say a prayer for a baby with lymphoma sent home to die, i referred her to grace gawler, thats all i can do. i know asir in hallwang is a genius at blood based cancers.
So instead of getting my 60th round of chemo, Dr. Lenz had a different plan. After emailing with him back and forth during my trip, lamenting about my lung issues and wanting to focus on the issue ...
Do your research on doctors, cancer centers, and treatment plans. Talk with several oncologists or surgeons before you choose yours. Speak up if you have questions or concerns. And always remember: your doctors are incredibly important to your victory over cancer, but the real leader of your team is YOU.
I spent alot of time checking glorias site, its so positive in many respects. the above commetn about finding doctors is incomplete, the omission of naturopaths and alternative doctor is a deadly omission. most usa based oncologists just kill most stage 4 colorectals, you need innovative out of the box therapies to help if your current efforts are failing keep on looking.
i dont know if gloria did do dca, b17 , ipt, tace, lung laser with doctor rolle. its not my business. her treatment, her life and effort is to be respected. i just wonder how she would have gone without 60 sessions of chemo and she had advice from any of the alternative usa based doctors featured in defeat cancer.
Her wonderful site highlights my greatest fear, our ability to influence others by our success and our passion. Many of my eloquent ex friends many on the cancer survivors network have the gift of popular appeal. i think gloria had this as well. often the conservative message being reinforced by vocal eloquent conservatives is really very palatable to the scared cancer masses. I just see those with conservative influence, all the cancer charities, conservative advocates leading so many to death and denying them any chance of life or extended remission
Its just I see so much suffering and death all around the net from colorectal, but i dont want any blind followers asking me questions, but thoughtful friends and supporters and encouragement well thats essential.
so i have always said study and exercise your asses off to have a chance of saving your ass.
I say follow the money trail, its driving all treatment decisions in good old greedy western world, of course greed is also in the alternative and breakthough world ie hallwang clinic aint cheap but probably you would still save some money instead of going to md andersen.
so i wondered what gloria tried, the above says it all, and yes lenz is there. no mention of axel rolle, prof vogel any of my immunotherapists.
so state of the art usa based care is tragically behind the times, if i live i am right, if i die i am wrong!!! as i have life i call it the way i see it. my handful of friends less than ten.
a wonderful friend said i am always on holidays. my answer.
if your lucky enough to get a 12 month terminal prognosis you too may have time for holidays, be careful for what you want.
survival is my work, but i know what you mean.
so my sense of humour is desserting me. i miss icecream. thats an example of ketogenic torture!!!!!!!!!!!
mornings glucose 97 and ketones 0.7 yesterdays exercise and clear broth soups worked. the old insulin resistance and exercise relationship.
i have been up studying immunoediting, and ctcs.
our biology is amazing and my survival depends on my grasping the keys parts of the science, i am blessed to have a brain and time to understand this and doctors to implement.
the cancer establishment can go f themselves... the pace of change and innovation to slow, if every oncologist was goal well survival rates would improve for most cancers!!!!!!!!!
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3082489/ does this turn you on ?
The main function of fibroblasts is to maintain the structural integrity of connective tissues by continuously secreting precursors of the extracellular matrix. Fibroblasts secrete the precursors of all the components of the extracellular matrix, primarily the ground substance and a variety of fibers. The composition of the extracellular matrix determines the physical properties of connective tissues.
Like other cells of connective tissue, fibroblasts are derived from primitive mesenchyme. Thus they express the intermediate filament protein vimentin, a feature used as a marker to distinguish their mesodermal origin. However, this test is not specific as epithelial cells cultured in vitro on adherent substratum may also express vimentin after some time.
In certain situations epithelial cells can give rise to fibroblasts, a process called epithelial-mesenchymal transition (EMT).
Conversely, fibroblasts in some situations may give rise to epithelia by undergoing a mesenchymal to epithelial transition (MET) and organizing into a condensed, polarized, laterally connected true epithelial sheet. This process is seen in many developmental situations (e.g. nephron and notocord development), as well as in wound healing and tumorigenesis.
The endoplasmic reticulum (ER) is a type of organelle in the cells of eukaryotic organisms that forms an interconnected network of flattened, membrane-enclosed sacs or tubes known as cisternae. The membranes of the ER are continuous with the outer membrane of the nuclear envelope. Endoplasmic reticulum occurs in most types of eukaryotic cell but is absent from red blood cells and spermatozoa. There are two types of endoplasmic reticulum, rough endoplasmic reticulum (RER)and smooth endoplasmic reticulum (SER). The outer (cytosolic) face of the rough endoplasmic reticulum is studded withribosomes that are the sites of protein synthesis. Rough endoplasmic reticulum is especially prominent in cells such ashepatocytes where active protein synthesis occurs. The smooth endoplasmic reticulum lacks ribosomes and functions inlipid metabolism, carbohydrate metabolism, and detoxification[citation needed] and is especially abundant in mammalian liver and gonad cells.
Discussion
The most striking or crucial characteristic of cancer disease is its ability to spread and produce new metastatic sites. In alignment with the scientific indications cited above, CTCs, which are part of the primary tumor, play an important role for the development of the disease, and later, of metastasis [15,16, 23, 24, 25].
Shortly, a tumor is formed when cancer cells grow as colonies. Many cellular and biochemical changes in the phenotype are responsible for the loss of epithelial hallmarks by the tumor cells.
Loss of epithelial polarity (interaction between tumor cells and stromal cells) drives CTCs to alter themselves and form spheres. This shape facilitates their immune escape, and finally reacts with the target. Ras/MAPK pathway is activated and EMT takes place. Expression levels of epithelial markers like E-cadherin and cytokeratin decrease and, as a result, the linkage between CTCs and actin cytoskeleton is weakened. In contrast, many mesenchymal markers, such as vimentin and fibronectin, are expressed in high levels and so cancer cells (CTCs) acquire a fibroblast-like shape and their mobility and invasiveness increases. As a result, circulation of tumor cells via proliferation through the blood circulation (intravasation) is taking place. CFS-1 and EGF are the major stimulators of this process, as well as a great range of metalloproteinases (MMPs), especially MMP-9 and G proteins (e.g., Ras, Rho). MMP-9 expression correlates with the tumorigenesis/metastasis cascade. It is well known that metalloproteinase plays a crucial role in normal tissues, as it is initially synthesized as soluble inactive pro-enzyme and acts like a caspase. Other caspases act then in order to stimulate the metastatic attitude of MMPs. On the contrary, G proteins like Ras and Rho are members of a signal transduction pathway, and their activation causes cell growth, differentiation and survival. Thus, using blood vessels, CTCs flow and reach the targeted place, where they are released via extravasation and produce new tumors (micrometastases). Since the environment lacks the previously owned signals and growth factors, CTCs need time in order to proliferate and find all necessary growth supplements to finally produce the detectable mass (macrometastasis) [10, 11, 14, 17].
Many efforts have been done by others in order to prove that cells which have detached from the primary tumor are CTCs [17, 24, 25, 26]. However, these methods present advantages and disadvantages. The first one is a PCR-based method which does not sustain cells as entity for analysis, meaning that there are limitations concerning further molecular analysis of CTCs. Furthermore, even if we have the ability to enumerate CTCs [4], we have identified only few molecular characteristics. The second widely used method is a magnetic bead-based method which uses a small range of markers in order to enrich the CTC population; hence, it is based on their positive selection [17].
In this research attempt, more than one method has been used to render the results more accurate and complete. CTCs isolation from the patient's blood sample was made using EpCAM magnetic beads, which is a pan-epithelial carcinoma-associated antigen that is expressed in almost all carcinomas, as mentioned before. Following isolation, CD45-negative selection was performed in order to isolate cells of epithelial origin from the remaining blood cells. Moreover, CD31-positive cells, endothelial cells or pericytes were excluded because they were considered normal.
The MET gene encodes protein that triggers tumor proliferation, neovascularization and metastases to distinct organs. Therefore, c-Met-positive cells are cells of interest. Expression of cytokeratins is organ and tissue specific. Moreover, the cytokeratin profile tends to remain intact when an epithelial cell undergoes a malignant transformation. Therefore, a cytokeratin profile study is helpful for tumor characterization [4, 24, 25].
The CD227 (Mucin-1 or Ca 15.3) antigen is highly expressed by virtually all mucosal epithelial tissues. It is aberrantly expressed in most human breast cancers, and in this study it was used as a breast cancer marker. CTCs were quantified in the sample [3, 27, 28].
The hypothesis that a population of CTCs has many CSC-like hallmarks is reinforced by the expression of related molecular markers. NANOG is a transcription factor which plays an important role in the self-renewal of undifferentiated embryonic stem cells. It is a nuclear protein and its function is correlated with other factors such as OCT4 [POU5F1 (POU class 5 homeobox 1)]. It has been shown that these genes play a key role in forming the identity of embryonic stem cells. Oct4 is initially active in the oocyte, and it remains active even later in the preimplantation period. It forms a dimmer with the Sox2 gene and so binds to the DNA. Studies claim that this dimmer activates the Nanog protein, and so this molecular cascade is responsible for the capability of tumor cells to differentiate into any of the 3 germ layers (pluripotency). Another protein that expresses early during cell development is Nestin. It is a marker that is not expressed in adults because it is replaced by tissue-specific intermediate filament proteins. Due to the above-mentioned reasons, these markers were chosen in order to prove the initial hypothesis. Since CSCs must hold the hallmark of self-renewal and asymmetric cell division, which is driven by the above factors, the present attempt shows that this hallmark also exists in CTCs [7, 19, 29,30].
I want my colorectal friends to reach out to me.
I know i cannot do this on my own, the research is beyond me and the life style and diet. Today this wonderful email came in, i want to share it.
I hope you don't mind if I email you directly. I've been reading your blog for some time. I believe I originally came across it while researching GCMAF yogurt.
Since then I've enjoyed following your adventures in Germany. I do not have cancer now, but am at high risk of recurrence, so I am learning as much as possible so as to be ready if things change.
I saw that you are concerned about a recurrence of your own cancer, so I wanted to write and tell you about some promising anticancer therapeutics that most oncologists are not aware of, or do not bother to prescribe. Most or all of these are commonly used, have little toxicity, and are quite inexpensive. I could write about many herbs and nutraceuticals as well, but there are many sources of information about that.
I will be very brief, as I'm sure you are capable of researching these drugs through Google and Google Scholar, both for their general anticancer effect and the specific evidence of their value against colon cancer. I have a different form of cancer, so the evidence in colon cancer may not be substantial.
Of course I'm not suggesting you abandon anything that has been working for you, but one or more of these could be good additions and might be a lot more affordable if you can find a doctor willing to prescribe them based on the research.
I hope some of these are new to you and prove to be useful The first two are probably my favorites, given how diverse and well-established their benefits are.
Good luck. YOU WILL SUCCEED. It's just a question of how.
Since then I've enjoyed following your adventures in Germany. I do not have cancer now, but am at high risk of recurrence, so I am learning as much as possible so as to be ready if things change.
I saw that you are concerned about a recurrence of your own cancer, so I wanted to write and tell you about some promising anticancer therapeutics that most oncologists are not aware of, or do not bother to prescribe. Most or all of these are commonly used, have little toxicity, and are quite inexpensive. I could write about many herbs and nutraceuticals as well, but there are many sources of information about that.
I will be very brief, as I'm sure you are capable of researching these drugs through Google and Google Scholar, both for their general anticancer effect and the specific evidence of their value against colon cancer. I have a different form of cancer, so the evidence in colon cancer may not be substantial.
Of course I'm not suggesting you abandon anything that has been working for you, but one or more of these could be good additions and might be a lot more affordable if you can find a doctor willing to prescribe them based on the research.
I hope some of these are new to you and prove to be useful The first two are probably my favorites, given how diverse and well-established their benefits are.
Good luck. YOU WILL SUCCEED. It's just a question of how.
Celebrex (celecoxib) - Anti-inflammatory, and COX-2 inhibitor, but it also has numerous anticancer effects INDEPENDENT of COX-2. Even the standard dose of 200 mg/day has proven to be beneficial in cancer patients. It is possible to go to 400 mg or 800 mg, maybe even further, but with increasing risk of longterm cardiac side effects.
yes, doing 200mg am and 200mg pm
Melatonin - There are many clinical trials showing its preventive effect against cancer, and a significantly improved outcome for cancer patients. This is non-prescription. I take 10 mg as a longterm preventive measure; many clinical trials have used 20 mg when used as an adjuvant to cancer therapy.
yes been on 20mg for 2 years
Mebendazole/Albendazole - Anti-parasitic agents.
yes its a vegf inhibitor with few side effects, i need to checkout gut bug , microbiome issues. my prof morris key researcher in its anticancer use.
Valproate (valproic acid) - An epigenetic drug that slows down the ability of cancer cells to reprogram their DNA and adapt to different types of attacks and stresses. This drug may even be able to REVERSE adaptations that have previously taken place, making cancer cells less invasive. There are several other HDAC inhibitors or demethylating agents that could be investigated instead.
no need to research
Propranolol - An anti-anxiety drug that blogs the signaling of stress hormones epinephrine and norepinephrine. The receptors for these hormones may also accelerate cancer growth. IMO this may be the source of the benefit of some "mind-body" cancer therapies.
no so if my cortisol is good and i meditate do i need it ?
Losartan - Anti-hypertension drug that inhibits the function of angiotensin II. This is a significant driver of most cancers, but it's beyond my ability to explain the biochemistry of it.
no but interested
Metformin - Anti-diabetes drug that cancer "stem cells" are especially susceptible to.
yes doing 2000 mg divided daily, doing it to also drive glucose down, as well as stem, also good for immunotherapy
Itraconazole - Anti-fungal that inhibits the Hedgehog Pathway, critical to cancer growth and especially to cancer "stemness", in other words their ability to remain immortal.
no but interested, researching
Tetrathiomolybdate - This drug chelates copper out of your system. Keeping copper at a low level (under 20 mg/dl, maybe under 15 mg/dl) can impair cancer's ability to trigger angiogenesis, also reduces growth and motility.
Itraconazole - Anti-fungal that inhibits the Hedgehog Pathway, critical to cancer growth and especially to cancer "stemness", in other words their ability to remain immortal.
no but interested, researching
Tetrathiomolybdate - This drug chelates copper out of your system. Keeping copper at a low level (under 20 mg/dl, maybe under 15 mg/dl) can impair cancer's ability to trigger angiogenesis, also reduces growth and motility.
no but my friend did this, its on the list, i'll measure copper to see where its at
nanog and cancer vaccines
