Sarcomas, Soft Tissue: Latest Research | The Cancer Disappeared

Sarcomas, Soft Tissue: Latest Research | The Cancer Disappeared

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

Effectively improve chemotherapy effect, treatment, immunity. 

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

Sarcomas, Soft Tissue: 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/

Sarcomas, Soft Tissue: Latest Research

Approved by the Cancer.Net Editorial Board, 06/2022

You will read about the scientific research being done to learn more about sarcomas and how to treat them.

Doctors are working to learn more about sarcoma, 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.

  • Immunotherapy. As discussed in Types of Treatment, immunotherapy comes in many forms. Immune checkpoint inhibitors have become the focus of a lot of research. These drugs are targeted monoclonal antibodies (proteins) that turn on immune responses in the body by taking the brakes off the immune system. The molecules that are blocked have names such as CTLA-4, PD-1, PD-L1, OX40, LAG3, and TIM3. This approach has proved helpful in treating many cancers and in research studies about sarcomas.

    Chimeric antigen receptor (CAR) T-cell therapy and T-cell receptor therapy use white blood cells from a patient’s blood to destroy cancer cells. The patient’s cells are removed and then changed so they have specific proteins called receptors. These receptors allow those T cells to recognize the cancer cells. The changed T cells are grown in large numbers and returned to the patient’s body. Once in the patient’s body, these T cells seek out and destroy cancer cells. This technique shows the most promise when there is a known target on the sarcoma, such as in synovial sarcoma and myxoid-round cell liposarcoma. Clinical trials are investigating this exciting but complex form of immunotherapy. Learn more about the basics of CAR T-cell therapy.

    Vaccines against specific sarcoma proteins or other molecules are also being studied, often in addition to immune checkpoint inhibitors. This type of vaccine is intended to treat cancer.

  • Improved drug delivery. Some chemotherapies are incorporated into fat molecules called liposomes to improve the absorption and distribution of the drug in the patient’s body. Other new ways to get a chemotherapy into a cancer cell are being studied. For example, chemotherapy can be attached to proteins, so the chemotherapy can enter into the cancer cells. In some cases, these proteins are antibodies that target, or bind to, a specific marker on a cancer cell, so the chemotherapy is delivered only to cancer cells and not to normal cells, which can improve effectiveness and decrease side effects. These are called antibody-drug conjugates.

  • New drugs. New medications are being developed and tested that may be effective in treating some subtypes of soft-tissue sarcoma. Learn more about the process of drug development and approval. As explained in Types of Treatment, several targeted therapies have been recently approved to treat specific types of sarcoma. This is an active area of research for sarcoma.

  • Targeted therapy. As described in Types of Treatment, targeted therapy is a treatment that targets the tumor’s specific genes, proteins, or the tissue environment that contributes to tumor growth and survival. Clinical trials led to the approval of a targeted drug, pazopanib, to treat some sarcomas. Clinical trials of other medications that work in different ways to block tumor growth and survival are also underway.

  • Tumor genetics. Researchers are learning that some sarcomas have unique genetic “fingerprints.” Understanding these fingerprints may help doctors make precise diagnoses, determine better treatments, and possibly better predict a patient’s prognosis. A number of cancer centers and companies now offer genetic tests of cancers to determine whether people with a sarcoma might benefit from newer treatments.

  • Palliative care/supportive care. Clinical trials are underway to find better ways of reducing symptoms and side effects of current sarcoma 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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