Treatment FAQ

what is treatment differentiation in research

by Winifred Murphy Published 2 years ago Updated 2 years ago
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Research: Treatment Adherence & Treatment Differentiation. Treatment adherence consists of 2 components: Treatment Adherence : degree in which the treatment is conducted in accordance with the theoretical model and prescribed technique. Treatment Differentiation: degree in which different treatments differ in the intended direction with respect to therapeutic interventions (e.g. comparative outcomes).

' (treatment differentiation). Establishing fidelity to the manualised therapy, and differentiation between the treatment arms, are essential validity step towards interpreting the relative effectiveness of different treatment approaches, which is key to the primary and secondary objectives of this study.

Full Answer

What is differentiation therapy for cancer?

Differentiation therapy is based on the concept that cancer cells are normal cells that have been arrested at or have gone back to an immature or less differentiated state, lack the ability to control their own growth, and so multiply at an abnormally fast rate.

How do you measure treatment integrity and treatment differentiation?

Once the treatment fidelity measure was finalized, we assessed treatment integrity and treatment differentiation by examining the mean number of times a therapist behavior occurred (e.g., “gave feedback on effort”), and mean competence scores in therapy sessions, in both the EMR group and the standard of care group.

What is treatment fidelity in outcomes research?

This issue is known as treatment fidelity. Attaining and demonstrating treatment fidelity in outcomes research enable researchers to isolate the active ingredients of an intervention, determine its efficacy, contrast it with a control or standard treatment, and replicate findings.

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What are the three major approaches to treatments?

With the agreement of these partners, the scope of the expert assessment covered three major psychotherapeutic approaches—the psychodynamic (psychoanalytical) approach, the cognitive-behavioural approach, and family and couple therapy—often used to care for defined disorders of adults, adolescents, or children.

What are the different treatment types?

This article will provide an overview of the different types of therapy available.Cognitive-behavioral therapy. ... Dialectical behavior therapy. ... Eye movement desensitization and reprocessing therapy. ... Exposure therapy. ... Interpersonal therapy. ... Mentalization-based therapy. ... Psychodynamic therapy. ... Animal-assisted therapy.More items...•

What are the two components of treatment fidelity?

Treatment fidelity consists of two general components: 1) treatment integrity, the degree to which a treatment is implemented as intended, and 2) treatment differentiation, the degree to which two or more study arms differ along critical dimensions (2, 3, 4, 5).

What is meant by treatment fidelity?

Purpose: Treatment fidelity is a measure of the reliability of the administration of an intervention in a treatment study. It is an important aspect of the validity of a research study, and it has implications for the ultimate implementation of evidence-supported interventions in typical clinical settings.

What are two types of treatments?

Types of Treatment MethodsTargeted Therapies: A targeted therapy is designed to treat only the cancer cells and minimize damage to normal, healthy cells. ... Chemotherapy: ... Surgery: ... Radiation Therapies: ... Biological Therapy: ... Hormonal Therapy:

What are the 5 therapy methods?

Approaches to psychotherapy fall into five broad categories:Psychoanalysis and psychodynamic therapies. ... Behavior therapy. ... Cognitive therapy. ... Humanistic therapy. ... Integrative or holistic therapy.

What does fidelity mean in research?

Perspective. Intervention fidelity refers to the degree to which a specific intervention is implemented as intended,1,2 critically supporting effectiveness research. Fidelity measurement underlies the reliable examination of the effect of interventions, particularly when 2 or more interventions are compared.

Why is treatment fidelity important?

Treatment fidelity means assuring that the treatment in a research study is conducted consistently and reliably. That is very important is because the outcomes of treatment research ends up affecting patient care and the quality of care that patients receive.

How do you assess treatment fidelity?

In clinical research treatment fidelity is typically attained by intensive training and supervision techniques and demonstrated by measuring therapist adherence and competence to the protocol using external raters.

What is fidelity in data collection?

Fidelity refers to implementing a program or curriculum as intended, which can be a key factor in its success and whether it positively moves youth outcomes. Fidelity monitoring refers to a system of measuring and analyzing the degree to which a program is implemented as intended.

How do you ensure fidelity in research?

Five main components of Fidelity in ResearchAdherence | Delivered program aligned to protocol. ... Exposure/Dose | Amount of program content that reached intended participants. ... Quality of Delivery | Intervention implementation success (not outcomes, just delivery)More items...

What is treatment feasibility?

In addition a dual treatment selection process may emerge. Specifically a feasible short-term treatment is immediately implemented while a long-term plan to build systematic capacity for a preferable treatment is developed and activated.

How does differentiation therapy work for cancer?

Differentiation therapy exerts its function by switching a malignant cancer cell into a benign phenotype as well as forcing CSCs to differentiate and lose their self-renewal properties . Similarly, the current treatment for APL, which consists of the combined use of all-trans retinoic acid (ATRA) and anthracycline-based chemotherapy, generally results in a high rate of complete cytogenetic remission (approximately 90%) and an overall survival rate of 80% in the initial phase [111]. It has been speculated that treatment with ATRA can induce apoptosis of leukemic cells due to its effect on the differentiation process [95]. There have been reports that ATRA could induce differentiation of EpCAM + LCSCs, which could be monitored by a notable reduction in the expression of CSC marker and the induction of expression of liver-specific genes. Furthermore, a more pronounced therapeutic effect could be observed when ATRA was combined with cisplatin compared with cisplatin treatment alone. This finding suggests that the combined treatment with differentiation therapy and conventional chemotherapy might be an effective strategy for HCC treatment [112]. Moreover, As 2 O 3 has been shown to be able to induce differentiation of LCSCs by inhibiting the expression of stemness-related genes in vitro and to decrease recurrence and prolong survival of mice in vivo without apparent toxicity. Mechanistic studies have revealed that As 2 O 3 promotes differentiation of LCSCs by targeting the expression of GLI1, further suggesting the clinical significance of As 2 O 3 in LCSC-targeted therapy [113]. A recent study showed that overexpression of TFPI-2 markedly suppressed proliferation and induced apoptosis of hepatoma cells. Moreover, the expression of LCSC markers was significantly reduced, while the expression of hepatocyte markers was notably elevated in the TFPI-2-overexpressing hepatoma cells, suggesting that TFPI-2 might differentiate LCSCs into hepatocytes [114].

What is the premise of differentiation therapy?

The underlying premise of differentiation therapy is that tumor cells can be reprogrammed to differentiate and to cease proliferation, thereby controlling their tumorigenic and malignant potential (Leszczyniecka et al., 2001; Staudt et al., 2007 ). Although a number of agents have been studied over the years, the most thoroughly examined and clinically tested as a differentiating agent is RA (Vitamin A), in particular ATRA. RA-induced differentiation therapy has acquired a therapeutic niche in treatment of APL and the ability of RA to prevent cancer and induce differentiation is currently being investigated ( Gudas & Wagner, 2011; Karsy, Albert, Tobias, Murali, & Jhanwar-Uniyal, 2010; Sell, 2004 ). Salinomycin is reported to induce expression of the epithelial/MET marker E-cadherin in these tumors, indicating that salinomycin might eradicate CSCs by inducing their differentiation ( Beug, 2009 ). CD105 + renal CSCs treated with rhIL-15 were observed to undergo epithelial differentiation of all CD105 + CSC subsets and blocked CSC self-renewal and their tumorigenic properties in severe combined immunodeficient mice ( Azzi et al., 2011 ).

What is the role of 1,25 OH 2 D in cancer?

A number of important mechanisms have been implicated in 1,25 (OH) 2 D 3 -mediated growth inhibition. These include (i) induction of cell cycle arrest, (ii) promotion of apoptosis, (iii) stimulation of differentiation, (iv) anti-angiogenesis, and (v) regulation of adherence and signaling between epithelial cells. Although the role of 1,25 (OH) 2 D in cancer has been traditionally linked strongly to antiproliferation and proapoptosis, there is now evidence for the role of 1,25 (OH) 2 D in other cancer-related signaling pathways. Studies in breast and prostate cancer have revealed anti-inflammatory effects of 1,25 (OH) 2 D 3 through the inhibition of prostaglandin synthesis and actions as well as the inactivation of stress-induced kinase signaling and downstream production of inflammatory cytokines, suggesting a role for vitamin D in cancer chemoprevention [379,380]. Vitamin D has broader anti-inflammatory actions [358], including inhibition of the NF-kappa-B pathway [381]. Other anticancer pathways have been discovered. In vitro and in vivo studies have demonstrated that 1,25 (OH) 2 D decreases estrogen signaling by inhibiting estrogen synthesis and action in breast cancer cells [382,383]. Disruption of the Wnt/β-catenin signaling pathway has been implicated in the actions of 1,25 (OH) 2 D [384], especially in colon cancers [333]. In addition to its impact on the VDR–β-catenin interactions, 1,25 (OH) 2 D is also known to regulate the expression of Wnt regulators such as Dickkopf (DKK) and DKK-1 [334].

Can biliary tumors be differentiated?

Biliary tract tumors may be particularly amenable to differentiation therapy given that more than 30% of CCA cells express cancer stem cell markers, which is in stark contrast to less than 3% in other cancer types.41 Indeed, such dedifferentiated features could be driven by epigenome remodeling. Evidence in support of these epimutational processes includes reactivation of the fetal oncoprotein IMP3 by promoter hypomethylation in 82% of iCCA patients. 42 More globally, HOX genes were among the earliest reported targets from epigenome-wide studies in CCA. As such, HOXA9 and HOXD9 have been shown to be hypermethylated in 86% and 89% of biliary tumors, respectively, and more broadly polycomb repressive complex 2 (PRC2) target genes were identified to be more susceptible to aberrant methylation in CCA. 43 Another study focusing on eCCA identified 970 hypermethylated CpG island promoters, 10% of which mapped to HOX genes. 44 Moreover, expression of these genes was restored by treatment with hypomethylating agent 5′-aza-2′-deoxycytidine. Such extensive, recurrent, and rescuable DNA methylome remodeling of particular developmental genes highlights the potential of differentiation therapy in these patients.

What is differentiation therapy?

Differentiation therapy: An approach to the treatment of advanced or aggressive malignancies in which the malignant cells are treated so that they can resume the process of maturation and differentiation into mature cells. Differentiation therapy is based on the concept that cancer cells are normal cells ...

Does ATRA induce remission?

It causes the promyelocytes to differentiate (to mature) and so deters them from proliferating. ATRA induces a complete remission in about 70% of cases. ATRA is the prototype of a differentiation therapy agent. CONTINUE SCROLLING OR CLICK HERE.

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