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Understanding Cancer and Its Possible Treatments


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In clinical practice[10], doctors observe that many cancer patients simply don't develop fevers, and cancer patients often report that they were never ill. Fever is the signal that launches our immune defenses.  Once a fever reaches 101.3oF (38.5oC), the level of immune defenses in the blood doubles within the next six hours.

Cancer patients also often report that long before they received a cancer diagnosis, they suffered from insomia in one form or another, with constant fatigue and sometimes feelings of depression or loss of control[10].

What's Cancer?

Cancer is a disease of our genes (or DNA) and their proteins. Like all living organisms, our bodies are making defective cells all the time.  Cancer lies dormant in all of us. Disturbing new research[3] suggests that microscopic cancer, small cancer cells (0.5mm3) that can only been seen under a microscope, is widely prevalent. A recent study of women in their 40s indicated that 40% of them had microscopic breast cancer. Even more shocking, almost 100% of people in their 70s will have microscopic cancer in their thyroid glands.
 
However, our bodies are also equipped with a number of mechanisms that detect and keep such cells in check. It is up to each of us to use our body's natural defenses. When we're healthy, there is an ongoing balance between the spontaneous development of new cancer cells and our bodies' immune activity to identify and eliminate the newly formed cancerous cells as rapidly as possible.[21,22] 

In Dr. Gorter's clinical practice[10], he has found that:
  • Some patients have impaired immune function, which occurs when the patient is unable to mount a fever.  This means that the immune system has no way to launch a major response to combat cancer cells that being amassing.
  • Some other patients have impaired immune signaling: the cells that normally identify cancer and trigger an immune response are inactive.
If not keeping cancer cells at bay, they can become wild and pursue their own longevity, immortality, or fountain of youth.[24] Wellsort of. Cancer cells selfishly consume resources to sustain its own perpetual life, they ultimately drain the life from the very body it is dependent upon for survival.

Growth-Signaling Pathways

Body grows and repairs by duplicating cells. Cell division normally begins with the tightly coiled DNA opening up to start copying itself in response to signals triggered from outside the cell. The message are carried along from the cell surface to its nucleus by a series of proteins that make up growth-signaling pathways. The human genome is loaded with genes which express proteins that make up these metabolic routes, and when the genes start barking out inappropriate orders to divide in an uncontrolled way, any one of them can become an oncogene.

Oncogenes can form at many points along this relay: growth factors outside the cell, specific growth receptors on the cell membrane that these factors lock onto, other proteins inside the cell that pick up signals from receptors and relay them to the cell nucleus, and ones that interact directly with the DNA to trigger or sustain the cell division process.

Apoptosis

Due to normal wears-and-tears and other environmental factors, DNA changes or mutates. These changes can accumulate over time and cause genetic errors. In Mother Nature's wisdom, adult cells age and will eventually be disposed of by the body. Apoptosis is used to describe this natural and purposeful cell death. Suicide genes lie dormant in all cells, waiting until they get a fateful call to trigger apoptosis. When the system is working, apoptosis eliminates rogue cancer cells long before they have a chance to form a tumor mass. However, sometimes cancer cells can evolve ways to outwit our many bodily defenses.

How Cancer Cells Outwit Bodily Defense

In the following table, I've listed different techniques that cancer cells use to survive or outwit bodily defense and perpetuate their uncontrolled growth as described in [1].  Based on these cancer cells' survival techniques, Dr Healy[1] has discussed the possible cancer treatment strategies.  At the end of article, you can also find useful sources that describe various cancer treatment strategies.  Using these information, you as a cancer patient can discuss these possible strategies with your caring doctors.

Cancer Cells' Survival Techniques Descriptions Cancer Treatment Strategies
Reactivate telomerase (or turning on telomerase gene) Telomeres cap the ends of chromosomes and keep the DNA strands from fraying or sticking each time they duplicate themselves. Each cell division telomeres get shorter, until they disappear. When the telomere is consumed, the cell can no longer clone itself. Therefore, they function like a timer counting off the number of times any given set of chromosomes can copy itself during normal growth and reproduction. By reactivating telomerase (an enzyme) which preserves and rebuilds telomere, cancer cells take this timeout mechanism off chromosome copying.
  • Health lifestyle with stress management[4] has been shown to prevent or even reverse stress-induced damage to DNA telomeres.
  • Could a telomerase blocker be a cancer therapy?[26]
  • Schmidt and others at at CU Boulder’s BioFrontiers Institute envision a new generation of targeted cancer drugs which would work by inhibiting telomerase's  cell-preserving process in cancer cells, while sparing healthy ones (thus avoiding the hair loss and other side effects that cancer drugs can bring).[62]
Block apoptosis by generating survival proteins or turning off the suicide gene
  • Apoptosis is the body's natural way of eliminating old or damaged cells to ensure orderly growth and repair. This targeted self-destruction (or recycling) is a natural process that makes room for new growth. Suicide genes lie dormant in all cells, waiting until they get a fateful call to trigger apoptosis. By blocking apoptosis, cancer cells can grow uncontrollably.
  • When we talk about inheriting a susceptibility to cancer, we usually mean that one of a pair of suppressor genes is abnormal at birth. Suppressor genes counter tumor growth and, if need be, destroy a hopelessly misbehaving cell by triggering apoptosis. Tumor suppressor gene[23] take many forms: some function as DNA's spell checkers, some repair damaged DNA segments, some slow down cell growth to allow time for natural repair mechanisms to kick in, some trigger suicide genes, etc.
  • Knock out the protein, such as BCL-2, that keeps cancer cells from self-destruction.
  • Chemotherapy and radiation wreak their havoc on actively replicating DNAs and damage them to the point of self-destruction.
  • Why elephants so rarely develop cancer?  The key may be p53 proteindue to extra copies of the p53 protein, the elephants' cells carry out apoptosis in response to DNA damage at much higher rates than do human cells.[48]
Form HSP (Heat Shock Proteins) It is now well established that HSP levels become amplified in a broad spectrum of cancers, are required for tumor progression.  HSP make cancer cells resilient to damage, particularly caused by environmental stress such as high temperature, low oxygen, or toxins, including chemotherapy or radiation. Cancer learns how to become more resilient to therapy by churning out abnormally high levels of these protective proteins. Target and reduce the high levels of HSP of tumors and make them more susceptible to therapy.[27,29,30]
Generate proteins that simulate cell growth Tyrosine kinase (a protein) is frequent oncogenic catalysts. They act as on-off switches, directing many of the core cell functions such as growth, development, and survivaland cancers use them to grow and prosper.
  • Hyaluronan appears to be part of the signalling that stops cells from multiplying uncontrollably. [45,46]
    • In other words, even if a mutation would cause a tumour to form, the hyaluronan stops it from developing further.
  • Search for new cancer therapies by mapping the cancer-stimulating proteins.
  • Find designer chemicals to block precisely the cancer-stimulating proteins on the surface or inside the cancer cell.
  • Cancer cells appear to have adapted in order to facilitate the incorporation of nutrients into cell building blocks (nucleotides, lipids, amino acids) to produce a new cell. 
    • Tumor's capability of metabolic reprogramming is induced by HIF-1, c-Myc, p53, PKM2, IDH, GLS and other molecules that act both independently and in concert with each other.[39]
    • These cancer-specific metabolic pathways have recently been used for cancer diagnosis and therapy.
Displace normal cells with tumors Cells organize into tissues by anchoring themselves to the 3D collagen web of the matrix. Certain tumors secrete a family of enzymes that work like meat tenderizer, helping the cancer cells break away their matrix restraints and tunnel through the surrounding space. MMP14 is the most important protein-cutting enzyme in terms of how cancer cells migrate throughout the body:[49]
  • Design drugs to dull the cancer cells' chemical drills as they invade.
Induce the growth of new blood vessels (or Angiogenesis) for cell growth The tumor must also initialize angiogenesis, without which the tumor would fail to develop, as local diffusion for transport of nutrients to and removal of waste products from the tumor site would suffice for tumors up to 2 mm in diameter.[35]

Cancer cells secrete chemicals that induce the formation of their own network of blood vessels. These new vessels are leakier than normal ones, causing them to bleed more easily. That's why blood in the sputum, stool, or urine can be first sign of a hidden cancer.

  1. Aim to inhibit Vascular Endothelial Growth Factor (VEGF), which is produced in abundance in tumors on the march.
  2. In Dr. Oz show[3], these 5 foods are said to be anti-angiogenesis:
    1. Bok Choy
    2. Strawberries
    3. Cooked tomatoes
    4. Flounder (for its omega-3)
    5. Artichokes
  3. Naturally-Occurring Antiangiogenic Substances
  4. A must-watch video from Angiogenesis Foundation
  5. Controlled Amino Acid Treatment
    1. Elastin is a protein essential to the formation of new blood vessels, therefore cancers must be deprived of elastin to minimise or inhibit growth. [37]
    2. The constituent amino acids found in elastin are: proline, leucine, isoleucine, valine and glycine; the latter comprising almost one quarter of the make-up of the elastin.
    3. Serine and glycine are biosynthetically linked, and together provide the essential precursors for the synthesis of proteins, nucleic acids, and lipids that are crucial to cancer cell growth.
    4. By functional and genetic evidence, it has been found that hyperactivation of the serine/glycine biosynthetic pathway drives oncogenesis.[38]
  6. Inducing blood vessel regression 
    • "The two together -- IFN-γ and tumor necrosis factor -- are a powerful team. TNF bursts tumor blood vessels, thus opening up the tissue, while IFN-γ cuts off the blood supply and keeps the tumor at bay over the long term."[64]
Hijack bodily defense (i.e., inflammation or white blood cell) mechanism to its advantage
  • Cancer cells can produce inflammation-promoting chemicals called cytokines and chemokines to summon white blood cells to its advantage. Inflammation reflects the surge of white blood cells and chemicals that rush to the sites in distress, where they loosen up the matrix and encourage cell growth. This stimulates blood vessels to sprout and helps to clear out dead cells, while laying down loose scar tissue to replace them. Being homegrown insurgents, disguised cancer cells can manage to slip through this white blood cells' attack while take advantage of our bodily defense mechanisminflammation. 
  • Researchers at Cold Spring Harbor Laboratory found that neutrophils – the most common type of white blood cell – can be ‘hijacked’ by cancer cells and used to aid the spread of breast tumors to the lungs in mice. 

  • Control inflammation and other immune responses[6]. For example, control COX-2 protein (which fosters inflammation).
  • A possible way can be identified to target this neutrophil activity using nanoparticles, which could be developed into a new treatment.[59]
Hijack transport systems to carry cancer cells to distant organs
  • To spread distantly, cancer cells must master the ability to set off and travel to outlying territories, establish a beachhead, and then build an outpost where they can thrive in alien tissues and organs composed of cells of a completely different type.
  • Cancer cells can spread throughout the body by hitching a ride through blood vessels and lymphatic ducts.


Find drugs to tackle metastatic cancer which is the greatest shortcoming of cancer medicine today.  However, there are some new findings provide a hope to patients:
  • The free radical involved in the metastacism of tumor cells is superoxide. Tests in mice on melanoma and breast cancer cells showed that administering an antioxidant stopped the production of superoxide. That, in turn, prevented cell changes that would lead to metastasis.[33]
  • Lymphoma cells only become truly dangerous when they leave the blood vessels and multiply in the lymphatic system. Since they cannot survive in the blood for long, these malignant cells are compelled to find a more accommodating environment – such as the lymphatic system – where they can proliferate. Scientists at UNIGE decided to focus on this Achilles heel by containing them in the blood so as to prevent any resulting harm.[56]
  • In a study to be published on December 26th in Nature, it has found that fat fuels lymphatics and using drugs to prevent fat utilization by lymphatics prevented lymphatic growth, an important step in the inhibition of metastasis.[60]
  • A study at UC Riverside sheds light on how ovarian cancer spreads.  Their findings emphasize the importance of Ncad in ovarian cancer metastasis and provide the rationale to support pre-clinical studies using Ncad-blocking molecules as a therapeutic strategy to suppress epithelial ovarian cancer metastatic anchoring.[70]
Disguise themselves as normal cells
  • Certain organs are more likely to be colonized by cancer than others. The liver, lungs, bones, and brain are the organs most vulnerable to metastases. Other organs, such as the heart and the skin, are more resistant.
  • For a metastatic cluster of cells to take hold, the new organ of residence must provide fertile ground for their growth, and in turn, the cancer cell must disguise itself as a welcome guest.
  • One example of such mutual affinity is seen in the particularly aggressive form of breast cancer that carries the HER2/neu gene. These cancer cells wrap their wolf nature in sheep's clothing, coating their outer surface with the HER2 receptor protein, which makes the cell look like a white blood cell. When distant sites in distress put out a call for white blood cells as part of an inflammatory response, it is the HER2-bearing cancer cells that respond.
  • Major histocompatibility class I antigens cease to be expressed on the tumor cell surface, thus masking the presence of the tumor proteome and evading CD8+ killing.[28]
  • Avoid chronic inflammation[6].
  • Design drugs to block cancer cells' magnetic draw to distant organs.
  • Dr. Gorter[10] uses fever-range and total-body hyperthermia to force cancer cell putting their energy into surviving, and thus dropping their escape mechanisms.
  • BUILDING A BETTER T-CELL
    • By modifying T cells to express chimeric antigen receptors (CARs) that recognize cancer-specific antigens, researchers can prime the cells to recognize and kill tumor cells that would otherwise escape immune detection.

Conclusions

We cannot emphasize more on the word "possible" in the title.  Cancer treatment is by no means straightforward.[69]  Cancer itself takes decades to develop.  So, we don't expect it could be easily cured.  One treatment focusing on one factor may also vary based on conditions.  For example,  TGF-beta can be either a tumor suppressor or a pro-oncogenic factor depending on:[31]
  • cell type
  • growth conditions
  • presence of other polypeptide growth factors, etc.
As noted in the book "The Death of Cancer", the author argued that:
  • A given tumor, for instance, can rarely be stopped with a single drug. Cancer is like a door with three [or more] (my own addition) locks, each of which requires a different key
Therefore, "if cancer drugs were used in extremely large doses, and in multiple combinations and repeated cycles, the cancer could be beaten," said the scientists.[50]

Today we’re also beginning to treat cancer in a whole new way. Rather than killing cancer cells directly with chemo or radiotherapy, the latest treatments are designed to target cancer cells selectively[51] and then promote the body’s natural immune control over the disease.

The most promising immunotherapies are antibody drugs, which target key switches on immune cells and fall into two main classes:[32]
  • Checkpoint blockers [44,52,68]
    • Drugs such as ipilimumab and nivolumab work by removing the cancer’s ability to switch off the immune system
    • Similarlly, Keytruda and durvalumab works by targeting the cellular pathway known as PD-1/PD-L1 (proteins found on the body’s immune cells and some cancer cells). [65]
      • By blocking this pathway, Keytruda and durvalumab may help the body’s immune system fight the cancer cells.
  • Immunostimulators 
    • such as anti-CD40 and anti-4-1BB, which promote active immune responses from the body.
Finally, as warned by Joy Victory, you should take any cancer-related news with a grain of salt from any source or from a conference like the annual meeting of American Society of Clinical Oncology that her article specifically addresses.[67]


References

  1. Living TimeFaith and Facts to Transform Your Cancer Journey, written by Dr. Bernadine Healy, which most of my writing is based on. She is a cancer survivor herself and have been the former director of the NIH. This book simply walks you through her cancer journey.
  2. Anti CancerA New Way of Life written by Dr. David Servan-Schreiber. He is also a cancer survivor and has been the Director of the Center for Integrative Medicine at the University of Pittsburgh. His book has become a big success and an international bestseller.
  3. 5 Foods That Starve Cancer
  4. Stress and How to Diffuse It
  5. Naturally-Occurring Antiangiogenic Substances
  6. Pros and Cons of Aspirin
  7. 天天蔬果,癌症Bye-Bye
  8. 如何將癌細胞變回成正常的細胞
  9. 早期肝癌治療找到新方法
  10. Fighting CancerA Nontoxic Approach to Treatment by Robert Gorter, MD, PhD and Erik Pepper, PhD.  The Gorter Model was developed by Robert Gorter, MD, PhD, who himself recovered from Stage IV testicular cancer in 1976 by using nontoxic treatment.
  11. Documentaries about the Gorter Model These videos include interviews with patients who have overcome cancer receiving the Gorter Model treatment.
  12. Foods to Fight Cancer: Essential Foods to Help Prevent Cancer by Beliveau, R., and D. Gingras.  Excellent overview and description of foods and herbs that help fight cancer and promote the immune system.
  13. Make Health Happen: Training Yourself to Create Wellness by Peper, E., K.H.Gibney, and C. Holt.  A sixteen-week structured stress-management and healing approach with detailed guided instructions that help us live with our bodies.
  14. Cancer as a Turning Point by LeShan, L.  Written by a master clinician using case studies to show how listening to yourself and doing what you truly want improves your quality of life.
  15. My Path by Van Leusden, C.  The book describes how the author chose a path through the cancer nightmare of metastatic breast cancer and is still here to enjoy the Now.
  16. Full Catastrophe Living by Kabat-Zinn, J.  Describes the basis of mindfulness mediation that is used with many cancer patients.
  17. Dr. Vincent Li from Angiogenesis Foundation

  18. How to reduce your risk of cancer
  19. What's Cancer—A Different Perspective (Travel and Health)
  20. How to Track down Bad Genes in Your Genome?
  21. Natural Immuninity Plays Important Roles in Your Health (Travel to Health)
  22. The Immune System and Cancer (Travel to Health)
  23. Hope Builds for a Drug that Might Shut Down a Variety of Cancers (Weill Cornell Medical College)
  24. Johns Hopkins Magazine -- April 2000
    • Henrietta Lacks's cells multiplied like nothing anyone had seen.
  25. Targeted Cancer Treatment
    • Some examples can be found to treat breast cancer, colorectal cancer, lung cancer and melanoma.
    • More researches are on the pipeline and can be found here.
  26. Telomerase inhibition as cancer therapy
    • This process is very slow and causes a long time lag between the onset of inhibition and the occurrence of senescence or apoptosis as a reversal of the immortal phenotype. 
    • Many telomerase inhibitors seem to be most efficient when combined with conventional chemotherapeutics
  27. Heat Shock Proteins, Autoimmunity, and Cancer Treatment
  28. Moller P, Hammerling GJ. The role of surface HLA-A,B,C molecules in tumour immunity. Cancer Surveys. 1992;13:101–127.
  29. Calderwood SK, Khaleque MA, Sawyer DB, Ciocca DR. Heat shock proteins in cancer: chaperones of tumorigenesis. Trends in Biochemical Sciences. 2006;31(3):164–172. 
  30. Ciocca DR, Calderwood SK. Heat shock proteins in cancer: diagnostic, prognostic, predictive, and treatment implications. Cell Stress and Chaperones. 2005;10(2):86–103.
  31. Transforming growth factor-beta in cancer and metastasis
  32. We're beginning to treat cancer in a whole new way
  33. Belgian Researchers Discover Way to Block Cancer Metastasis
  34. Email reply from cancer.net:
    • If we may explain, systemic cancer treatments, be they intravenous or oral chemothearpy / targeted therapies, are aimed at killing cancer cells no matter where they are located within the body. For instance, the primary cancer (lets use colon cancer as an example) that may have started as a tumor in the colon and diagnosed as colon cancer, may spread to the other parts of the body like the liver or lungs, and yet it is still colon cancer even though it has been found in another place in the body where it just happens to be able to grow.
    • So to answer your question directly, the primary cancer type is the same as the metastatic cancery type. Therefore, taking a targeted therapy aims to treat both the primary tumor and/or any metastatic spread throughout the body. You may find our section on What is Cancer helpful in explaining this relationship between an original tumor and it’s metastatic spread.
  35. Brooks PC. Cell adhesion molecules in angiogenesis. Cancer Metastasis Rev. 1996;15:187–94.http://dx.doi.org/10.1007/BF00437471 .
  36. Cancer Invasion and Metastasis: Molecular and Cellular Perspective
    • Metastasis is the leading reason for the resultant mortality of patients with cancer. 
    • The research on cancer metastasis focuses on the following areas:
      • Cell adhesion
      • Epithelial to mesenchymal transition
      • Angiogenesis
      • Lymphangiogenesis 
      • Organ specific metastasis in cancer.
  37. Controlled Amino Acid Treatment (CAAT)
    • The way CAAT works on a tumour is by:
      • Preventing the production of new blood vessels
      • Blocking the process of glycolysis 
      • Preventing growth of cancer cells being stimulated.
  38. Serine and glycine metabolism in cancer
  39. Cancer metabolism: Key players in metabolic reprogramming
  40. The CAR T-Cell Race
  41. Evolution, not just mutation, drives development of cancer
    • The ecosystem of a healthy tissue landscape lets healthy cells outcompete ones with cancerous mutations; it is when the tissue ecosystem changes due to aging, smoking, or other stressors, that cells with cancerous mutations can suddenly find themselves the most fit, allowing their population to expand over generations of natural selection.
  42. RETHINKING CARCINOGENS: “HALLMARKS OF CANCER:” HOW NORMAL CELLS TURN INTO CANCER CELLS
  43. Thyroid Cancer Cases Soar Due To Overdiagnosis Of Tumors
    • Research has suggested that certain cancers of the prostate, breast and lung as well as thyroid grow so slowly that they will never become deadly, and that overzealous screening leads to overtreatment.
  44. Cancer Immunotherapy Pioneer Nets Major Prize
    •  “Checkpoint blockade” therapy will be more effective for cancer types with lots of mutations such as lung cancer or melanoma.
    • When you get to cancers like breast, prostate and kidney, which have smaller numbers of mutations, the drugs aren’t quite as effective. 
  45. The secrets of living to 200 years old
  46. High molecular weight hyaluronan mediates the cancer resistance of the naked mole-rat
  47. Antioxidants Facilitate Melanoma Metastasis
  48. How Elephants Stay Cancer-Free
  49. New Studies Create Better Understanding of Cancer-Spreading Enzymes
    • We now understand that MMP7 signals to cancer cells to become more aggressive when the enzyme cuts off specific proteins as it binds to those cancer cells. Knowing this, we hopefully can find ways to prevent these enzymes from binding and signaling to these cancer cells in the first place. The end result could be a way to prevent cancer cells from spreading so rapidly.
  50. Tough Medicine — A disturbing report from the front lines of the war on cancer.
    • A given tumor, for instance, can rarely be stopped with a single drug. Cancer is like a door with three locks, each of which requires a different key.
  51. New treatment a ‘huge milestone’ in curing cancer
    • FDA newly approved new treatment (i.e., T-VEC) that can intelligently target cancer cells while leaving healthy ones alone
  52. FDA approves Keytruda for advanced non-small cell lung cancer
  53. Glowing Tumors That Could Improve Cancer Surgery Are Getting Closer To Reality
  54. Scientists root out the ‘bad seeds’ of liver cancer
    • Researchers want to target the bad seeds (NANOG) in cancer to eradicate recurrence problems and metastasis. 
  55. Scientists may have accidentally found the cure for cancer (good news for cancer research)
  56. Blocking the migration of cancer cells to destroy them
  57. Researchers discover how cancer’s ‘invisibility cloak’ works
    • When IL-33 disappears in the tumour, the body’s immune system has no way of recognizing the cancer cells and they can begin to spread, or metastasize.
    • The researchers found that the loss of IL-33 occurs in epithelial carcinomas, meaning cancers that begin in tissues that line the surfaces of organs. These cancers include prostate, kidney breast, lung, uterine, cervical, pancreatic, skin and many others.
  58. Flicking the switch on cancer’s immaturity
  59. Tumour cells may ‘hijack’ white blood cells to help spread
  60. Fat fuels the road to cancer cell spread
  61. Why vitamin pills don't work, and may be bad for you (good)
  62. Battling aging by preserving telomeres could backfire, fueling cancer
  63. Asian Fund for Cancer Research Limited
  64. Fighting cancer with immunotherapy: Signaling molecule causes regression of blood vessels
  65. AstraZeneca immunotherapy wins first approval in bladder cancer
    • The drug belongs to a new class of medicines called PD-L1 inhibitors that block a mechanism tumors use to evade detection from the immune system.
  66. Platelets suppress T cell immunity against cancer
    • The researchers noted that antiplatelet drugs (i.e., aspirin and clopidogrel) by themselves were not successful in combating melanoma in their experiments.  However,  mice with normal platelets that were given melanoma and then adoptive T cell therapy survived longer and relapsed less when aspirin and clopidogrel, two antiplatelet drugs, were added
  67. 6 things to keep in mind if you read cancer-related news (must read)
  68. Immune Checkpoint Inhibitors (Cleveland Clinic)
    • Immunotherapy does not currently offer a cancer cure, but the novel checkpoint inhibitors have allowed doctors to make significantly more progress against advanced cancer than they had been able to achieve in decades.
  69. Grand Challenges―Some of the Greatest Obstacles Facing Cancer Research Today (06/22/2017)
  70. Study sheds light on how ovarian cancer spreads
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