fission yeast appear to be dispensable, we asked why similarly simplified circuits were not selected over the complex endogenous network during evolution. This led us to investigate the limits of such minimal systems, in particular when challenged by different stresses. Unexpectedly, we uncovered that simplification of the CDK network confers resistance to replication stress. We showed that this phenotype is independent from the CDK inhibitor Rum1 and the existing checkpoint pathways. It solely relies on operating the entire cell cycle with a single cyclin, Cdc13, and is associated with reduced genome instability when replication is challenged. However, it is not the consequence of changes in replication organisation along the chromosomes. Our data suggest that G1/S cyclin-associated Cdc2 activity may represent an alternative as yet unknown means of modulating cellular response to DNA stress. We also took advantage of a derivative of the minimal cell cycle network, in which Cdc2 is made sensitive to specific chemical inhibition. As a result, CDK activity can be externally modulated and cell cycle phases can be precisely controlled. Using this system, we re-visited the interplay between CDK and periodic transcription, a highly conserved process that is critical for proper cell proliferation. In contrast with previous studies in budding yeast, we demonstrate that periodic transcription in fission yeast is not independent from cell cycle progression. On the contrary, our work reveals that cell cycle transcriptional oscillations rely on quantitative changes in CDK activity levels. We therefore propose a new model, in which cell cycle progression and periodic transcription are intimately coupled through their common dependency on a unique input, namely CDK activity levels

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Tikad, Abdellatif. "Développement de nouvelles pyrido[3,2-d]pyrimidines polyfonctionnalisées : application à la synthèse d’inhibiteurs de CDKs." Orléans, 2008. http://www.theses.fr/2008ORLE2079.

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Les pyrido[d]pyrimidines constituent une classe de composés intéressants tant sur le plan chimique que biologique. Une des applications courante pour cette famille concerne leur utilisation dans l’élaboration de nouvelles drogues inhibitrices de kinases. Dans ce travail nous nous sommes intéressés aux pyrido[3,2-d]pyrimidines, les moins décrites dans la littérature, car leurs voies d’accès sont souvent difficiles et les produits de départ sont très onéreux. Dans le cadre de la recherche de nouveaux agents cytotoxiques et d’inhibiteurs de kinases toujours plus sélectifs, nous avons développé de nouvelles méthodologies originales, efficaces et moins coûteuses, pour la synthèse des 2,4-dichloro et 2,4,7-trichloro pyrido[3,2-d]pyrimidines. La réactivité de ces deux synthons clés a été étudiée lors de réactions de substitutions nucléophiles aromatiques et divers couplages pallado-catalysés qui ont permis l’obtention d’un large panel de molécules polyfonctionnalisées en position 2, 4 et 7. Différentes analyses pharmacologiques ont été réalisées. L’inhibition des kinases (DYRK1A, CDK5, GSK3) par nos produits originaux et l’évaluation de leur cytotoxicité sur diverses cellules humaines cancéreuses ont été réalisées. Certaines molécules ont donné des résultats extrêmement prometteurs. Les relations entre structure et activité de ces nouvelles familles de composés sont discutées.

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Books on the topic "CDKIs"

1

Lehr, Margaret B. Best practices for CDFIs: Key principles for performance. Philadelphia, PA (924 Cherry St., Second Fl, Philadelphia 19107): National Community Capital, 1998.

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Treasury, Great Britain, ed. Mapping of credit unions and community development finance institutions (CDFIs). London: HMSO, 2005.

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Chapman, Deborah Lynne. Identification of murine B-type cyclins expressed during gametogenesis and examination of their potential functions in association with CDC2 and CDKS. [New York]: [Columbia University], 1993.

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Immergluck, Daniel. CRA & CDFIs: The Community Reinvestment Act and community development financial institutions : qualified investments, community development lending, and lessons from the new CRA performance evaluations. Chicago (407 S. Dearborn, Chicago 60605): Woodstock Institute, 1998.

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Community development financial institutions (CDFIs): Their unique role and challenges serving lower-income, underserved, and minority communities : hearing before the Committee on Financial Services, U.S. House of Representatives, One Hundred Eleventh Congress, second session, March 9, 2010. Washington: U.S. G.P.O., 2010.

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United States. National Aeronautics and Space Administration, ed. Crustal Dynamics Data Information System: CDDIS. [Washington, DC: National Aeronautics and Space Administration, 1993.

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Tansey, Charles, Michael Swack, and Michael Tansey. Capital Markets, Cdfis, and Organizational Credit Risk. Lulu Press, Inc., 2010.

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Macarthur Communicative Development Inventories (Cdis): Words And Sentences. Brookes Publishing Company, 2003.

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Staff, International Monetary Fund. Coordinated Direct Investment Survey Guide 2015 (CDIS 2015). International Monetary Fund, 2015.

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Macarthur Communicative Development Inventories (Cdis): Words And Gestures. Brookes Publishing Company, 2003.

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Book chapters on the topic "CDKIs"

1

Solomon, M. J., and P. Kaldis. "Regulation of CDKs by phosphorylation." In Results and Problems in Cell Differentiation, 79–109. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-540-69686-5_4.

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Mir, Manzoor Ahmad, and Abrar Yousuf Mir. "Breast Tumor Microenvironment and CDKs." In Therapeutic potential of Cell Cycle Kinases in Breast Cancer, 149–74. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-8911-7_7.

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Gupta, Anand, Anita Kumari, Boris Kundu, and Isha Agarwal. "CDIS: Circle Density Based Iris Segmentation." In Communications in Computer and Information Science, 295–306. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03547-0_28.

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Mir, Manzoor Ahmad, and Burhan Ul Haq. "Therapeutic Implications of CDKs in Breast Cancer." In Therapeutic potential of Cell Cycle Kinases in Breast Cancer, 233–52. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-8911-7_11.

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Mir, Manzoor Ahmad, and Umar Y. Mir. "Targeting CDKs with Other Chemotherapeutic Drugs: A Combinatorial Approach." In Therapeutic potential of Cell Cycle Kinases in Breast Cancer, 269–89. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-8911-7_13.

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Noll, Carey E. "Data archiving and distribution for the Crustal Dynamics Project: The CDDIS." In Contributions of Space Geodesy to Geodynamics: Technology, 27–45. Washington, D. C.: American Geophysical Union, 1993. http://dx.doi.org/10.1029/gd025p0027.

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Pinhero, Reena, and Krassimir Yankulov. "Expression and Purification of Recombinant CDKs: CDK7, CDK8, and CDK9." In Methods in Molecular Biology, 13–28. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2926-9_3.

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Williams, Paul D., Kevin P. Anchor, John L. Bebo, Gregg H. Gunsch, and Gary D. Lamont. "CDIS: Towards a Computer Immune System for Detecting Network Intrusions." In Lecture Notes in Computer Science, 117–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/3-540-45474-8_8.

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McClendon, A. Kathleen, Jeffry L. Dean, and Erik S. Knudsen. "Regulation of Pre-RC Assembly: A Complex Symphony Orchestrated by CDKs." In Cell Cycle Deregulation in Cancer, 43–55. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_3.

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Gallastegui, Edurne, and Oriol Bachs. "Expression and Purification of Recombinant Cyclins and CDKs for Activity Evaluation." In Methods in Molecular Biology, 9–12. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2926-9_2.

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Conference papers on the topic "CDKIs"

1

Chen, Da-Ming, Y. F. Xu, and W. D. Zhu. "Non-Model-Based Multiple Damage Identification of Beams Under Spatially Dense Vibration Measurement." In ASME 2017 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/imece2017-72430.

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An effective non-model-based multiple damage identification method for beams by using a continuously scanning laser Doppler vibrometer (CSLDV) system is presented. Velocity response of a beam along a scan line under sinusoidal excitation is measured by the CSLDV system and a spatially dense operating deflection shape (ODS) of the beam along the scan line is obtained by the demodulation method from velocity response. The ODS of an associated undamaged beam is obtained by using a polynomial with a proper order to fit the ODS from the demodulation method. The curvature of an ODS (CODS) is used to identify abnormality induced by multiple damage. A curvature damage index (CDI) using differences between CODSs associated with ODSs that are obtained by the demodulation method and the polynomial fit is proposed to identify multiple damage. An auxiliary CDI obtained by averaging CDIs at different excitation frequencies is defined to further assist identification of multiple damage. Experiments on three beams with three damage on each beam in the form of three small cuts are conducted. Widths and depths of the three damage are varied from 3 mm to 9 mm with an increment of 3 mm and from 5% of thickness reduction to 15% with an increment of 5%, respectively, and their effects on ODSs, CODSs, and CDIs are investigated. Three frequencies close to natural frequencies of the beams and one randomly selected frequency that is not close to any natural frequencies of the beams are used as sinusoidal excitation frequencies. Each damage is successfully identified near regions with consistently high values of CDIs at different excitation frequencies when the damage is not close to a nodal point of an ODS. The three damage on each beam is successfully identified with the auxiliary CDI by obvious peaks at locations of the three damage.

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Saxena, Bhawanjali, Kumud Pant, Bhasker Pant, and K. R. Pardasani. "Dipeptide based SVM model for prediction of CDKs and cyclins." In 2nd International Conference on Computer and Automation Engineering (ICCAE 2010). IEEE, 2010. http://dx.doi.org/10.1109/iccae.2010.5451233.

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Saxena, Bhawanjali, Kumud Pant, Bhasker Pant, and Neeru Adlakha. "Hybrid based SVM model for prediction of CDKs and cyclins." In 2nd International Conference on Computer and Automation Engineering (ICCAE 2010). IEEE, 2010. http://dx.doi.org/10.1109/iccae.2010.5451262.

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Zhao, Tianna, Riccardo Serra, Michelle Guo, Peter C. Burger, Lisa M. Rooper, Betty Tyler, Christine L. Hann, and Gary L. Gallia. "CDKS Blockade Enhances In Vivo Efficacy of EGFR Inhibition in Chordomas." In Special Virtual Symposium of the North American Skull Base Society. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725264.

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Stevens, K. J., K. Lichti, I. A. Minchington, N. Janke-Gilman, T. Mactutis, D. Rook, and P. Bondurant. "Conductor Damage Inspection System for overhead ACSR power cables CDIS on ACSR." In 2013 Seventh International Conference on Sensing Technology (ICST). IEEE, 2013. http://dx.doi.org/10.1109/icsenst.2013.6727780.

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Rajput, Sandeep, Zhanfang Guo, and Cynthia Ma. "Abstract 3097: CDKs inhibitor: potential monotherapy for treatment of triple-negative breast cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3097.

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Lu, Shuyan, Wenyue Hu, Tae Sung, Brad Hirakawa, Marina Amaro, and Bart Jessen. "Abstract 99: Phenotypic characterization of knockdown of CDKs in the intestinal epithelial cells." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-99.

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Tadesse, Solomon, Laychiluh Bantie, Khamis Tomusange, Saiful Islam, Muhammed H. Rahaman, Benjamin Noll, Frankie Lam, Mingfeng Yu, and Shudong Wang. "Abstract 2353: CDKI-15, a novel and highly selective CDK4/6 inhibitor: discovery,in vitroandin vivoanticancer efficacy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2353.

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Rieß, C., CF Classen, and C. Maletzki. "CDKs as target structures for cancer therapy – an in vitro analysis on patient-derived glioblastoma cell lines." In 28th Annual Meeting of the working group “Experimental Neuro-Oncology”. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1696331.

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Shapiro, G. "Abstract MS1-1: Beyond CDK 4/6: Targeting additional cell cycle and transcriptional CDKs in breast cancer." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-ms1-1.

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Reports on the topic "CDKIs"

1

Tansey, Charles, Michael Swack, Michael Tansey, and Vicky Stein. Capital markets, CDFIs, and organizational credit risk. University of New Hampshire Libraries, 2010. http://dx.doi.org/10.34051/p/2020.123.

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Jayson Wharton, Edward Seabury, Gus Caffrey, and Phili. Summary Report: INL CDCIS Cask Scanner Testing at. Office of Scientific and Technical Information (OSTI), April 2013. http://dx.doi.org/10.2172/1087695.

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Swack, Michael, Eric Hangen, and Jack Northrup. CDFIs Stepping into the Breach: An Impact Evaluation—Summary Report. University of New Hampshire Libraries, 2015. http://dx.doi.org/10.34051/p/2020.228.

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Northrup, Jack, Eric Hangen, and Michael Swack. CDFIs and Online Business Lending: A Review of Recent Progress, Challenges, and Opportunities. University of New Hampshire Libraries, 2016. http://dx.doi.org/10.34051/p/2020.276.

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Williams, Teshanee, Jamie McCall, Natalie Prochaska, and Tamra Thetford. How Community Development Financial Institutions (CDFIs) are shaped by Funders through Data Collection, Impact Measurement, and Evaluation. Carolina Small Business Development Fund, November 2022. http://dx.doi.org/10.46712/cdfi.evaluation.pressures.

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Community Development Financial Institutions (CDFIs) are grassroots organizations that provide equitable access to financial capital. While a robust body of evidence supports the ability of CDFIs to promote holistic and sustainable development, attempts to systematically evaluate the industry have yielded disparate and often confounding results. We apply an institutional theory lens to examine challenges to meaningful data collection, impact measurement, and program evaluation. Our data show how regulators, major funders, and third-party rating organizations have applied indirect and direct pressures that have systematically lowered the capacity of nonprofit CDFI loan funds. This combination of coercive, mimetic, and normative isomorphic forces has (1) hampered meaningful data collection, (2) created a lack of staff expertise in these areas, (3) raised the cost and complexity of utilizing technology systems to improve evaluation processes, and (4) fostered industry norms which de-prioritize meaningful evaluation. The data suggest several ways for stakeholders to improve these trends. For example, funders might consider providing support which builds organizational capacity via unrestricted operating grants and recurring financial commitments.

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Tansey, Charles, and Michael Swack. The Potential Role For CDFIs in the Opportunity Zones of the Investing in Opportunities Act (IIOA). University of New Hampshire Libraries, 2019. http://dx.doi.org/10.34051/p/2020.350.

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McCall, Jamie, and Emily Stallings. Assessing Public, Private, and Philanthropic Support for CDFIs: Data on Contributing Operating Revenues and Measures of Efficiency. Carolina Small Business Development Fund, December 2020. http://dx.doi.org/10.46712/cdfi.revenue.sources.

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Hangen, Eric, and Michael E. Hangen. CDFIs Can Make the SBA PPP Loan Program Work for Smaller, Minority-Owned, and Women-Owned, Small Businesses. University of New Hampshire Libraries, 2020. http://dx.doi.org/10.34051/p/2020.386.

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McCall, Jamie, Nora Anzawi, Miles Zeller, and James Onorevole. Growth, Equity, and Individual Welfare: A Theoretical Framework for “Moving the Needle” on CDFI Impact Evaluation. Carolina Small Business Development Fund and AltCap, January 2023. http://dx.doi.org/10.46712/evaluation.frameworks.

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Community development financial institutions (CDFI) are grassroots entities that guide sustainable economic growth by prioritizing the needs of marginalized populations. Traditionally, CDFIs have been evaluated by the extent to which their activities foster local development or lessen economic inequities. Our analysis suggests this phenomenon is the result of deeply entrenched alliances between the public sector and the interests of CDFI stakeholders. These institutions are major resource providers and thus have set the narrative around CDFI impact measurement and evaluation. We propose an alternative framework that prioritizes changes in individual welfare which foster economic autonomy and improve relationships with community institutions. Our framework is admittedly theoretical, and further iteration will be required to operationalize it into a workable concept. Ultimately though, the existing framework around these issues is broken – and we find scant evidence that it can be salvaged.

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