“I tried to find out how to get this [reversing MS with stem cells] done and all the companies I called require you to pay $15,000 for stem cells they already have and go to Mexico for the procedure. I wanted to use the baby’s cord tissue stem cells”
Archive for the ‘PHARMA AND DRUGS’ Category
A little over a week ago, I posted an article that described:
Of the 100 million BULK CANCER CELLS in a 1-cm cancer tumor, there are about 1,000 to 10,000 CANCER STEM CELLS and those cells are up to 15 times more active and may be the only cells responsible for cancer cell reproduction and metastasis.
Scientists have zeroed in even deeper and targeted a new ‘CD99’ molecule expressed on certain stem cells that drive human leukemia malignancies. They’ve designed antibodies that can directly kill human acute myeloid leukemia (AML) stem cells.
protein-sugar molecule, CD99
Researchers design antibody that recognizes and destroys blood cancer stem cells
Published on January 25, 2017 at 9:44 PM ·
Building on this discovery, the study authors designed an antibody that recognizes and destroys CD99-covered leukemia cells while sparing normal blood stem cells, a finding confirmed by experiments in human cells and in mice with AML cells. Antibodies are immune system proteins that stick to a specific target, like a protein on the surface of invading bacterium. In recent years, researchers have become capable of engineering antibodies so that they target disease-related molecules.
“Our findings not only identify a new molecule expressed on stem cells that drive these human malignancies, but we show that antibodies against this target can directly kill human AML stem cells,” says corresponding study author, Christopher Y. Park, MD, PhD, associate professor in the Department of Pathology at NYU Langone and its Perlmutter Cancer Center.
“While we still have important details to work out, CD99 is likely to be an exploitable therapeutic target for most AML and MDS patients, and we are working urgently to finalize a therapy for human testing,” says Park.
Direct Cell Killing
Acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) arise from abnormal stem cells that build up in bone marrow until they interfere with normal blood cell production. Patients struggle with anemia, increased risk for infection, and bleeding.
The study results are based on the understanding that cancers, like normal tissues, contain stem cells that give rise to all the other cells. Such “cancer stem cells” are known to be major drivers of many cancer types. In AML, a small group of leukemic stem cells become incapable of maturing into red or white blood cells as intended. Most leukemias respond initially to standard treatment, but relapse is common as standard treatments fail to kill leukemia stem cells, which continue to multiply.
The research team became interested in CD99 when they observed that it occurs frequently on AML and MDS cells, and then noted in the literature that CD99 is elevated in a rare bone cancer called Ewing’s Sarcoma. This prompted them to see if CD99 was important in the development of these blood diseases.
When researchers examined stem cell populations from 79 AML and 24 MDS patients, they found that approximately 85 percent of stem cells in both groups expressed high levels of CD99. The levels were so high that diseased stem cells could be cleanly separated from related, normal stem cells in AML patients.
Upon confirming that CD99 was abundant on leukemia stem cells, the research team then made several CD99 antibodies, and chose to focus on the one that most effectively killed those cells. Researchers found that when the study antibody attaches itself to CD99 on the surface of a cancer stem cell, it sends a signal inside the cell that increases the activity of enzymes called SRC-family kinases.
While the team does not yet know why, the binding of their antibody to CD99, and the subsequent activation of these enzymes, causes leukemia stem cells to die. Most cells with genetic mistakes leading to cancer “sense” they are flawed and self-destruct, but CD99, so the theory goes, may be part of a mechanism that prevents this. As the antibody binds to CD99, it appears to undo this block on self-destruction.
“With the appropriate support, we believe we can rapidly determine the best antibodies for use in patients, produce them at the quality needed to verify our results, and apply for permission to begin clinical trials,” says Park.
While the most common acute leukemia affecting adults (22,000 new cases each year) and expected to become more prevalent as the population ages, AML it is still relatively rare, accounting for 1.2 percent of U.S. cancer deaths. About 15,000 mostly elderly patients are diagnosed with MDS each year as well.
Did we just figure out which cells actually cause the creation of more cancer cells?
- A 1-cm cancer tumor has about 100 million BULK CANCER CELLS.
- A 1-cm cancer tumor has about 1,000 to 10,000 CANCER STEM CELLS.
- We know that cancer cells may pass through blood vessel walls to metastasize Moses-stem-cell-pathways-and-maybe-metastatic-cancers/
- We know that long telomeres increase risk of cancer in cells.
Scientists found that cancer stem cells which have the enzyme called Telomeras, were found to be up to 15 times more active and may be the only cells responsible for cancer cell reproduction and metastasis.
“We can now begin to think of cancer stem cells as being at the heart of tumour regrowth and turn our efforts away from ‘bulk cancer cells’, which don’t really drive tumour recurrence and metastasis.”
Now, we know how to aim at the cells responsible for tumor growth we can change how we fight cancer!
Puts a whole new spin on the Niki Lauda quote:
Stem cell ‘marking’ study offers alterative hypothesis of cancer metastasis
- Date:January 18, 2017- Source: University of Salford – Summary: Stem cells are among the most energetically activated, migratory and proliferative sub-populations of tumour cells, according to observations by scholars at the Biomedical Research Centre at the University of Salford.
Cancerous stem cells are often left behind after chemotherapy with the potential to create new tumours — a process called recurrence and metastasis.
In research published in the journal Oncotarget, the Salford team conclude that stem cell characteristics and behaviour are instrumental in metastasis and believe the key to their reactivation is an enzyme called Telomerase, or hTERT.
Using lung, breast and ovarian cancer cells, the team set out to identify which cells are cancerous by their levels of Telomerase, an enzyme which endows cells with the ability to multiply.
To achieve this, they followed Telomerase activity with a fluorescent protein, GFP, more commonly found in jellyfish, effectively colouring each cells to mark it either ‘active’ or ‘inactive’.
Cells highlighted ‘fluorescent’ (hTERT-high) were found to be up to 15 times more active than others with an vastly increased capacity for migration and cell proliferation.
Michael Lisanti, Professor of Translational Medicine at the University of Salford said: “We reasoned that if we could spot the telomerase activity, we could identify which cells were cancerous.
“What we had not expected was to find the very rapid rate of proliferation of the cancer stem cells.
“Clearly, this contradicts the accepted view that stem cells do not proliferate quickly, and offers an alternative view of the process of metastasis, and moreover, a method of identifying, isolating and potentially killing tumour-forming cells.”
As part of the study, the team found that FDA-approved drugs, such as doxycycline and palbociclib, were effective at halting cancer stem cell propagation. Palbociclib blocks the activity of proteins known as cyclin-dependent kinases (CDK) and inhibits the division of cancer cells, but until now hadn’t been shown to effectively block cancer stem cell reproduction.
“The use of these FDA-approved drugs may provide a mechanism for treating metastatic disease on a larger scale and certainly opens the way for new Phase II clinical trials in multiple cancer types,” adds Professor Lisanti.
Dr Federica Sotgia, Reader of Translational Medicine at the University of Salford said: “We can now begin to think of cancer stem cells as being at the heart of tumour regrowth and turn our efforts away from ‘bulk cancer cells’, which don’t really drive tumour recurrence and metastasis.”
- Gloria Bonuccelli, Maria Peiris-Pages, Bela Ozsvari, Ubaldo E. Martinez-Outschoorn, Federica Sotgia, Michael P. Lisanti. Targeting cancer stem cell propagation with palbociclib, a CDK4/6 inhibitor: Telomerase drives tumor cell heterogeneity. Oncotarget, 2016; DOI: 10.18632/oncotarget.14196
EVERY TIME A CELL DIVIDES, A TELOMERE LOSES IT’S WINGS
- The length of a telomere controls cell age.
- Each time a cell splits, the telomere gets smaller.
- Too long and cancer risk increases.
- Too short and no more cell division.
Scripps Research Institute discovered the TZAP that controls telomere length. “TZAP: a Telomere-Associated Protein involved in telomere length control”
Master regulator of cellular aging discovered
- Date: January 12, 2017 – Source: Scripps Research Institute – Summary: Scientists have discovered a protein that fine-tunes the cellular clock involved in aging.
This novel protein, named TZAP, binds the ends of chromosomes and determines how long telomeres, the segments of DNA that protect chromosome ends, can be. Understanding telomere length is crucial because telomeres set the lifespan of cells in the body, dictating critical processes such as aging and the incidence of cancer.
“Telomeres represent the clock of a cell,” said TSRI Associate Professor Eros Lazzerini Denchi, corresponding author of the new study, published online today in the journal Science. “You are born with telomeres of a certain length, and every time a cell divides, it loses a little bit of the telomere. Once the telomere is too short, the cell cannot divide anymore.”
Naturally, researchers are curious whether lengthening telomeres could slow aging, and many scientists have looked into using a specialized enzyme called telomerase to “fine-tune” the biological clock. One drawback they’ve discovered is that unnaturally long telomeres are a risk factor in developing cancer.
“This cellular clock needs to be finely tuned to allow sufficient cell divisions to develop differentiated tissues and maintain renewable tissues in our body and, at the same time, to limit the proliferation of cancerous cells,” said Lazzerini Denchi.
In this new study, the researcher found that TZAP controls a process called telomere trimming, ensuring that telomeres do not become too long.
“This protein sets the upper limit of telomere length,” explained Lazzerini Denchi. “This allows cells to proliferate — but not too much.”
For the last few decades, the only proteins known to specifically bind telomeres is the telomerase enzyme and a protein complex known as the Shelterin complex. The discovery TZAP, which binds specifically to telomeres, was a surprise since many scientists in the field believed there were no additional proteins binding to telomeres.
“There is a protein complex that was found to localize specifically at chromosome ends, but since its discovery, no protein has been shown to specifically localize to telomeres,” said study first author Julia Su Zhou Li, a graduate student in the Lazzerini Denchi lab.
“This study opens up a lot of new and exciting questions,” said Lazzerini Denchi.
In addition to Lazzerini Denchi and Li, authors of the study, “TZAP: a telomere-associated protein involved in telomere length control,” were Tatevik Simavorian, Cristina Bartocci and Jill Tsai of TSRI; Javier Miralles Fuste of the Salk Institute for Biological Studies and the University of Gothenburg; and Jan Karlseder of the Salk Institute for Biological Studies.
The study was supported by the American Cancer Society (grant RSG-14-186-01), the Swedish Research Council International (grant D0730801) and the National Institutes of Health (grant R01GM087476 and R01CA174942).
- Julia Su Zhou Li, Javier Miralles Fuste, Tatevik Simavorian, Cristina Bartocci, Jill Tsai, Jan Karlseder, Eros Lazzerini Denchi. TZAP: A telomere-associated protein involved in telomere length control. Science, 2017; DOI: 10.1126/science.aah6752
Heart drug linked to higher breast cancer risk
Women taking the heart drug digoxin have an increased risk of breast cancer, according to a study of more than 2 million Danes.
By Genevra Pittman – NEW YORK |
(Reuters Health) –
Digoxin, marketed as Lanoxin and Digitek, is used by people with heart failure or with abnormal heart beats. But it can also act like the female hormone estrogen in the body…
those currently on it were about 40 percent more likely to get breast cancer.