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High Fat Diets Are Linked to Colon Cancer

High Fat Diets Are Linked to Colon Cancer
High Fat Diets Are Linked to Colon Cancer

Doctors regularly warn patients that obesity is linked to an increased risk of cancer. A study by researchers at MIT has shed some light on how high-fat diets can trigger colon cancer.

The Role of Stem Cells in Colon Cancer

Colon cancer arises from mutations that tend to accumulate among intestinal stem cells, which last a lifetime. Omer Yilmaz, an assistant professor of biology at MIT, led a team that set out to discover the process behind these cellular changes.

For nine months to a year, Yilmaz and his team fed healthy mice a diet composed of 60 percent fat. In addition to gaining up to 50 percent more body mass, these mice developed more intestinal tumors than those on a healthy diet.

Effects of High-Fat Diet on Intestinal Cells

Researchers observed significant changes in the intestinal stem cells of the mice:

  • The mice eating a high-fat diet had a higher number of intestinal stem cells. In addition, they were able to operate free of input from niche cells that normally regulate stem cell activity.
  • Progenitor cells, which are differentiated “daughters” of stem cells, began to take on characteristics of stem cells, including longer life span and ability to generate mini-intestines outside the body.

Yilmaz is hopeful that, with further investigation, this information will lead to identifying new methods of cancer treatment for obesity-related tumors.

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The Connection Between Tumors and Blood Vessels

Stop Cancer
Stop Cancer

The medical community has long believed that cancer cells support their growth by generating blood vessels. A recent study suggests that blood vessels may actually begin the cycle of tumor development.

“Hijacking” Blood Vessels for Tumor Development

According to cancer biologist Dr. Lan Ko, one of the authors of the study, the team found evidence that blood vessels can create tumors. In turn, the cancer cells then produce blood vessels to further sustain their growth.

Researchers focused on GT198, a gene generally found in low levels within the body. It has a natural ability to repair DNA and regulate stem cells, but in mutated form it creates cancer cells.

Pericytes, found in the outer layer of blood vessels, resemble stem cells in the way they can form different types of tissue. During the study, researchers found abnormally high levels of GT198 in pericytes supporting a number of human tumors.

Even more surprising was that the GT198 was located in the pericytes’ cytoplasm instead of the nucleus. This enabled malignant pericytes to multiply into cancer cells and detach from blood vessels to promote spread of the tumors.

Application for Cancer Treatment

As Dr. Ko explained, these results indicate that GT198 is a viable target for immunotherapy for cancer treatments. Further testing will explore use of existing cancer drugs and development of new ones.

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New Guidance on Lymph Node Removal for Melanoma Patients

New Guidance on Lymph Node Surgery
New Guidance on Lymph Node Surgery

Aggressive surgery has often been the preferred approach for patients in whom melanoma has spread to the lymph nodes. Results of a recent trial suggest that a conservative treatment of watchful waiting may actually be more beneficial.

Is Completion Surgery Necessary?

Once a patient is diagnosed with melanoma, the traditional procedure has been to conduct a sentinel lymph node biopsy. If cancer cells are detected, the next step is usually immediate removal of the remaining regional lymph nodes in the surrounding area.

Surgery vs. Watchful Waiting

MSLT-II involved 1,934 participants who had been diagnosed with skin melanoma of medium thickness that had spread to sentinel lymph nodes but nowhere else in the body. Half underwent immediate lymph node removal surgery while the other half were monitored for signs of cancer in the regional lymph nodes.

After three years, 86 percent of patients in each group had not succumbed to melanoma. In addition, 68 percent of the surgery group and 63 percent of the monitored group had not experienced any recurrence of cancer.

Greater Risk of Complications

While difference in recurrence rate was negligible, the surgery group was found to be far more susceptible to complications. Those patients were approximately four times more likely to experience lymphedema, which is a buildup of excess lymph fluid that causes swelling.

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What is Recurrent Cancer – What Do I Need to Know?

What Do I Need to Know?
What Do I Need to Know?

Have you ever heard stories about patients undergoing immunotherapy for cancer and experiencing no recurrence? Here’s what you need to know about recurrent cancer and what it means in terms of your overall health.

When Cancer Comes Back

Recurrence refers to cancer that returns after treatment has been completed. It originates with cancer cells that remained after the first course of treatment but were too small to show up in post-treatment testing.

Recurrent cancer is the same form as the original tumor, as opposed to a new type of cancer that may develop in patients who have a history of tumors. The latter is known as second primary cancer.

Types of Recurrent Cancer

Cancer recurs in three different ways:

• Local recurrence is in the same general area as the original tumor.

• Regional recurrence describes cancer that has grown into lymph nodes or other tissues near the original cancer.

• Distant recurrence is when cancer has spread to organs or other tissues far from the original site.

Another term that describes distant recurrence is metastatic cancer. Regardless of where the cancer has spread, it’s still the same type as the original tumor.

Testing and Treatment

Your doctor will likely repeat many of the same tests that resulted in the first diagnosis. These tests provide information to help determine the appropriate course of treatment.

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How the Presence of Estrogen Protects Women from Gastric Inflammation Leading to Cancer

Advanced Cancer Research
Advanced Cancer Research

In the past, scientists have attributed gender discrepancies in cancer rates to lifestyle differences. Recent evidence strongly indicates that the cause may actually lie in biological differences instead.

This theory was bolstered by the results of an MIT study involving male mice infected with H. pylori, a bacterium that can lead to gastric cancer. More than 50 percent of people around the globe are infected with H. pylori, and while many remain asymptomatic, gastric cancer is the second-leading cause of cancer deaths worldwide.

How Gastric Cancer Develops

H. pylori infections are controlled by the body’s immune system, but a common side effect is gastritis, which is an inflammation of the stomach. The result is conditions that lead to the development of gastric cancer.

Studies have indicated that estrogen can protect women from gastritis, lowering their gastric cancer risk. Conversely, Tamoxifen and other drugs that block estrogen have been linked to higher risk of gastric cancer in women.

Testing the Theory

The mice in the MIT study were treated with estrogen, Tamoxifen or both. None of them developed cancer despite a prior history of gastritis, suggesting that Tamoxifen in the stomach may mimic rather than block estrogen. In the untreated control group, 40 percent of the mice developed gastric cancer.

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Scientists Uncover a Key Step in Lung Cancer Progression Which May Lead to New Treatments

Advanced Cancer Research
Advanced Cancer Research

Approximately 40 percent of lung cancer cases in the United States involve an aggressive form called adenocarcinoma. Researchers recently identified a vital step in this cancer’s development that could be the key to successful early cancer treatment.

The Path from Benign to Malignant

Lung adenocarcinoma gets its name from adenomas, which are a form of benign tumors. Scientists believe that lung adenocarcinomas begin as adenomas that transition to the more aggressive type.

A team of researchers at MIT’s Koch Institute for Integrative Cancer Research set out to study the process behind the change from benign to malignant. According to lead author Tuomas Tammela, at some point the tumor cells begin acting like stem cells, allowing for rapid reproduction.

Flipping the Switch

Wnt is a signaling pathway that maintains cells in a stem cell-like state. The team focused on the activity of this pathway in a group of mice programmed to develop lung adenomas that were likely to progress to adenocarcinomas.

While they found that the Wnt pathway was not active in the adenomas, about five to 10 percent of the cells turned it on during the transition. When the mice received cancer treatment that interfered with the Wnt proteins, tumor growth was halted and the mice lived 50 percent longer.

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