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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

A In the CRPC II trial, median OS has not been achieved after 3 years, although 39 % of the patients did not show objective response (>50 % PSA response) to cellular therapy in situ. B Response in bone scan was observed in six of six patients. C Control of paraneoplastic lupus erythematosus was associated with objective tumor response. D Therapy response was on-going in six patients beyond stop of study medication (5 to 18 months) due to non-oncologic surgery. Following resistance to cellular therapy in situ, 60 % of the studied patients regained responsiveness against gonadotropin-releasing hormone (GnRH) agonists
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Fig2: A In the CRPC II trial, median OS has not been achieved after 3 years, although 39 % of the patients did not show objective response (>50 % PSA response) to cellular therapy in situ. B Response in bone scan was observed in six of six patients. C Control of paraneoplastic lupus erythematosus was associated with objective tumor response. D Therapy response was on-going in six patients beyond stop of study medication (5 to 18 months) due to non-oncologic surgery. Following resistance to cellular therapy in situ, 60 % of the studied patients regained responsiveness against gonadotropin-releasing hormone (GnRH) agonists

Mentions: A limited pattern of hallmarks of cancer could be clinically monitored, such as inflammation, via CRP response, in RCCC I/II (n = 18; n = 31) (Fig. 1), in MM (n = 6) and mLCH (n = 2), immune response in one patient with CRPC (CRPC I) (Fig. 2).Fig. 1


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)

A In the CRPC II trial, median OS has not been achieved after 3 years, although 39 % of the patients did not show objective response (>50 % PSA response) to cellular therapy in situ. B Response in bone scan was observed in six of six patients. C Control of paraneoplastic lupus erythematosus was associated with objective tumor response. D Therapy response was on-going in six patients beyond stop of study medication (5 to 18 months) due to non-oncologic surgery. Following resistance to cellular therapy in situ, 60 % of the studied patients regained responsiveness against gonadotropin-releasing hormone (GnRH) agonists
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig2: A In the CRPC II trial, median OS has not been achieved after 3 years, although 39 % of the patients did not show objective response (>50 % PSA response) to cellular therapy in situ. B Response in bone scan was observed in six of six patients. C Control of paraneoplastic lupus erythematosus was associated with objective tumor response. D Therapy response was on-going in six patients beyond stop of study medication (5 to 18 months) due to non-oncologic surgery. Following resistance to cellular therapy in situ, 60 % of the studied patients regained responsiveness against gonadotropin-releasing hormone (GnRH) agonists
Mentions: A limited pattern of hallmarks of cancer could be clinically monitored, such as inflammation, via CRP response, in RCCC I/II (n = 18; n = 31) (Fig. 1), in MM (n = 6) and mLCH (n = 2), immune response in one patient with CRPC (CRPC I) (Fig. 2).Fig. 1

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