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Anakoinosis: Communicative Reprogramming of Tumor Systems - for Rescuing from Chemorefractory Neoplasia.

Hart C, Vogelhuber M, Wolff D, Klobuch S, Ghibelli L, Foell J, Corbacioglu S, Rehe K, Haegeman G, Thomas S, Herr W, Reichle A - Cancer Microenviron (2015)

Bottom Line: Cellular therapy in situ consisted of repurposed drugs, pioglitazone plus all-trans retinoic acid or dexamethasone or interferon-alpha (dual transcriptional modulation) combined with metronomic low-dose chemotherapy or low-dose 5-azacytidine, plus/minus classic targeted therapy.The novel therapeutic tools for specifically designing communication processes within tumor diseases focus on redirecting (1) rationalizations of cancer hallmarks (constitution of single cancer hallmarks), (2) modular events, (3) the 'metabolism' of evolutionary processes (the sum of therapeutically and intrinsically inducible evolutionary processes) and (4) the holistic communicative context, which determines validity and denotation of tumor promoting communication lines.Published data on cellular therapies in situ (6 histologic tumor types, 144 patients, age 0.9-83 years) in castration-resistant prostate cancer, pretreated renal clear cell carcinoma, chemorefractory acute myelocytic leukemia, multiple myeloma > second-line, chemorefractory Hodgkin lymphoma or multivisceral Langerhans cell histiocytosis, outline the possibility for treating refractory metastatic cancer with the hope that this type of reprogrammed communication will be scalable with minimal toxicity.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine III, Haematology & Oncology, University Hospital of Regensburg, Regensburg, Germany.

ABSTRACT
Disruptive technologies, such as communicative reprogramming (anakoinosis) with cellular therapies in situ for treating refractory metastatic cancer allow patient care to accelerate along a totally new trajectory and highlight what may well become the next sea change in the care of patients with many types of advanced neoplasia. Cellular therapy in situ consisted of repurposed drugs, pioglitazone plus all-trans retinoic acid or dexamethasone or interferon-alpha (dual transcriptional modulation) combined with metronomic low-dose chemotherapy or low-dose 5-azacytidine, plus/minus classic targeted therapy. The novel therapeutic tools for specifically designing communication processes within tumor diseases focus on redirecting (1) rationalizations of cancer hallmarks (constitution of single cancer hallmarks), (2) modular events, (3) the 'metabolism' of evolutionary processes (the sum of therapeutically and intrinsically inducible evolutionary processes) and (4) the holistic communicative context, which determines validity and denotation of tumor promoting communication lines. Published data on cellular therapies in situ (6 histologic tumor types, 144 patients, age 0.9-83 years) in castration-resistant prostate cancer, pretreated renal clear cell carcinoma, chemorefractory acute myelocytic leukemia, multiple myeloma > second-line, chemorefractory Hodgkin lymphoma or multivisceral Langerhans cell histiocytosis, outline the possibility for treating refractory metastatic cancer with the hope that this type of reprogrammed communication will be scalable with minimal toxicity. Accessibility to anakoinosis is a tumor inherent feature, and cellular therapy in situ addresses extrinsic and intrinsic drug resistance, by redirecting convergent organized communication tools, while been supported by quite different pattern of (molecular-)genetic aberrations.

No MeSH data available.


Related in: MedlinePlus

Left site showing C-reactive protein (CRP) follow-up during chemo- and brentuximab-vedotin refractory cHL. The add-on of everolimus to combined transcriptional modulation with pioglitazone and dexamethasone plus metronomic low-dose chemotherapy led to PET negativity and continuous CR following allogeneic blood stem cell transplantation. The right site indicates that chemorefractory mLCH may respond with cCR following cHL-therapy without everolimus. But patient two with chemorefractory mLCH needed the add-on of temsirolimus to achieve cCR
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Fig3: Left site showing C-reactive protein (CRP) follow-up during chemo- and brentuximab-vedotin refractory cHL. The add-on of everolimus to combined transcriptional modulation with pioglitazone and dexamethasone plus metronomic low-dose chemotherapy led to PET negativity and continuous CR following allogeneic blood stem cell transplantation. The right site indicates that chemorefractory mLCH may respond with cCR following cHL-therapy without everolimus. But patient two with chemorefractory mLCH needed the add-on of temsirolimus to achieve cCR

Mentions: In mLCH, CRP levels normalized in response to compassionate use therapy (Fig. 3) [25].Fig. 3


Anakoinosis: Communicative Reprogramming of Tumor Systems - for Rescuing from Chemorefractory Neoplasia.

Hart C, Vogelhuber M, Wolff D, Klobuch S, Ghibelli L, Foell J, Corbacioglu S, Rehe K, Haegeman G, Thomas S, Herr W, Reichle A - Cancer Microenviron (2015)

Left site showing C-reactive protein (CRP) follow-up during chemo- and brentuximab-vedotin refractory cHL. The add-on of everolimus to combined transcriptional modulation with pioglitazone and dexamethasone plus metronomic low-dose chemotherapy led to PET negativity and continuous CR following allogeneic blood stem cell transplantation. The right site indicates that chemorefractory mLCH may respond with cCR following cHL-therapy without everolimus. But patient two with chemorefractory mLCH needed the add-on of temsirolimus to achieve cCR
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4542828&req=5

Fig3: Left site showing C-reactive protein (CRP) follow-up during chemo- and brentuximab-vedotin refractory cHL. The add-on of everolimus to combined transcriptional modulation with pioglitazone and dexamethasone plus metronomic low-dose chemotherapy led to PET negativity and continuous CR following allogeneic blood stem cell transplantation. The right site indicates that chemorefractory mLCH may respond with cCR following cHL-therapy without everolimus. But patient two with chemorefractory mLCH needed the add-on of temsirolimus to achieve cCR
Mentions: In mLCH, CRP levels normalized in response to compassionate use therapy (Fig. 3) [25].Fig. 3

Bottom Line: Cellular therapy in situ consisted of repurposed drugs, pioglitazone plus all-trans retinoic acid or dexamethasone or interferon-alpha (dual transcriptional modulation) combined with metronomic low-dose chemotherapy or low-dose 5-azacytidine, plus/minus classic targeted therapy.The novel therapeutic tools for specifically designing communication processes within tumor diseases focus on redirecting (1) rationalizations of cancer hallmarks (constitution of single cancer hallmarks), (2) modular events, (3) the 'metabolism' of evolutionary processes (the sum of therapeutically and intrinsically inducible evolutionary processes) and (4) the holistic communicative context, which determines validity and denotation of tumor promoting communication lines.Published data on cellular therapies in situ (6 histologic tumor types, 144 patients, age 0.9-83 years) in castration-resistant prostate cancer, pretreated renal clear cell carcinoma, chemorefractory acute myelocytic leukemia, multiple myeloma > second-line, chemorefractory Hodgkin lymphoma or multivisceral Langerhans cell histiocytosis, outline the possibility for treating refractory metastatic cancer with the hope that this type of reprogrammed communication will be scalable with minimal toxicity.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine III, Haematology & Oncology, University Hospital of Regensburg, Regensburg, Germany.

ABSTRACT
Disruptive technologies, such as communicative reprogramming (anakoinosis) with cellular therapies in situ for treating refractory metastatic cancer allow patient care to accelerate along a totally new trajectory and highlight what may well become the next sea change in the care of patients with many types of advanced neoplasia. Cellular therapy in situ consisted of repurposed drugs, pioglitazone plus all-trans retinoic acid or dexamethasone or interferon-alpha (dual transcriptional modulation) combined with metronomic low-dose chemotherapy or low-dose 5-azacytidine, plus/minus classic targeted therapy. The novel therapeutic tools for specifically designing communication processes within tumor diseases focus on redirecting (1) rationalizations of cancer hallmarks (constitution of single cancer hallmarks), (2) modular events, (3) the 'metabolism' of evolutionary processes (the sum of therapeutically and intrinsically inducible evolutionary processes) and (4) the holistic communicative context, which determines validity and denotation of tumor promoting communication lines. Published data on cellular therapies in situ (6 histologic tumor types, 144 patients, age 0.9-83 years) in castration-resistant prostate cancer, pretreated renal clear cell carcinoma, chemorefractory acute myelocytic leukemia, multiple myeloma > second-line, chemorefractory Hodgkin lymphoma or multivisceral Langerhans cell histiocytosis, outline the possibility for treating refractory metastatic cancer with the hope that this type of reprogrammed communication will be scalable with minimal toxicity. Accessibility to anakoinosis is a tumor inherent feature, and cellular therapy in situ addresses extrinsic and intrinsic drug resistance, by redirecting convergent organized communication tools, while been supported by quite different pattern of (molecular-)genetic aberrations.

No MeSH data available.


Related in: MedlinePlus