Pancreatic Cancer: Latest Research | The Cancer Disappeared

Pancreatic Cancer: Latest Research | The Cancer Disappeared

Best adjuvant (assist) for chemotherapy | 1+1>487% |

Effectively improve chemotherapy effect, treatment, immunity. 

Reduce side effects and recurrence.  

Overview / Relation / Abstract / Role / Principle / Action / Mechanism / Function / Work | 

Pancreatic Cancer: Latest Research

Abstract / Summary / Overview of Apoptosis.

Why do cells undergo apoptosis?

The relationship between cancer cells and apoptosis.

Where are the weaknesses and symptoms of cancer cells?

Are cancer cells aggressive?

Extraordinary Solamargine (Role, Principle, Action, Mechanism, Function, Work)

Solamargine's major function mechanism:

Solamargine vs cancer

Best Chemotherapy Adjuvant.  (1+1>478%) 

Effectively improve chemotherapy effect and cure.

When cancer cells are less resistant to drugs, chemotherapy becomes more effective. 



Extract : https://www.cancer.net/cancer-types/

Pancreatic Cancer: Latest Research

Approved by the Cancer.Net Editorial Board, 07/2022

You will read about the scientific research being done to learn more about pancreatic cancer and how to treat it.

Doctors are working to learn more about pancreatic cancer, ways to prevent it, how to best treat it, and how to provide the best care to people diagnosed with this disease. The following areas of research may include new options for patients through clinical trials. Always talk with your doctor about the best diagnostic and treatment options for you.

  • Early detection. The best chance of successful treatment is when pancreatic cancer is found early. This is why ongoing research is focused on finding and using special blood tests, diagnostic imaging tools, and other approaches to find pancreatic cancer at its earliest stages before it spreads. This includes finding it at precancerous stages, known as pancreatic intraepithelial neoplasia, or PanIN lesions. These screening approaches are typically being used for people who have a high risk for pancreatic cancer, such as those with a strong family history or a known genetic condition that increases the risk of pancreatic cancer. It is not yet known if these screening tools could be used effectively for the general population.

  • Genetic/molecular studies. In cancer, damaged or abnormal genes cause uncontrolled cell growth. Many new research developments are based on identifying damaged genes and proteins and repairing them or changing how they work.

    Pancreatic tumor samples can be analyzed using a variety of molecular techniques, such as DNA sequencing and mutational analysis, to look for genetic changes. Some of these same analyses can now even also be performed on blood samples, as newer technologies allow for collection and analysis of tumor DNA present in the blood.

    This information can then be used to develop new drugs that target these changes (see "Immunotherapy" and "Targeted therapy," below), as well as to potentially screen for pancreatic cancer in people who have a high risk of the disease. At this point, these tools are only being used in clinical trials.

  • Circulating tumor (ct)DNA. This refers to DNA that is shed by cancer cells into the bloodstream. It can now be detected and analyzed through a simple blood draw (or, less commonly, a urine sample) using current technologies. ctDNA is being studied as a tool for monitoring response to treatment, for observing early signs of disease recurrence, and as a way to determine the disease's resistance to ongoing treatment.

  • Immunotherapy. As explained in the Types of Treatment section, cancer researchers are studying several types of immunotherapyas potential treatments for pancreatic cancer.

    • A number of clinical trials have been done or are ongoing that use cancer vaccines to try to treat a variety of types of cancer, including pancreatic cancer. Such vaccines may be made from various sources, including pancreatic cancer cells, bacteria, or a person’s specific tumor cells. Depending on the circumstances, vaccines may be given either after, during, or instead of chemotherapy.

    • Immune checkpoint inhibitors, such as anti-PD-1 antibodies, are already approved for other types of cancer, including melanoma and lung cancer. However, they are not yet approved for pancreatic cancer except for the few patients with tumors that have high microsatellite instability (see Types of Treatment). Researchers are looking at other drugs that can harness a person's immune system in different ways. Ongoing studies in pancreatic cancer are testing the combination of different immunotherapies with each other or with chemotherapy, radiation therapy, or other targeted agents.

    • In addition, researchers are studying methods to collect and genetically modify a person’s T cells, which are a type of white blood cell. This is called adoptive immunotherapy. While this approach (such as chimeric antigen receptor therapy, or CAR T-cell therapy) has advanced the way doctors treat some blood-based cancers such as leukemia and myeloma, researchers are still trying to learn how to apply it in solid tumors such as pancreatic cancer.

  • Targeted therapy. As discussed in the Types of Treatment section, the only targeted therapies currently approved for pancreatic cancer are erlotinib, which is no longer commonly used; olaparib, which is limited to pancreatic cancers associated with a germline (hereditary) BRCA mutation; and larotrectinib and entrectinib, which are limited to pancreatic cancers that harbor an NTRK fusion. Other drugs that may help block tumor growth and spread are being studied for pancreatic cancer, both as single drugs and as part of combination therapy. A gene called KRAS is often mutated in pancreatic cancer, and new drugs that target specific RAS mutations (in particular one called KRAS G12C that is present in about 2% of pancreatic cancers) show promising results. An additional strategy under evaluation entails inhibiting autophagy, a process used by cancer cells for self-protection by providing extra nutrients and keeping anticancer drugs from destroying them. Researchers are also studying drugs that can break down the stroma, which is the fibrous-like connective tissue that surrounds cancer cells and is involved in maintaining the cancer. By disrupting the tumor-associated stroma, these drugs may allow chemotherapy to reach and destroy cancer cells more effectively. Learn more about the basics of targeted therapy.

  • Gene therapy. Gene therapy is the delivery of specific genes to cancer cells, which are often carried by specially designed viruses. These include normal genes that are delivered into the center of cancer cells. Then, as the cancer cells divide, the working genes that were inserted in the cell replace the abnormal genes that contribute to cancer growth.

  • Chemotherapy. Newer, more effective types of standard chemotherapy continue to be researched.

  • Cancer stem cells. Pancreatic cancer stem cells are cells in the tumor that may be particularly resistant to standard therapies. Research is currently focused on identifying treatments that may specifically target those cancer stem cells.

  • Palliative care/supportive care. Clinical trials are underway to find better ways of reducing symptoms and side effects of current pancreatic cancer treatments to improve comfort and quality of life for patients.



Abstract / Summary / Overview of Apoptosis. 

Apoptosis.jpg

Overview of apoptosis

•Programmed cell death

•Apoptosis is a form of programmed cell death, or “cellular suicide.”

•Apoptosis is different from necrosis, in which cells die due to injury.

•Apoptosis removes cells during development, eliminates potentially cancerous and virus-infected cells, and maintains balance in the body.


Why do cells undergo apoptosis?

  • Basically, apoptosis is a general and convenient way to remove cells that should no longer be part of the organism.
  • Some cells are abnormal and could hurt the rest of the organism if they survive, such as cells with viral infections or DNA damage.
  • Apoptosis is part of development
  • In many organisms, programmed cell death is a normal part of development.


The relationship between cancer cells and apoptosis

Apoptosis can eliminate infected or cancerous cells.

When a cell’s DNA is damaged, it will typically detect the damage and try to repair it. 

If the damage is beyond repair, the cell will normally send itself into apoptosis, ensuring that it will not pass on its damaged DNA. 

When cells have DNA damage but fail to undergo apoptosis, they may be on the road to cancer.

However, “successful” cancer cells successfully evade the process of apoptosis.

This allows them to divide out of control and accumulate mutations (changes in their DNA).

Apoptosis is key to immune function

Apoptosis also plays an essential role in the development and maintenance of a healthy immune system. 


Where are the weaknesses and symptoms of cancer cells?

The symptoms of cancer cells are in the nucleus.

The nucleus controls the outer cytoplasm, cell composition, cell viability, etc.

DNA mutations also mutate in the nucleus.

Therefore, to treat cancer cells, we must first enter the nucleus.

Let the “regulatory cell gene” mechanism enter the nucleus to regulate


Are cancer cells aggressive?

After the action of Solamargine, the aggressiveness of cancer cells is alleviated.

So after using Solamargine, many patients feel that I am half better.

Although the tumor does not disappear quickly, patients feel that the degree of aggressiveness is reduced.



Extraordinary Solamargine (Role, Principle, Action, Mechanism, Function, Work). 

sr-t100_apoptosis_mechanism005.jpg


Solamargine's major function mechanism:

When Solamargine enter,

Solamargine activates receptors that are turned off by cancer cells, allowing cancer cells to modulate again.

Solamargine modulates the anti-modulates genes of cancer cells, making cancer cells less resistant.

Reduced drug resistance

When cancer cells are less resistant to drugs, chemotherapy becomes more effective.

Solamargine modulates the mutated genes in cancer cells and then initiates cancer cell apoptosis to achieve anti-cancer effects.


Solamargine combined with which chemotherapy drugs are more effective in treating cancer cells?

Chemotherapy_01.jpg



Solamargine vs cancer

cell apoptosis.jpg

Solamargine vs cancer

The picture shows the death of cancer cells.

The black and black parts are cancer cell nuclei.

Even if the nucleus ruptures, the cancer cells will die.

The figure shows that cancer cells can cause death. 

cancer cell apoptosis_01_800.jpg

The figure shows that cancer cells can cause death.

The figure shows that the death of lung cancer cells is relatively slow, and it will not be obvious until eight hours later.

The figure shows that the death of liver cancer cells is very obvious, even more obvious in eight hours.

The graph shows that breast cancer cells die faster. It was obvious from the beginning that breast cancer is easy to treat, and patients with breast cancer need not worry.



Best Chemotherapy Adjuvant. (1+1>487%) 

Effectively improve chemotherapy effect and treatment.solamargine vs cancer_lung cancer cell.jpg

ANTI-CANCER 

Patent protection in 32 nations. 

A comparison study showing Solamargine vs. other therapeutic drugs with respect to lung cancer cells.

solamargine vs cancer_breast cancer cell_01_800.jpgA comparison study showing Solamargine vs. other chemotherapeutic drugs with respect to breast cancer cells.

solamargine combined treatment therapy_01_800.jpg

SR-T100 combination therapy with effective result against breast cancer cells.


solamargine combined treatment therapy_03R12_800.jpg

Combination Therapy   |   Research results for lung cancer cells. 

A. Chemotherapy    (100μM), 16% of cancer cell apoptosis. 

B. Alone SM (4.8μM), 28% of cancer cell apoptosis. 

C. SM (4.80μM) + Chemotherapy (40μM), 66% of cancer cells apoptosis.  

D. SM (4.80μM) + Chemotherapy (100μM), 78% of cancer cell apoptosis.  

SM has a clearing effect better than Chemotherapy. 

The combined treatment of Solamargine and Chemotherapy significantly increased the apoptosis of lung cancer cells.  

SM (4.8μM) + Chemotherapy (40μM), increased from 16% to 66% (up to 4.125 times).  

SM (4.8μM) + Chemotherapy (100μM), increased from 16% to 78% (up to 4.875 times).  

Reorganized from: BBRC. Action of Solamargine on TNFs and drug-resistant human lung cancer cells 2004.


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The best solution for cancer cells.

Solamargine Q&A (English)






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