Gastrointestinal Stromal Tumor (GIST)

An image of a cancer cell in a blue background.

GIST is the most common form of sarcoma (a type of cancer that develops from the cells of the body’s connective or supportive tissues) involving the gastrointestinal tract. GIST can occur anywhere along the GI tract but is most often found in the stomach (40-70 percent of cases) or the small intestine (20-40 percent of cases).1

In Europe, there are an estimated 10-20 GIST cases per million2 and, in the U.S., there are approximately 4000-6000 cases diagnosed each year3.


GIST represents a life-threatening malignancy if the disease has spread to other parts of the body (metastasized) or is unable to be surgically removed with curative intent.


The discovery of oncogenic KIT kinase mutations in GISTs and the introduction of kinase inhibitor therapies have led to a rapid evolution in the understanding of these tumors. It is now established that over 80% of GISTs harbor a KIT gene mutation, that these mutations lead to the continued activation of the kinase and that mutant KIT is a clinically important therapeutic target in GIST4.


Unless they are located in certain regions of the digestive system, GIST may not cause any noticeable symptoms until they reach a certain size. As a result, GIST is often not diagnosed until later stages of disease, at which point 15-25% of people diagnosed will have developed metastatic disease5.


GIST is often diagnosed when blood is detected in the stool or vomit. Should the tumor grow large enough, it can block the passage of food to the stomach or intestine, resulting in severe abdominal pain and vomiting.


Over time, the continued blood loss will lead to anemia, or low red blood cell count, causing patients to feel tired and weak.

Advice for patients

Each body reacts differently to medicines. Therefore it is impossible to tell which medicine works best for you. Please consult your physician.

Treating GIST

The treatment of GIST depends on a number of factors, including the patients’ general health and the size and position of the tumor. Surgery is the main treatment option for GIST that has not spread or has only spread into nearby tissue. Tumors that are larger or located in places where the cancer may be harder to remove without causing potential health problems later on are often prescribed targeted therapies. These are known as growth inhibitors and work by blocking growth signals, preventing the GIST cells from multiplying. Chemotherapy and radiotherapy are not effective for this type of cancer and are therefore rarely used.


Three growth inhibitors have been approved for the treatment of GIST if the tumor cannot be surgically removed and/or has already spread. With the entrance of ewer precision oncology treatments, some of the GIST cases can now also be treated based on their specific genomic alteration.

Bayer Treatments for GIST

Bayer has a targeted treatment which is approved in many countries around the world, including the U.S., Japan and countries of the European Union, for the treatment of patients with metastatic and/or unresectable GIST whose disease has progressed even after treatment with all standard approved therapies.

Bayer also has a precision oncology treatment approved in the U.S., the EU, Brazil and Canada for the treatment of solid tumors with particular alteration in the tumor’s genome , which occurs also in approximately 3% of GIST cases.



1 The Life Raft Group. GIST 101. 2013. Available at: Accessed May 2019

Union for International Cancer Control. Gastrointestinal Stromal Tumour - 2014 Review of Cancer Medicines on WHO List of Essential Medicines. Available at:
medicines/committees/expert/20/applications/GastrointestinalStromalTumour.pdf?ua=1. Accessed May 2019

American Cancer Society. Gastrointestinal Stromal Tumor (GIST). 2017.
Available at: Accessed November 2019.

OncologyPro. KIT in Gastrointestinal Stromal Tumours (GIST): ESMO Biomarker Factsheet.
Available at:

Ford SJ., Gronchi A., Indications for surgery in advanced/metastatic GIST. Eur J Cancer, 2016 Aug; 63: 154-67