Regelmatig kijk ik op slideshare naar presentaties van oncologen wereldwijd (in de hoop recente nuttige behandelinformatie aan te treffen). Behoudens het feit dat ik letterlijk lees dat artsen vb. in Maleisie 350 dollar per maand bonus ontvangen van verzekeraars om bepaalde kostenefficiente kankermedicatie voor te schrijven (en dit voor hun patienten verzwijgen), en het feit dat mensenlevens alleen maar gerelateerd worden aan zgn kosteneffeciente behandelingen (waarbij men zelfs niet schroomt om oude medicatie her in te voeren en te beperken door vb. maximaal 3 behandelmogelijkheden!), werd mijn aandacht getrokken naar de volgende presentatie ....
http://www.slideshare.net/planet--ayurveda/herbs-for-breast-cancer?qid=2f18df66-d9ed-4908-a1e0-2b6ff04f5d46&v=default&b=&from_search=11
Presentatie is van een ayurvedische arts uit India, die weliswaar geld hieraan verdient, maar zeer uitgebreid beargumenteerd wat waarvoor te gebruiken is en vooral waarom.
(eerst account aanmaken bij slideshare)
Blijkbaar heb ik mijn huiswerk vanaf het begin al goed gedaan.
Inmiddel gebruik ik al geruime tijd dagelijks flexseed (lijnzaadolie vloeibaar en zaadjes), garlic (verse knoflook), curcumine (long curcumine met zwarte peper), en sinds kort wheetgrass (opbouwende relatief hoge dosering gerstegras).
Ik raak steeds meer geboeid door de ayervedische kruiden en ondersteuning bij kanker-behandeling(en) die uiteraard uit gaat van bestaande ayurvedische kruiden o.a. uit het Himalaya gebergte.
Nu nog de leefstijlverandering consequent gaan toepassen (waar langzaam naar toe gewerkt wordt) .... .
dinsdag 31 maart 2015
donderdag 26 maart 2015
Potassium, sodium en kanker (update met link naar uitgebreide - zeer interessante - presentatie over potassium houdende voedingswaren)
Potassium.. toen ik in Duitsland was werd dit direct opgemeten. Pas nu heb ik de tijd, de kracht en de energie om uit te zoeken waarom men dit in Duitsland opmeet en men hier zoveel waarde aan hecht.
Volgend onderzoeksresultaat uit 1996 (van het MD Anderson Cancer centrum uit Texas) vond ik in pubmed..
Volgend onderzoeksresultaat uit 1996 (van het MD Anderson Cancer centrum uit Texas) vond ik in pubmed..
J Environ Pathol Toxicol Oncol. 1996;15(2-4):65-73.
Potassium, sodium, and cancer: a review.
Abstract
Agents
known or believed to be carcinogenic decrease the concentration of
potassium and increase the concentration of sodium in the cells.
Anticarcinogenic agents have the opposite effect. In all cases where we
have information on an agent's carcinogenicity or anticarcinogenicity
and on that agent's effects on cellular potassium and sodium
concentrations the above relationships have been found to be true.
Dietary carcinogenic agents studied include sodium, cadmium, fat,
cholesterol, calories, and alcohol; dietary anticarcinogenic agents
include potassium, vitamins A, C, and D, selenium, and fiber. The effect
of calcium intake is less clear as that effect depends on the
concentrations on sodium and potassium. Not only dietary agents but also
other carcinogenic and anticarcinogenic agents work in the same way.
The cancer-causing drug dimethylhydrazine increases sodium and decreases
potassium in the cells, whereas, for example, indomethacin, an
anticarcinogen, has the opposite effect. In aging potassium leaves the
cells, sodium enters them, and the rates of cancer increase. Patients
with hyperkalemic diseases (Parkinson, Addison) have reduced cancer
rates, and patients with hypokalemic diseases (alcoholism, obesity,
stress) have increased cancer rates.
Sinds vandaag neem ik 1000 mg organische gerstengras (barley grass) per dag.
Gerstengras werkt ook als Detox vandaar dat je eerst moet starten met 2 x 500 mg. per dag (aanbevolen hoeveelheid 6 tot 10 capsules per dag).
Ik gebruik dit na extensive research en op aanraden van een medekankerpatient van de biomed kliniek uit Duitsland (inmiddels kankervrij verklaard).
Gedroogde abrikozen en pruimen bevatten de meeste potassium. Een overdosis innemen aan potassium is onmogelijk.
In gerstengras zit o.a. vitamine A, C, en Potassium.
Selenium nam ik al. Alcohol nuttig ik nooit. Stress probeer ik te vermijden....
Voor meer informatie
http://www.rainforestfoods.co.uk/barley-grass/
Van elk product dat verkocht wordt bij Rain Forest wordt er 1 m2 cloud forest in Ecuador gesponserd.
Onderstaande presentatie van een ayurveda arts uit India is zeer boeiend (geeft ook meer uitleg over waarom je potassium waarde niet (te) hoog mag zijn. Overigens wordt de potassiumwaarde ook verhoogd door medicatie (oa ontstekingsremmende middelen).
http://www.slideshare.net/planet--ayurveda/foods-with-low-and-high-potassium-ckd-diet?related=2
Ik denk dat je eerst even een account moet aanmaken om toegang te krijgen tot slideshare.
Sinds vandaag neem ik 1000 mg organische gerstengras (barley grass) per dag.
Gerstengras werkt ook als Detox vandaar dat je eerst moet starten met 2 x 500 mg. per dag (aanbevolen hoeveelheid 6 tot 10 capsules per dag).
Ik gebruik dit na extensive research en op aanraden van een medekankerpatient van de biomed kliniek uit Duitsland (inmiddels kankervrij verklaard).
Gedroogde abrikozen en pruimen bevatten de meeste potassium. Een overdosis innemen aan potassium is onmogelijk.
In gerstengras zit o.a. vitamine A, C, en Potassium.
Selenium nam ik al. Alcohol nuttig ik nooit. Stress probeer ik te vermijden....
Voor meer informatie
http://www.rainforestfoods.co.uk/barley-grass/
Van elk product dat verkocht wordt bij Rain Forest wordt er 1 m2 cloud forest in Ecuador gesponserd.
Onderstaande presentatie van een ayurveda arts uit India is zeer boeiend (geeft ook meer uitleg over waarom je potassium waarde niet (te) hoog mag zijn. Overigens wordt de potassiumwaarde ook verhoogd door medicatie (oa ontstekingsremmende middelen).
http://www.slideshare.net/planet--ayurveda/foods-with-low-and-high-potassium-ckd-diet?related=2
Ik denk dat je eerst even een account moet aanmaken om toegang te krijgen tot slideshare.
dinsdag 24 maart 2015
Kahlers disease preliminary study of the effect of CURCUMIN p53 protein in a human multiple myeloma cell line.
Curcumin
inhibited the proliferation of the MM RPMI 8226 cells in a dose- and
time-dependent manner. In the MM RPMI 8226 cells treated with curcumin, the expression of the p53 and Bax genes was upregulated, while the expression of the MDM2 gene was downregulated. p53 protein expression was higher in the curcumin experimental group compared with the control group. Subsequent to treatment with curcumin,
the growth of the MM RPMI 8226 cell line was inhibited in a
concentration- and time-dependent manner. In the MM RPMI 8226 cells
treated with curcumin, p53 protein levels were upregulated, which suggested that curcumin may promote the apoptosis of MM cells by upregulating p53 protein expression.
Curcumine kan op internet besteld worden (beste is denk ik, van Jacob Hooy - Nederlands bedrijf die ook bijvoorbeeld excellente losse groene thee verkoopt).
Let op dit is geen gewone curcumine maar de curcumine LONGA.
Op de volgende site voor 110 gram kost dit slechts 7,99 euro (excl verzendkosten).
http://puurenkracht.nl/products/curcuma-longa-110-gram-jacob-hooy
Curcumine kan op internet besteld worden (beste is denk ik, van Jacob Hooy - Nederlands bedrijf die ook bijvoorbeeld excellente losse groene thee verkoopt).
Let op dit is geen gewone curcumine maar de curcumine LONGA.
Op de volgende site voor 110 gram kost dit slechts 7,99 euro (excl verzendkosten).
http://puurenkracht.nl/products/curcuma-longa-110-gram-jacob-hooy
zondag 22 maart 2015
Geneeskundige kracht van ongekookte brocolli(spruiten)/koolsoorten, enzymen antikankereigenschappen en detoxeigenschappen
([Systemic enzymotherapy as a method of prophylaxis of postradiation complications in oncological patients].
[Article in Ukrainian]Hubarieva HO, Kindzel's'kyĭ LP, Ponomar'ova OV, Udatova TV, Shpil'ova SI, Smolanka II, Korovin SI, Ivankin VS.)
Abstract
Set out in the paper are results of treatment of those patients with carcinoma of the lung, uterine cervix, hysterocarcinoma, breast cancer, malignant thymomas, malignant non-Hodgkin's lymphomas, and lymphogranulematosis having been administered combined, chemoradiation or radiation treatments against the background of a complex of accompanying therapy involving systemic enzymotherapy. Polyenzymic drugs were found to be capable of improving results of treatment of acute radiation reactions and preventing postradiation fibrous changes in the lungs, skin, fatty tissue, soft tissue, liver, kidneys. Thus, systemic enzymotherapy is capable of improving the quality of life and results of treatment of oncological patients.
http://www.ncbi.nlm.nih.gov/pubmed/16786662http://www.ncbi.nlm.nih.gov/pubmed/16786662Systemic enzymotherapy as a method of prophylaxis of postradiation complications in oncological patients
http://mens-en-gezondheid.infonu.nl/gezonde-voeding/134463-de-geneeskracht-van-broccolispruiten-of-broccolikiemen.html#enzymen-met-antioxidantwerking.
In verband met de auteursrechten kan ik alleen deze link vermelden maar de inhoud van dit artikel gaat veel verder dan een publicatie vd kankerstichting over gezonde voeding voor kankerpatienten. Dat is wat ik mis.Miljoenen worden gespendeerd aan research...kankerpatienten kunnen actief bijdragen aan hun herstel maar missen de kennis terzake!
Patent op voeding is niet mogelijk dus commercieel niet belangrijk maar zo ontzetend belangrijk voor alle kankerpatienten!
Duitse behandelaars schrijven Wobenzymen P voor...
Nederlandse artsen bestempelen het als kwakzalverij.
[Article in Ukrainian]Hubarieva HO, Kindzel's'kyĭ LP, Ponomar'ova OV, Udatova TV, Shpil'ova SI, Smolanka II, Korovin SI, Ivankin VS.)
Abstract
Set out in the paper are results of treatment of those patients with carcinoma of the lung, uterine cervix, hysterocarcinoma, breast cancer, malignant thymomas, malignant non-Hodgkin's lymphomas, and lymphogranulematosis having been administered combined, chemoradiation or radiation treatments against the background of a complex of accompanying therapy involving systemic enzymotherapy. Polyenzymic drugs were found to be capable of improving results of treatment of acute radiation reactions and preventing postradiation fibrous changes in the lungs, skin, fatty tissue, soft tissue, liver, kidneys. Thus, systemic enzymotherapy is capable of improving the quality of life and results of treatment of oncological patients.
http://www.ncbi.nlm.nih.gov/pubmed/16786662http://www.ncbi.nlm.nih.gov/pubmed/16786662Systemic enzymotherapy as a method of prophylaxis of postradiation complications in oncological patients
http://mens-en-gezondheid.infonu.nl/gezonde-voeding/134463-de-geneeskracht-van-broccolispruiten-of-broccolikiemen.html#enzymen-met-antioxidantwerking.
In verband met de auteursrechten kan ik alleen deze link vermelden maar de inhoud van dit artikel gaat veel verder dan een publicatie vd kankerstichting over gezonde voeding voor kankerpatienten. Dat is wat ik mis.Miljoenen worden gespendeerd aan research...kankerpatienten kunnen actief bijdragen aan hun herstel maar missen de kennis terzake!
Patent op voeding is niet mogelijk dus commercieel niet belangrijk maar zo ontzetend belangrijk voor alle kankerpatienten!
Duitse behandelaars schrijven Wobenzymen P voor...
Nederlandse artsen bestempelen het als kwakzalverij.
donderdag 19 maart 2015
Interview Shanon .. van stage 3 naar stage 4 borstkanker naar genezing ..met alternatieve behandeling....!!
Hyperthermie
Vitamine C
Vitamine D
Vitamine B17 (zit ook in abrikozenpitten)
Stress
Onverwerkte trauma
etc. ...
Vitamine C
Vitamine D
Vitamine B17 (zit ook in abrikozenpitten)
Stress
Onverwerkte trauma
etc. ...
https://www.youtube.com/watch?v=v4-tgpp7kkk
Metabolic stress on cells? Het belang van voeding!
Kanker bestrijden met een gigantische anti kankersalade, met Chris Wark?https://www.youtube.com/watch?v=BORz-CNszes (blog van 24 januari jongstleden)
Waarom Nederlandse kankerpatienten gewezen moeten worden op het belang van voeding.
Research at the University of Adelaide has discovered cancer cells may be particularly susceptible to metabolicstress - opening the way for new targeted therapy that won't harm normal cells.The researchers showed that chromosomal instability - which is a hallmark of rapidly dividing cancer cells - makes them stressed and vulnerable to mild metabolic disruption. Metabolism is the normal process by which the body turns food into energy."A common problem in treating cancers is that they don't respond to chemotherapy, or they respond for a while, but then come back," says lead author Dr Stephen Gregory, Senior Postdoctoral Fellow with the University's School of Molecular and Biomedical Sciences."One reason this happens is because a tumour is usually not made up of identical cells but rather a diverse population of cells that changes all the time, losing and gaining chromosomes as they divide - so-called chromosomal instability. Sooner or later they change enough to be able to resist chemotherapy drugs."Our research has shown that chromosomal instability has some consequences for cells - they get stressed, and it only takes a small metabolic push to kill them."Current chemotherapy is also very toxic to all dividing cells, particularly affecting cells in hair follicles, the gut lining and blood, often causing hair loss, pain and making patients unwell."We need to find ways to target cancer cells without affecting other normal dividing cells," says Dr Gregory.The researchers induced chromosomal instability in small experimental flies, Drosophila, and found that the unstable cells were "on the edge" of how much stress they could tolerate."This is significant because a change in metabolism is something people cope with very well normally," says Dr Gregory. "That means that we hope to be able to develop treatments that have no side effects on patients, but are able to kill off the unstable tumour cells that cause relapses."Dr Gregory says this may give some validity to theories of alternative treatments such as going on a radical diet."People who have advanced cancer which isn't responding to chemotherapy often try a range of different treatments such as a radical diet in the hope it may help," he says. "In some situations, it may in fact work; but we hope to be able to point the way to a more targeted approach - finding the most appropriate steps for intervention in the metabolic process that will give the best results."h at the University of Adelaide has discovered cancer cells may be particularly susceptible to metabolicstress - opening the way for new targeted therapy that won't harm normal cells.The researchers showed that chromosomal instability - which is a hallmark of rapidly dividing cancer cells - makes them stressed and vulnerable to mild metabolic disruption. Metabolism is the normal process by which the body turns food into energy."A common problem in treating cancers is that they don't respond to chemotherapy, or they respond for a while, but then come back," says lead author Dr Stephen Gregory, Senior Postdoctoral Fellow with the University's School of Molecular and Biomedical Sciences."One reason this happens is because a tumour is usually not made up of identical cells but rather a diverse population of cells that changes all the time, losing and gaining chromosomes as they divide - so-called chromosomal instability. Sooner or later they change enough to be able to resist chemotherapy drugs."Our research has shown that chromosomal instability has some consequences for cells - they get stressed, and it only takes a small metabolic push to kill them."Current chemotherapy is also very toxic to all dividing cells, particularly affecting cells in hair follicles, the gut lining and blood, often causing hair loss, pain and making patients unwell."We need to find ways to target cancer cells without affecting other normal dividing cells," says Dr Gregory.The researchers induced chromosomal instability in small experimental flies, Drosophila, and found that the unstable cells were "on the edge" of how much stress they could tolerate."This is significant because a change in metabolism is something people cope with very well normally," says Dr Gregory. "That means that we hope to be able to develop treatments that have no side effects on patients, but are able to kill off the unstable tumour cells that cause relapses."Dr Gregory says this may give some validity to theories of alternative treatments such as going on a radical diet."People who have advanced cancer which isn't responding to chemotherapy often try a range of different treatments such as a radical diet in the hope it may help," he says. "In some situations, it may in fact work; but we hope to be able to point the way to a more targeted approach - finding the most appropriate steps for intervention in the metabolic process that will give the best results."
Bron : zie bovenstaande internetlink (december 2014)
Ik verwijs naar mijn blogspotvan 24 januari jl. :
Waarom Nederlandse kankerpatienten gewezen moeten worden op het belang van voeding.
Research at the University of Adelaide has discovered cancer cells may be particularly susceptible to metabolicstress - opening the way for new targeted therapy that won't harm normal cells.The researchers showed that chromosomal instability - which is a hallmark of rapidly dividing cancer cells - makes them stressed and vulnerable to mild metabolic disruption. Metabolism is the normal process by which the body turns food into energy."A common problem in treating cancers is that they don't respond to chemotherapy, or they respond for a while, but then come back," says lead author Dr Stephen Gregory, Senior Postdoctoral Fellow with the University's School of Molecular and Biomedical Sciences."One reason this happens is because a tumour is usually not made up of identical cells but rather a diverse population of cells that changes all the time, losing and gaining chromosomes as they divide - so-called chromosomal instability. Sooner or later they change enough to be able to resist chemotherapy drugs."Our research has shown that chromosomal instability has some consequences for cells - they get stressed, and it only takes a small metabolic push to kill them."Current chemotherapy is also very toxic to all dividing cells, particularly affecting cells in hair follicles, the gut lining and blood, often causing hair loss, pain and making patients unwell."We need to find ways to target cancer cells without affecting other normal dividing cells," says Dr Gregory.The researchers induced chromosomal instability in small experimental flies, Drosophila, and found that the unstable cells were "on the edge" of how much stress they could tolerate."This is significant because a change in metabolism is something people cope with very well normally," says Dr Gregory. "That means that we hope to be able to develop treatments that have no side effects on patients, but are able to kill off the unstable tumour cells that cause relapses."Dr Gregory says this may give some validity to theories of alternative treatments such as going on a radical diet."People who have advanced cancer which isn't responding to chemotherapy often try a range of different treatments such as a radical diet in the hope it may help," he says. "In some situations, it may in fact work; but we hope to be able to point the way to a more targeted approach - finding the most appropriate steps for intervention in the metabolic process that will give the best results."h at the University of Adelaide has discovered cancer cells may be particularly susceptible to metabolicstress - opening the way for new targeted therapy that won't harm normal cells.The researchers showed that chromosomal instability - which is a hallmark of rapidly dividing cancer cells - makes them stressed and vulnerable to mild metabolic disruption. Metabolism is the normal process by which the body turns food into energy."A common problem in treating cancers is that they don't respond to chemotherapy, or they respond for a while, but then come back," says lead author Dr Stephen Gregory, Senior Postdoctoral Fellow with the University's School of Molecular and Biomedical Sciences."One reason this happens is because a tumour is usually not made up of identical cells but rather a diverse population of cells that changes all the time, losing and gaining chromosomes as they divide - so-called chromosomal instability. Sooner or later they change enough to be able to resist chemotherapy drugs."Our research has shown that chromosomal instability has some consequences for cells - they get stressed, and it only takes a small metabolic push to kill them."Current chemotherapy is also very toxic to all dividing cells, particularly affecting cells in hair follicles, the gut lining and blood, often causing hair loss, pain and making patients unwell."We need to find ways to target cancer cells without affecting other normal dividing cells," says Dr Gregory.The researchers induced chromosomal instability in small experimental flies, Drosophila, and found that the unstable cells were "on the edge" of how much stress they could tolerate."This is significant because a change in metabolism is something people cope with very well normally," says Dr Gregory. "That means that we hope to be able to develop treatments that have no side effects on patients, but are able to kill off the unstable tumour cells that cause relapses."Dr Gregory says this may give some validity to theories of alternative treatments such as going on a radical diet."People who have advanced cancer which isn't responding to chemotherapy often try a range of different treatments such as a radical diet in the hope it may help," he says. "In some situations, it may in fact work; but we hope to be able to point the way to a more targeted approach - finding the most appropriate steps for intervention in the metabolic process that will give the best results."
Bron : zie bovenstaande internetlink (december 2014)
Ik verwijs naar mijn blogspotvan 24 januari jl. :
dinsdag 10 maart 2015
Huidige medische stand van zaken ...
Tumormarker (weer) gezakt van 333 naar 258 in 8 weken tijd ...!
Oncoloog kan geen receptje van een medicijn v 20 € voorschrijven en geeft eerlijk toe dat de verzekeraar in zijn nek hijgt en het medicijnenbeleid letterlijk bepaalt. Hoe triest!
Zelfs het tonen van een email met de medische verklaring van een Duitse chefarts die zich jaarlijks door Japanse oncologen laat bijscholen over de noodzaak van dit medicijn voor mij, kan hem niet over de streep trekken!
Het was en is mij inmiddels wel duidelijk waar ik de beste kankerbehandeling krijg nl. in Duitsland! Daar word men boos omdat ik geen Endoxan tegen de uitzaaiingen inneem.
Daar worden zelfs nog bisfosfornaten voorgeschreven (zie bisfosfornaten wikipedia dient vnl om progressie van botmetastasen te voorkomen dus PREVENTIEF medicijnenbeleid).Ik heb dit gevraagd aan de Nederlandse oncoloog maar die reageert hier niet op.
Binnenkort weer hyperthermie, andulation, massage, etc. .. .Ik verheug me er op.Elke keer weer een stapje verder...
Duitse verzekeraars vergoeden zelfs 2 weken kankerrevalidatie (met begeleider) in welness oorden...wat een contrast met het karige kankerbeleid in Nederland, waar je na 10 minuten weer buiten staat!
Oncoloog kan geen receptje van een medicijn v 20 € voorschrijven en geeft eerlijk toe dat de verzekeraar in zijn nek hijgt en het medicijnenbeleid letterlijk bepaalt. Hoe triest!
Zelfs het tonen van een email met de medische verklaring van een Duitse chefarts die zich jaarlijks door Japanse oncologen laat bijscholen over de noodzaak van dit medicijn voor mij, kan hem niet over de streep trekken!
Het was en is mij inmiddels wel duidelijk waar ik de beste kankerbehandeling krijg nl. in Duitsland! Daar word men boos omdat ik geen Endoxan tegen de uitzaaiingen inneem.
Daar worden zelfs nog bisfosfornaten voorgeschreven (zie bisfosfornaten wikipedia dient vnl om progressie van botmetastasen te voorkomen dus PREVENTIEF medicijnenbeleid).Ik heb dit gevraagd aan de Nederlandse oncoloog maar die reageert hier niet op.
Binnenkort weer hyperthermie, andulation, massage, etc. .. .Ik verheug me er op.Elke keer weer een stapje verder...
Duitse verzekeraars vergoeden zelfs 2 weken kankerrevalidatie (met begeleider) in welness oorden...wat een contrast met het karige kankerbeleid in Nederland, waar je na 10 minuten weer buiten staat!
CRCI of Cancer related cognitive impairment PRIOR to treatment!!
Prevalence, mechanisms, and management of cancer-related cognitive impairment.
Authors
Janelsins MC1, Kesler SR, Ahles TA, Morrow GR.
Author information
Journal
Int Rev Psychiatry. 2014 Feb;26(1):102-13. doi: 10.3109/09540261.2013.864260.
Affiliation
Abstract
This review summarizes the current literature on cancer-related cognitive impairment (CRCI) with a focus on prevalence, mechanisms, and possible interventions for CRCI in those who receive adjuvant chemotherapy for non-central nervous system tumours and is primarily focused on breast cancer. CRCI is characterized as deficits in areas of cognition including memory, attention, concentration, and executive function. Development of CRCI can impair quality of life and impact treatment decisions. CRCI is highly prevalent; these problems can be detected in up to 30% of patients prior to chemotherapy, up to 75% of patients report some form of CRCI during treatment, and CRCI is still present in up to 35% of patients many years following completion of treatment. While the trajectory of CRCI is becoming better understood, the mechanisms underlying the development of CRCI are still obscure; however, host characteristics, immune dysfunction, neural toxicity, and genetics may play key roles in the development and trajectory of CRCI. Intervention research is limited, though strategies to maintain function are being studied with promising preliminary findings. This review highlights key research being conducted in these areas, both in patient populations and in animals, which will ultimately result in better understanding and effective treatments for CRCI.
CRCI +chronische stress = meer cognitieve problemen en natuurlijk geen dementieverschijnsel!
Authors
Janelsins MC1, Kesler SR, Ahles TA, Morrow GR.
Author information
Journal
Int Rev Psychiatry. 2014 Feb;26(1):102-13. doi: 10.3109/09540261.2013.864260.
Affiliation
Abstract
This review summarizes the current literature on cancer-related cognitive impairment (CRCI) with a focus on prevalence, mechanisms, and possible interventions for CRCI in those who receive adjuvant chemotherapy for non-central nervous system tumours and is primarily focused on breast cancer. CRCI is characterized as deficits in areas of cognition including memory, attention, concentration, and executive function. Development of CRCI can impair quality of life and impact treatment decisions. CRCI is highly prevalent; these problems can be detected in up to 30% of patients prior to chemotherapy, up to 75% of patients report some form of CRCI during treatment, and CRCI is still present in up to 35% of patients many years following completion of treatment. While the trajectory of CRCI is becoming better understood, the mechanisms underlying the development of CRCI are still obscure; however, host characteristics, immune dysfunction, neural toxicity, and genetics may play key roles in the development and trajectory of CRCI. Intervention research is limited, though strategies to maintain function are being studied with promising preliminary findings. This review highlights key research being conducted in these areas, both in patient populations and in animals, which will ultimately result in better understanding and effective treatments for CRCI.
CRCI +chronische stress = meer cognitieve problemen en natuurlijk geen dementieverschijnsel!
donderdag 5 maart 2015
Indol carbinol 3--) p53 to trigger its apoptotic response
.Essential role of the cancer stem/progenitor cell marker nucleostemin for indole-3-carbinol anti-proliferative responsiveness in human breast cancer cells.
Authors
Tin AS, Park AH, Sundar SN, Firestone GL.
Journal
BMC Biol. 2014 Sep 12;12:72. doi: 10.1186/s12915-014-0072-6.
Affiliation
Abstract
BACKGROUND: Nucleostemin is a nucleolus residing GTPase that is considered to be an important cancer stem/progenitor cell marker protein due to its high expression levels in breast cancer stem cells and its role in tumor-initiation of human mammary tumor cells. It has been proposed that nucleostemin may represent a valuable therapeutic target for breast cancer; however, to date evidence supporting the cellular mechanism has not been elucidated.RESULTS: Expression of exogenous HER2, a member of the EGF receptor gene family, in the human MCF-10AT preneoplastic mammary epithelial cell line formed a new breast cancer cell line, 10AT-Her2, which is highly enriched in cells with stem/progenitor cell-like character. 10AT-Her2 cells display a CD44+/CD24-/low phenotype with high levels of the cancer stem/progenitor cell marker proteins nucleostemin, and active aldehyde dehydrogenase-1. The overall expression pattern of HER2 protein and the stem/progenitor cell marker proteins in the 10AT-Her2 cell population is similar to that of the luminal HER2+ SKBR3 human breast cancer cell line, whereas, both MCF-7 and MDA-MB-231 cells display reduced levels of nucleostemin and no detectable expression of ALDH-1. Importantly, in contrast to the other well-established human breast cancer cell lines, 10AT-Her2 cells efficiently form tumorspheres in suspension cultures and initiate tumor xenograft formation in athymic mice at low cell numbers. Furthermore, 10AT-Her2 cells are highly sensitive to the anti-proliferative apoptotic effects of indole-3-carbinol (I3C), a natural anti-cancer indolecarbinol from cruciferous vegetables of the Brassica genus such as broccoli and cabbage. I3C promotes the interaction of nucleostemin with MDM2 (Murine Double Mutant 2), an inhibitor of the p53 tumor suppressor, and disrupts the MDM2 interaction with p53. I3C also induced nucleostemin to sequester MDM2 in a nucleolus compartment, thereby freeing p53 to mediate its apoptotic activity. siRNA knockdown of nucleostemin functionally documented that nucleostemin is required for I3C to trigger its cellular anti-proliferative responses, inhibit tumorsphere formation, and disrupt MDM2-p53 protein-protein interactions. Furthermore, expression of an I3C-resistant form of elastase, the only known target protein for I3C, prevented I3C anti-proliferative responses in cells and in tumor xenografts in vivo, as well as disrupt the I3C stimulated nucleostemin-MDM2 interactions.
CONCLUSIONS: Our results provide the first evidence that a natural anti-cancer compound mediates its cellular and in vivo tumor anti-proliferative responses by selectively stimulating cellular interactions of the stem/progenitor cell marker nucleostemin with MDM2, which frees p53 to trigger its apoptotic response. Furthermore, our study provides a new mechanistic template that can be potentially exploited for the development of cancer stem/progenitor cell targeted therapeutic strategies
Authors
Tin AS, Park AH, Sundar SN, Firestone GL.
Journal
BMC Biol. 2014 Sep 12;12:72. doi: 10.1186/s12915-014-0072-6.
Affiliation
Abstract
BACKGROUND: Nucleostemin is a nucleolus residing GTPase that is considered to be an important cancer stem/progenitor cell marker protein due to its high expression levels in breast cancer stem cells and its role in tumor-initiation of human mammary tumor cells. It has been proposed that nucleostemin may represent a valuable therapeutic target for breast cancer; however, to date evidence supporting the cellular mechanism has not been elucidated.RESULTS: Expression of exogenous HER2, a member of the EGF receptor gene family, in the human MCF-10AT preneoplastic mammary epithelial cell line formed a new breast cancer cell line, 10AT-Her2, which is highly enriched in cells with stem/progenitor cell-like character. 10AT-Her2 cells display a CD44+/CD24-/low phenotype with high levels of the cancer stem/progenitor cell marker proteins nucleostemin, and active aldehyde dehydrogenase-1. The overall expression pattern of HER2 protein and the stem/progenitor cell marker proteins in the 10AT-Her2 cell population is similar to that of the luminal HER2+ SKBR3 human breast cancer cell line, whereas, both MCF-7 and MDA-MB-231 cells display reduced levels of nucleostemin and no detectable expression of ALDH-1. Importantly, in contrast to the other well-established human breast cancer cell lines, 10AT-Her2 cells efficiently form tumorspheres in suspension cultures and initiate tumor xenograft formation in athymic mice at low cell numbers. Furthermore, 10AT-Her2 cells are highly sensitive to the anti-proliferative apoptotic effects of indole-3-carbinol (I3C), a natural anti-cancer indolecarbinol from cruciferous vegetables of the Brassica genus such as broccoli and cabbage. I3C promotes the interaction of nucleostemin with MDM2 (Murine Double Mutant 2), an inhibitor of the p53 tumor suppressor, and disrupts the MDM2 interaction with p53. I3C also induced nucleostemin to sequester MDM2 in a nucleolus compartment, thereby freeing p53 to mediate its apoptotic activity. siRNA knockdown of nucleostemin functionally documented that nucleostemin is required for I3C to trigger its cellular anti-proliferative responses, inhibit tumorsphere formation, and disrupt MDM2-p53 protein-protein interactions. Furthermore, expression of an I3C-resistant form of elastase, the only known target protein for I3C, prevented I3C anti-proliferative responses in cells and in tumor xenografts in vivo, as well as disrupt the I3C stimulated nucleostemin-MDM2 interactions.
CONCLUSIONS: Our results provide the first evidence that a natural anti-cancer compound mediates its cellular and in vivo tumor anti-proliferative responses by selectively stimulating cellular interactions of the stem/progenitor cell marker nucleostemin with MDM2, which frees p53 to trigger its apoptotic response. Furthermore, our study provides a new mechanistic template that can be potentially exploited for the development of cancer stem/progenitor cell targeted therapeutic strategies
Low-Dose Cyclophosphamide Synergizes with Dendritic Cell-Based Immunotherapy in Antitumor Activity
Low-Dose Cyclophosphamide Synergizes with
Dendritic Cell-Based Immunotherapy in Antitumor Activity
Joris D. Veltman, Margaretha E. H. Lambers, Menno van Nimwegen, Sanne de Jong,
Rudi W. Hendriks, Henk C. Hoogsteden, Joachim G. J. V. Aerts, and Joost P. J. J. Hegmans
Department of Pulmonary Medicine, Erasmus Medical Center Rotterdam, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands
Correspondence should be addressed to Joost P. J. J. Hegmans,
j.hegmans@erasmusmc.nl Received 30 November 2009; Revised 5 February 2010; Accepted 7 March 2010 Academic Editor: Zhengguo Xiao Copyright © 2010 Joris D. Veltman et al.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Clinical immunotherapy trials like dendritic cell-based vaccinations are hampered by the tumor’s offensive repertoire that suppresses the incoming effector cells. Regulatory T cells are instrumental in suppressing the function of cytotoxic T cells. We studied the effect of low-dose cyclophosphamide on the suppressive function of regulatory T cells and investigated if the success rate of dendritic cell immunotherapy could be improved. For this, mesothelioma tumor-bearing mice were treated with dendritic cell-based immunotherapy alone or in combination with low-dose of cyclophosphamide. Proportions of regulatory T cells and the cytotoxic T cell functions at different stages of disease were analyzed. We found that low-dose cyclophosphamide induced beneficial immunomodulatory effects by preventing the induction of Tregs, and as a consequence, cytotoxic T cell function was no longer affected. Addition of cyclophosphamide improved immunotherapy leading to an increased median and overall survival. Future studies are needed to address the usefulness of this combination treatment for mesothelioma patients.
© kanker gezond(er) benaderen 2015.
j.hegmans@erasmusmc.nl Received 30 November 2009; Revised 5 February 2010; Accepted 7 March 2010 Academic Editor: Zhengguo Xiao Copyright © 2010 Joris D. Veltman et al.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Clinical immunotherapy trials like dendritic cell-based vaccinations are hampered by the tumor’s offensive repertoire that suppresses the incoming effector cells. Regulatory T cells are instrumental in suppressing the function of cytotoxic T cells. We studied the effect of low-dose cyclophosphamide on the suppressive function of regulatory T cells and investigated if the success rate of dendritic cell immunotherapy could be improved. For this, mesothelioma tumor-bearing mice were treated with dendritic cell-based immunotherapy alone or in combination with low-dose of cyclophosphamide. Proportions of regulatory T cells and the cytotoxic T cell functions at different stages of disease were analyzed. We found that low-dose cyclophosphamide induced beneficial immunomodulatory effects by preventing the induction of Tregs, and as a consequence, cytotoxic T cell function was no longer affected. Addition of cyclophosphamide improved immunotherapy leading to an increased median and overall survival. Future studies are needed to address the usefulness of this combination treatment for mesothelioma patients.
© kanker gezond(er) benaderen 2015.
CYCLOPHOSPHAMIDE INDUCES DIFFERENTIATION OF Th17 CELLS IN CANCER PATIENTS
- Authors:
Nathalie Chaput and Laurence Zitvogel, Centre d'Investigation Clinique Biothérapie 507, Institut de Cancérologie Gustave Roussy, 114 rue Edouard Vaillant, 94805 Villejuif, France.PHONE
: 33142116616; Fax: 33142116094. E-MAIL: chaput@igr.fr, zitvogel@igr.fr
Abstract
Low doses of the alkylating agent cyclophosphamide (CTX) mediate antiangiogenic and immunostimulatory effects, leading to potent tumoricidal activity in association with various immunotherapeutic strategies. Here, we show in rodents and cancer patients that CTX markedly promotes the differentiation of CD4+ T helper 17 (Th17) cells that can be recovered in both blood and tumor beds. However, CTX does not convert regulatory T cells into Th17 cells. Because Th17 are potent inducers of tissue inflammation and autoimmunity, these results suggest impact ON the clinical management of various types of malignancies treated with alkylating agents and a potential need to optimize CTX-based immunotherapy in patients. Cancer Res; 71(3); 661–5. ©2010 AACR.
© kanker gezond(er) benaderen 2015.
the clinical management of various types of malignancies treated with alkylating agents and a potential need to optimize CTX-based immunotherapy in patients. Cancer Res; 71(3); 661–5. ©2010 AACR.© kanker gezond(er) benaderen 2015.
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