Major advances in history and a common link
The 1950's and anti-folate metabolism
An earlier advance in cancer treatments were the anti-folates, which prevent metabolism of folic acid. Inititally in the 1950's anti-folates were used to prevent remission in childhood leukemias and then later in solid tumours. Methotrexate is still a cornerstone of cancer treatment today. Findings from a study found that a diet high in synthetic folate may be associated with increased progesterone levels. In other words there is a link between folate and hormones. (‘The impact of dietary folate intake on reproductive function in premenopausal women,’ Perkins, Schisterman et al, 26th September 2012.) Methotrexate is effective for the treatment of a number of cancers, alone or in combination including: breast, head and neck, leukemia, lymphoma, lung, osteosarcoma, bladder, and trophoblastic neoplasms [1a]. It works on fast-dividing cells by inhibiting the metabolism of folate. Low-dose methotrexate is also used for certain autoimmune diseases like rheumatoid arthritis and it is used to cause abortion.
The 1980's and neutrally-charged platinum
A second major advance occurred when platinum therapy in the 1980's sent cure rates from 10% to 90% for testicular cancer, harnessing the electrical properties of platinum to kill cancer cells. Platinum provided an electrical current that was able to interact with salt, water and nitrogen. Courtesy of its neutral charge, platinum can go across cell membranes, (like hormones do). And ultimately stop cancer cells from dividing by binding to DNA – through the process of water replacing salt (cells are “less salty” than blood) – and then nitrogen replacing water.
The 1990's – chromosomal mutations and inhibiting tyrosine
A third advance in the nineties was when the cure rates for chronic myeloid leukemia (CML), a blood cancer, went from 5% to 90%. This was due to the development of tyrosine kinase inhibitors (TKI's). In cancer, there is a gene mutation that can produce abnormal amounts of tyrosine. Inhibiting the abnormal protein that the cancer needs to grow can stop certain cancer growth. In chronic myeloid leukemia there was only one driver mutation caused by translocation and it was easier to inhibit the protein produced by this gene mutation. In many other cancers multiple mutations need to be addressed.
A fourth advance involved drugs that inhibit estrogen. Cells are sensitive and reactive to this hormone. This is true in both men and women. Estrogen blockers help with both breast and prostate cancer. High estrogen can be involved in prostate cancer since the estrogen receptor and testosterone receptor are close together and may fuse. This can result in excess estrogen being produced by the testosterone receptor and can contribute to prostate cancer. Blocking estrogen does not stop cancer cells specifically, but stops proliferation of all cells and means mutated cancer cells have a lower chance of proliferating. (Is it possible the immune system therefore has less mutant T-cells to deal with?)
A fifth advance started around 2015 with Immunotherapy, which has changed the standard of care in melanoma, lung cancer, kidney cancer and other indications due to significantly superior survival rates and a better safety profile. These treatments turn immune cells such as T-cells back on so that tumours are attacked.
*The advances in cancer have a common link: hormones.
1. Platinum therapy stops cell growth by crossing cell membranes, like hormones.
2. TKI's inhibit tyrosine, a precursor for hormones.
3. Estrogen Blockers inhibit estrogen, a hormone.
4. Immuno-oncology turns the immune system back on by reactivating T-cells. Hormones also govern T-cells. For instance estrogen up-regulates natural killer cells (see below)..
Links between tyrosine, estrogen, tryptophan, serotonin and the immune system
Like phenylalanine and tyrosine, tryptophan is an olfactory amino acid impacting metabolism. Tryptophan is converted into NADH (refer chapter on stem cells in the book) and is also a precursor for serotonin. Estrogen and progesterone impact expression of serotonin receptors in the central nervous system. The liver can synthesize niacin from tryptophan, but excess estrogen can inhibit the conversion of tryptophan to niacin (vitamin B3).
Estrogen also protects against atherosclerosis (when arteries are clogged by fatty substances ) and estrogen up-regulates the immune system, through the activation of natural killer cells to fight infection. Estrogen also offers protection of immune cells from apoptosis  (programmed cell death) and production of pro-inflammatory cytokines such as IL- 6  . In addition progesterone and testosterone can down-regulate the immune system.
 Collins P, Rosano GM, Sarrel PM, Ulrich L, Adamopoulos S, Beale CM, McNeill JG, Poole-Wilson PA (1995)"17 beta-Estradiol attenuates acetylcholine-induced coronary arterial constriction in women but not men with coronary heart disease".
 Vegeto E, Pollio G, Pellicciari C, Maggi A. Estrogen and progesterone induction of survival of monoblastoid cells undergoing TNF-α-induced apoptosis. FASEB Journal. 1999.
 Sorachi KI, S. Kumagai M. Sugita et al. ‘Enhancing effect of 17β-estradiol on human NK cell activity.’ Immunology Letters. 1993.
 L. Miller, J.S. Hunt. ‘Sex steroid hormones and macrophage function.’ Life Sciences. 1996.
Hormones and immuno-oncology
The hormone estrogen up-regulates the immune system
Estrogen or estradiol is a hormone and steroid affecting reproductive tissue and other tissue, including bone. It also has essential functions in men for instance to stop apoptosis of sperm cells. It is made from progesterone, arriving in 2 steps from cholesterol . It affects the liver and heart since it has a protective role in both organs. It affects the production of many proteins, including lipoproteins and proteins responsible for blood clotting. It affects blood vessels and it is speculated that it may activate certain oncogenes (cancer genes) especially in breast cancer and cancer of the uterine lining. Estradiol is a hormone, which activates the immune system, for instance enhancing natural killer cells (NK cells) allows for bacterial clearance and recovery from infection.
Hormones and bacteria
Hormones such as estrogen, testosterone and progesterone are linked to bacteria
They participate in the communication between microorganisms and mammal hosts. This type of communication is commonly referred to as “interkingdom signaling” and can be used by microbial pathogens to activate their virulence factors and control the course and outcome of infection .
Certain bacteria can degrade estradiol . For instance In Stenotrophomonas maltophilia, a bacterium that degrades estradiol, it was determined that estrone is converted into the amino acid tyrosine, this amino acid in turn can be utilized in protein biosynthesis; however, the enzyme responsible of this conversion was not identified  . Grapefruit juice and antibiotics like erythromycin and clarithromycin can increase estrogen levels in the blood by slowing down it's metabolism. If estrogen is not metabolized, it stays in the blood. Antibiotics can play a role in the metabolism of hormones since we know fecal bacteria, can be reduced when antibiotics are taken. Such bacteria may be needed to metabolise estradiol and testosterone.
Testosterone and progesterone down-regulate the immune system
Testosterone suppresses the immune system, for instance by suppressing natural killer cells and suppressing pro-inflammatory cytokines such as TNF alpha. Progesterone reduces natural killer cell activity and suppresses production of IFNy and TNF alpha, which deal with bacterial infections for instance. For this reason when progesterone is high in pregnancy, it can predispose to infection.
Fertility and cancer cells
The molecule JQ1 stopped the growth of lymphomas in mice models and is related to MYC levels, but more interestingly it was found, that JQ1 blocked sperm functioning .
Sleep and cancer cells
Fertility and sleep have a relationship to cancer cells. It was found that a protein regulating circadian rhythms and sleep - is also an important tumour suppressor (the PER2 clock protein). It may be able to turn off the function of the MYC gene. It appears to turn MYC off, since MYC levels rise in its absence (refer section on James Watson for more on how high MYC levels may be implicated in advanced cancers).
Autoimmune disease and cancer cells
CTLA4 or CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), also known as CD152 (cluster of differentiation 152), is a protein receptor, found on the surface of T-cells, and acts as an "off" switch when bound to CD80 or CD86 on the surface of antigen presenting cells. In other words puts the brakes on T-cells and instructs them not to attack cancer cells. It is also known as an immune checkpoint inhibitor, which downregulates the immune system. I think of protein 4 as a brake protein on T-cells.
Vitamin D and anti cancer therapies
Taking Vitamin D has been associated with a decrease in autoimmune disease, but in cancer immunotherapy we try to tip the balance in favour of immune response, which may increase autoimmune disease. For autoimmune disease we desire the protein 4 (CTLA4) brakes to work so that the immune system is not over-active, but in cancer we generally desire that the protein 4 brakes do not work so that T-cells are more active. In a recent research paper on Vitamin D, Jeffery and Qureshi et al. discuss how TH17 can inhibit or suppress CTLA4 brakes. However Vitamin D can enhance CTLA4, especially in the presence of TH17 (reference: ‘Vitamin D antagonises the suppressive effect of inflammatory cytokines on CTLA-4 expression and regulatory function. Louisa E. Jeffery, Omar S. Qureshi et al. Plos, 2nd July 2015). As opposed to automimmune disease where we try to put the brakes on T-cells, in cancer we do the opposite and use anti-CTLA4 therapies to take the brakes off. We may wish to explore whether lower vitamin D levels (and cholesterol which is related to Vitamin D) may help the anti-CTLA4 immunotherapies. Vitamin D comes from cholesterol and vice versa. There is also a link of vitamin D to NAD - the adenine in NAD and NADH, strongly absorbs UV light. As a recap insufficient NAD can lead to ‘excess’ ROS and ‘excess’ antioxidants. Insufficient NAD/low tryptophan/low vitamin B3 can lead to a lowered immune system (see stem cells section). NADH absorbs UV light (see end of viruses and bacteria section).
Side effects of treatments
When anti-cancer agents are given, the side effects can often include blood clotting (thickening), blood thinning or a cardiovascular event such as a heart attack. That raises the question 'Is cancer initiated in our bodies in order to remedy or address larger issues such as cardiovascular problems or appropriate regulation of blood flow?'
Some cancers appear to result in a higher incidence of cardiovascular disease.
In a Nordic study, cardiovascular disease was diagnosed in 8.1% of childhood cancer survivors. Survivors of childhood hepatic (liver) tumor, hodgkin lymphoma and leukemia had the highest overall risks for cardiovascular disease, although each main type of childhood cancer had increased risk with different risk profiles. The highest relative risks measured by standardized hospitalization rate ratio (RR) were seen for heart failure (RR, 5.2; 95% CI 4.5–5.9), valvular dysfunction (4.6; 3.8–5.5) and cerebrovascular diseases (3.7; 3.4–4.1). These findings, according to the study, indicate the need for preventive interventions and continuous follow-up for this rapidly growing population. (‘Cardiovascular disease in Adult Life after Childhood Cancer in Scandinavia: A population-based cohort study of 32,308 one-year survivors, T. Gudmundsdottir, J.F. Winther et al. March 2015). In many cases the cardiovascular disease can be as a result of the medications given to treat the cancers. Interestingly, the majority of patients with hodgkin lymphoma are now cured - around 80% versus only 20% about a decade ago. But these cures come at the price of long-term side-effects such as a secondary tumours (around 10% at 15 years) and cardiovascular and pulmonary events (around 10% at 20 years). (Source: A presentation by Dr Michele Ghielmini, Oncology Institute of Southern Switzerland, European School of Oncology (ESO)). These long-term side effects are caused by a combination of chemotherapy, especially alkylating agents and radiotherapy, therefore we try to give just enough for a cure and here positive PET-CT scans are used to guide intensifying the dose. As we start to ‘cure’ more cancers, we may have to learn more about side effects like these; and also use scans and other markers to identify appropriate doses.
Side effects of immunotherapy
Immunotherapy can cause side effects associated with an overactive immune system and autoimmune disease. This may involve a range of symptoms from mild itching to inflammation of the intestines, which can be serious if not treated with prednisolone (steroids). An interesting hormonal link with immunotherapy is that the immune system can infiltrate some endocrine (hormonal) organs such as the thyroid, which controls metabolism, and the pituitary gland, a kind of master regulator controlling the rest of the body and many other glands. We don’t completely understand why. If these glands stop working as they become full of immune cells, the glands stop producing the hormones needed and it may be necessary to take lifelong hormone replacement therapy .
Same treatment different diseases (cardiovascular, respiratory, multiple sclerosis, viruses, clotting)
Below see some common drugs for other diseases that may also be useful in treating cancer:
Metformin, the anti diabetic drug, may help with cancer according to James Watson. Molecules called reactive oxygen species (ROS) help stabilize proteins as they fold. When there is not enough oxidation Watson says proteins emerge unfolded, and cannot function. This, he proposes, causes the inflammation that harms the pancreas, sometimes causing Type 2 diabetes. Watson suggests that taking the diabetes drug Metformin may help reduce cancers, especially at their late stage, since it may reduce cancer stem cells. Furthermore ROS are needed to ensure programmed cell death, or apoptosis, of cancer cells. There is conflicting evidence in studies about whether Metformin can benefit cancer patients. Studies are small and I do not know if they were performed on late stage cancers (refer stem cell section in this website.)
Gilenya, a fungus based treatment for multiple sclerosis, may be benefical in pancreatic cancer. (‘A preclinical evaluation of minnelide as a therapeutic agent against pancreatic cancer’ Rohit Chugh Veena Sangwan et al. 17 Oct 2012.) Myriocin, or minnelide was isolated from a type of fungus, Isaria sinclairii, and used in traditional Chinese medicine. This is now the successful drug Gilenya used for multiple sclerosis (extracts from an article in the Register, 18 October 2012, Phil Muncaster).
Lemtrada, an approved drug for multiple sclerosis; is also used in cancer.
Paclitaxel, a fungus-based medicine for cancer is also used as an anti-viral and to widen the arteries - see more below.
Methotrexate used for certain autoimmune diseases like rheumatoid arthritis (at low doses) is a mainstay cancer drug, which works on fast-dividing cells by inhibiting the metabolism of folate.
Propranolol, the most common type of non-selective beta-blocker, improved survival for patients with cancer by 4 years in one study: when cancer patients were also taking this drug for heart conditions, average survival was 95 months versus 38 months for patients not taking a beta-blocker . Stress hormones bind to receptors causing a fight-or-flight response such as rapid heartbeat and sweaty palms. These stress hormones may lead to suppression of the immune system when binding with stress receptors. Cancer cells may have similar receptors which stress hormones can bind to to cause spread of cancer cells. Work funded by the Cancer Research Institute has shown that T-cells that are supposed to attack cancer may also have these receptors, and this could dampen their killing ability. Beta-blockers may work in part by relieving this immune suppression . Beta-blockers, especially non-selective ones, may help in ovarian, breast and other cancers, but they have side effects, so it is too soon to recommend them as cancer treatment according to this cancer study.
Combination treatments work across diseases
In finding the cure for Hepatitis C, we drew from our knowledge of anti-retrovirals in HIV, showing that combination treatments were much more successful than single agents, partially because combinations were able to target different genotypes. We also know that in HIV one percent of the population have shortened CCR5 receptors, conveying immunity to HIV! More work on such receptors seems warranted.
Cancer and cardiovascular disease
There is a relationship between cancer and thromboembolic complications. Thromboembolic complications (lack of blood flow) is the 2nd leading cause of death in cancer patients (pubmed 2011.) In the Murchison study 2004 it was found patients had a 420% higher chance of getting cancer after 6 months if they have thromboembolic problems. Also notable, the side effects of many of the new tyrosine inhibitors (for chronic myeloid leukemia for instance) often have the side effect of either thickening the blood too much (thromboembolic events) or thinning the blood too much. There is also a higher risk of heart attacks (for instance with Ariad’s drug Iclusig for leukemia, see label). Cancer drugs like Herceptin for breast cancer punch holes in the heart when they combine with iron. Drugs for prostate cancer, which block the hormones like androgens, can affect the heart, blood pressure, blood sugar and cholesterol. Refer to propranolol above for a relationship between drugs for cardiovascular disease and cancer.
Thrombosis, genetics and cancer
The connection of ‘thick’ blood and cancer is becoming more obvious with the discovery of new genetic markers. For instance in 2005 a number of studies identified that 95% of patients with the disease Polythemia Vera (PV), have an acquired gene mutation (acquired genetic mutations are not inherited). PV is a condition affecting almost 100 000 people world wide where blood is too thick due to too many red blood cells being produced in the bone marrow. PV can lead to blood clots, heart attacks, lack of oxygen to the legs/lungs, dizziness and other symptoms. In addition 45% of people with Myelofibrosis (a rare blood/bone marrow cancer with prevalence of almost 20 000 in the U.S. according to Incyte) have this acquired mutation as well and there is now a treatment called Ruxolitinib (Jakafi) by Incyte for people with these aqcuired genetic markers (it is also linked to JCV virus antibodies.) This same Myelofibrosis cancer drug, Jakafi, was approved for Polythemia Vera in December 2014. It is a good example of where a cancer drug now works for a disease where our blood is too thick, based on a common genetic mutation that we only identified 10 years ago. This genetic mutation is found in PV and cancer. A few years ago it was too expensive to do these acquired gene mutation tests, but it is now becoming cheaper and more viable.
About Paclitaxel (Gemzar, Abraxane)
Paclitaxel an anti-cancer drug sourced from yeast, a fungus that grows on the bark of the yew tree Taxus Brevifolia. Taxanes are now synthesized rather than coming directly from the tree. Paclitaxel can prevent cancer cells from dividing by stabilising microtubules. It also increases reactive oxygen species (ROS), was used as an anti-viral in the past and it can be used to widen the arteries. Since it can be used to widen arteries it is worth observing that estrogen plays a role in that it reduces atherosclerosis. Incidentally in pancreatic cancer we often find clots, and these might serve as clues to the causes of cancer -the cause and reason for the clots is unknown. It is possible that the yeast-based anti-cancer agents reduce clotting, which could be from many sources including viruses and bacteria? Is Paclitaxel connected to estrogen? For instance, might the yeast or 'fungi' in Paclitaxel inhibit conversion to estrogen or degrade estrogen, like bacteria do? This could be similar to how mushrooms stop aromatase and conversion to estrogen. There is weak evidence for this. Refer ‘Anti-aromatase activity of phytochemicals in white button mushrooms ’Chen S, Oh SR, et al. 2006).
Stabilisation of microtubules to prevent cancer cells from dividing
Normally microtubules become too strained when tubulin stops growing, and so the microtubules peel off, like when banana skins are peeled, to allow continued growth of dividing cells and the release of tubulin for recycling into other microtubules. Taxol inserts itself in the microtubule, preventing this ‘peeling off action’ and thereby preventing the cancer cell from dividing. The epothilone B analogue, ixabepilone, stabilises microtubules in a similar way to taxanes, although it has not shown increased survival. 'Earlier in 2011 Eribulin, a non-taxane inhibitor of microtubule dynamics with a distinctly different mode of interaction with microtubules, achieved a statistically significant and clinically meaningful improvement in overall survival compared with physician’s choice of treatment in women with heavily pre-treated metastatic breast cancer' (sources: ‘How bark from the Pacific yew tree improved the treatment of breast cancer’ Jenny Bryan, The pharmaceutical Journal September 2011; ‘Discovery of how Taxol works could lead to better anticancer drugs’, Robert Sanders, May 2014). Because taxanes are originally from yeast, it is interesting that they are able to stabilise microtubules and prevent division of fast-dividing cells, including preventing release of tubulin for recycling into other microtubules. Since yeasts may in some form be able to inhibit conversion to estrogen; I am querying whether there is a dual function here, whereby microtubules are stabilised, fast-dividing cells are arrested in the actions described above and the aromatase enzyme is inhibited at the same time, reducing estrogen levels? Since beneficial bacteria can also degrade estrogen, it might be interesting to know if the yeast from the bark of the yew tree has a similar function here in degrading estrogen. Furthermore, can Paclitaxel's potential to 'turn off' the estrogen receptor, be linked to clotting? Also refer resistance and link to antioxidants, diabetes and Metformin as a possible treatment for cancer.
Anti clotting and Paclitaxel
Gemzar can be used to widen the arteries; therefore it is useful to ask whether there is a clotting link related to infection (clots may be ‘walling off’ infections) or lack of blood flow and oxygen, and whether Paclitaxel plays its anti-cancer role here via reducing or modulating clotting?
Anti-virals for pancreatic
Do compounds similar to Gemzar exist, which viruses are not resistant to? Paclitaxel used to be given for viruses. Refer also James Watson in the stem cell chapter at the beginning of this book (he recommends looking into the Piper Longum plant which might increase ROS and apoptosis, through reducing antioxidants which limit ROS). Given it takes on average 28 years to die of liver cancer from contracting Hep C, should we be more focused on administering vaccines and anti-virals earlier on in life? Can anti-virals be given for cancer patients? If anti-virals are working, we may not know it, since a cancer like pancreatic may kill the patient before the treatment takes effect. Note that in biological development the liver, pancreas and bladder all come from the endoderm (the first layer of cells in the embryo). Both liver and pancreatic cancer are rising in incidence, but bladder cancer incidence, which occurs more in men, is falling.
The measles virus (and HIV)
The measles virus tested against a variety of tumours in animal models where it shows a broad spectrum of activity against lymphoma, multiple myeloma, ovarian cancer, brain cancer and pancreatic cancer. Ovarian cancer was one of the first cancers where activity was shown. (Ref: ‘Measles virus for cancer therapy’ Stephen J. Russell, M.D., Ph.D. and Kah Whye Peng, Ph.D. 17 Feb 2014, Pubmed.)
Fighting a virus with a virus
In a similar vein when we modify T-cells in CAR-T immunotherapy, we use an inactivated HIV virus as the growth vector to grow T-cells before reinfusing them back into the body. Since the HIV virus has a long life cycle, this also gives the T-cells a more durable killing effect. It is possible, however that the HIV virus is playing an additional role in attacking other viruses; which may be creating cross talk within the body. This would assume you are fighting a virus with another virus.
BRCA1 gene for DNA repair and Alzheimers
On 30 November 2015 the NIH said research funded by them revealed deficient DNA repair might lead to dementia. The breast cancer factor 1 (BRCA1) gene associated with breast and ovarian cancers may also be linked to Alzeimer’s disease. The results published in Nature Communications, suggest that low levels of BRCA1 protein in the brain may contribute to dementia. Researchers also found reductions of the BRCA1 protein in brains of mouse models. When researchers reduced BRCA1 levels in the brains of healthy mice, the animals developed learning and memory problems and incurred DNA damage. Moreover adding beta-amyloid - which can lead to death of neurons (nerve cells) and is a hallmark of Alzheimer’s disease - lowered levels of BRCA1. ‘An emerging theme in neurodegeneration research is that normal DNA repair protects against damage that causes neurons to die’ says Roderick Corriveau, Ph.D. at the NIH. Senior author Lennart Mucke, MD, director of Gladstone Institute of Neurological disease said ‘it is extremely interesting that one molecule can be critically involved in two apparently opposing conditions: cancer, in which too many cells are born and neurodegenerative disease, in which too many brain cells die off.“ BRCA1 plays a key role in repairing DNA, our genetic code. When DNA strands break and are not repaired properly by DNA proteins including BRCA1, the cell may die.
Summing up, when BRCA1 levels were reduced in mouse models (by adding beta-amyloid for instance), learning and memory problems and DNA damage was incurred. Low BRCA1 protein levels were also found in dementia patients. Deficient DNA repair could contribute to death of neurons.
Can we block progesterone so that the immune system is not suppressed?
Is it possible to use bacteria instead of estrogen inhibitors to degrade estrogen? (When the immune system is overactvated?)
When we find high estrogen levels in blood tests, is the estrogen there to fight infection and to reduce clotting?
Why do we sometimes have clots in pancreatic cancer?
Is it possible that an immune system is unable to fight cancer, because it is fighting something else like bacteria?
Can we find out what causes the immune system to be elevated? (I.e what causes the elevated TNF-Alpha or elevated natural killer cells)?
Can the immune system be elevated to fight bacteria, but suppressed to fight cancer (in other words it has two states at the same time?)
When we inhibit estrogen, do we also inhibit tyrosene (explaining the success of both estrogen blockers and TKI’s in treating cancer)?
Are we preventing the immune system from dealing with cancer and/ or bacteria when we inhibit tyrosene?
When we inhibit estrogen with breast cancer drugs for instance, are we contributing to resistance to treatments? (Possibly because existing infection is not fought and therefore new cancer stem cells must grow to fight infection?)
Do cancer cells grow initially to fight infection?
When we treat with estrogen blockers and tyrosene kinase inhibitors (TKI's) do we make it more difficult for immuno-oncology to work? (We know estrogen inhibitors and tyrosine inhibitors can switch off the immune system).
When we use estrogen blockers and TKI's do we also cause an 'original problem' to return? (Estrogen is used to reduce clotting and fight infection).
Does Paclitaxel impact estrogen?
 "Synaptocrine signaling: steroid synthesis and action at the synapse." Endocrine reviews (2011).
 Hughes DT, Sperandio V. ‘Inter-kingdom signalling: communication between bacteria and their hosts.’ Nature reviews microbiology, 2008.
 Role of Sex Steroid Hormones in Bacterial-Host Interactions Elizabeth García-Gómez, Bertha González-Pedrajo
 Saldanha, Colin J., Luke Remage-Healey, and Barney A. Schlinger.
 Li Z, Nandakumar R, Madayiputhiya N, Li X. Proteomic analysis of 17beta-estradiol degradation by Stenotrophomonas maltophilia. Environmental science & technology, 2012, Pubmed.
 (Delmore JE, et al.2011 BET bromodomain inhibition as a therapeutic strategy to target c-MYC. Cell 146,904–917. doi: 10.1016/j.cell.2011.08.017).
 Source: Talk by Dr Jedd Wolcheck, Webinar Cancer research Institute.
 The study, in the Cancer journal, led by Anil Sood, M.D., at The University of Texas MD Anderson Cancer Center, looked at 1,425 patients who were treated for cancer between 2000 and 2010 according to the Cancer Research Institute blog in October 2015.
 The Cancer Research Institute is funding the work of Ming O. Li, Ph.D., an immunologist at Memorial Sloan Kettering Cancer Center through a Clinical and Laboratory Integration Program (CLIP) grant. Dr. Li is looking at the role that signaling through beta-adrenergic receptors on specific immune cells called T cells has on the ability of these cells to fight cancer. - See more at: