A Few Cancer Stem Cell Articles
Cancer stem cell theories offers the prospect that various types of cancer spawn from characteristic stem-cell-like initial populations. Cancer exists because random mutations that occur in our cells as a result of damage and age will eventually produce one of these prolific and damaging cell types, possibly by damaging an existing adult stem cell, or possibly by radically mutating a normal somatic cell. Cancer stem cells are hard to eradicate completely through old-style chemotherapy, radiotherapy, or surgery, which is why cancers tend to recur - all it takes is one remaining errant stem cell to rebuild the cancer anew. But the nature of cancer stem cells also means that they are the weak link: destroy them and the cancer cannot survive. Fortunately, identifying and safely destroying specific cell types based on their biochemical differences is a core focus for biotechnology research these days. This is one of the reasons I am confident that my generation will not suffer greatly from cancer in later life: the cancer-killing therapies of three decades from now will be very safe, very effective, and very cheap.
On this topic, I noticed a few recent articles on cancer stem cell research and development today, and thought I would share.
Possible Prostate Cancer Culprit:
"Think about cancer as a disease of stem cells," said study coauthor Owen Witte, a Howard Hughes Medical Institute investigator at the University of California, Los Angeles. Mutations in these cells can cause "normal stem cells to lose their regularized behavior and instead turn into an incipient cancer," he said. Like many other tissues in the body, prostate tissue is made up of several different kinds of cells, including a class called basal stem cells. Normally these cells divide to replenish prostate tissue, but sometimes they become cancerous. Instead of producing normal cells, these stem cells lead to tumors.
$11.5 million NIH Center grant funds novel cancer stem cell research:
"Targeting cancer stem cells, rather than cancer cells, is a completely new strategy for treating cancer," said Dr. Stephen Wong, director of the Center for Bioengineering and Informatics at The Methodist Hospital Research Institute and principal investigator for the grant study. "By attacking the cancer stem cell, we hope to eliminate cancer’s ability to grow, recur or metastasize."
Researchers identify a potential therapeutic target for brain cancer:
Recent studies have increased our understanding of cancer by elucidating some of the differences that exist between tumor cells among patients and even between distinct subsets of tumor cells within the same patient. Evidence suggests there are subgroups of cells - called cancer stem cells or tumor initiating cells - within tumors that are harder to kill with current therapies than other cells within these tumors. Cancer stem cells may in fact be more important to destroy than non-cancer stem cells because they may be responsible for metastasis and for tumor recurrence after therapy. Identifying therapies which specifically target cancer stem cells therefore hold great promise for effective and lasting treatment.
The original paper for that last item makes for interesting reading. You should take a look. But of course things are never as simple as we'd like them to be. Cancer stem cells may not be at the base of all cancers, and there are strong arguments that might lead us to expect this to be the case. This final article from earlier in the month delves into some of these complications.
Dissecting Cancer Stem Cell Theories:
The stochastic, or clonal evolution, model dictates that, "despite the heterogeneity (in cancer), cells of many different phenotypes are capable of proliferating extensively and forming new tumors," Dr. Morrison summarized. The cancer stem cell model, in contrast, says that "cancer stem cells are uniquely capable of proliferating extensively and forming new tumors, and that they go through an aberrant process of differentiation giving rise to phenotypically diverse cancer cells with a limited capacity to divide." Which of these two theories is correct seems to depend upon the type of cancer.
I do not remember where I read the statistics, but I think that wiping out cancer would increase life-span in the developed world by two years, while wiping out arterial diseases would add more than a decade. (If anyone knows where this data comes from or any contrary data tell me...)
Are their any similar innovations to declog the arteries that in the pipeline yet? What are the time horizons?
So far war on cancer had been a failure -- that is the conclusion of an article in SCEPTICAL INQUIRER magazine for january of this year. After U.S. government spent 109 billion bucks since 1971, cancer survivor rate improved only by five percent. Realistically it doesn't bode well for the future. And it shows that spending hundreds of billions of bucks doesn't necessarily solve health problems.
There is a more rational hypothesis than the CSC hypothesis, which does not have any documented evidence. Nobody knows the source of CSCs; there is no evidence for its potential to undergo asymmetric division. On the other hand, the neosis paradigm of carcinogenesis has documented proof You can find all about the neosis paradigm of carcinogenesis from the internet by googling for the words "Neosis + Rajaraman". Neosis is a novel mode of cell division involved in the birth and self-renewal of all types of cancers. Senescent cell is supposed to be a tumor suppressor; therefore, it has to escape senescence if it want to become tumorigenic. This is what happens during the birth of tumor cells. The mitotically non-viable polyploid genome of the senescent cell undergoes neosis with an intact nuclear envelope during karyokinesis, this involves Epithelial-mesenchymal transition, during which the chromatin modulation occurs giving rise to the mitotically viable genomes of the neotic offspring. We have shown that this process is repetitive producing newer Raju cells, the neotic offspring, with transient stemness. Thus neosis appears to be the morphological manifestation of the epithelial-mesenchymal transition, which precedes neosis. The cells escape senescence-induced mitotic catastrophe via Neosis.
New evidence indicates that neosis executes Epithelial-Mesenchymal transition. This tells us that EMT is not just transition but transformation of cells. We also know that EMT involves the birth of new tumor initiating cells, termed Raju cells, which are produced every time a cell undergoes neosis. New evidence indicates that the so called Cancer Stem Cells are only short-lived as opposed to the original concept of the CSC hypothesis. Just as the EMT and the reverse process MET occurs several times during embryogenesis, tumor cells undergo several EMTs and METs during its growth, each time yielding newer Raju cells, with slightly different gene expression profiles. This will explain the confusion due to the CSC hypothesis, which would like us to believe that CSCs are a constant part of the tumor cells just like normal stem cells, with unlimited division potential.