Targeted cancer therapy

The term targeted cancer therapy ( Engl. Targeted therapy ) refers, in contrast to traditional chemotherapy with cytotoxic drugs that treat cancers with various new drugs that exploit certain biological and cytological characteristics of cancer tissue. These include, for example, genetically engineered monoclonal antibodies (name ending '-mab') or so-called small molecules (name ending '-mib' or '-nib'). Since these features rarely or not at all appear on healthy cells, targeted cancer therapy should be more tolerable and effective. As a rule, the new substances are combined with conventional therapy methods ( surgery , chemotherapy and radiation therapy ). Some of the active ingredients or therapeutic approaches, such as monoclonal antibodies, fall into the area of cancer immunotherapy , which is a form of targeted cancer therapy.

Receptor Based Therapy

Some cancer cells have unique structures on the surface of their cell membrane , such as receptors and other membrane proteins , which distinguish them from other body cells. With the development of the monoclonal antibody rituximab in 1997, proof of the effectiveness of such a therapy was first achieved. Today a variety of monoclonal antibodies such as B. trastuzumab , cetuximab and bevacizumab approved for the targeted cancer therapy of various tumors and many more are in development.

Disruption of metabolic pathways

With a new class of drugs, the so-called small molecules , it is possible to specifically intervene in the metabolism of cancer cells and thus prevent them from growing:

• Tyrosine kinase inhibitors such. B. Imatinib , Gefitinib , Erlotinib or Pazopanib block the transmission of growth signals to the cell nucleus and are used in a number of cancers.
• Bortezomib is a proteasome inhibitor that is used in the treatment of multiple myeloma . It leads to programmed cell death in cancer cells ( see below ).
• Immucillin-H is a purine nucleoside phosphorylase (PNP)inhibitorand is currentlyundergoing clinical testsin the treatment of acute lymphoblastic leukemia .

Inhibition of the formation of new blood vessels (antiangiogenesis)

The formation of new blood vessels ( angiogenesis ) is rare in a healthy body - however, a growing tumor requires oxygen and nutrients; It therefore stimulates the surrounding tissue with messenger substances such as the growth factor VEGF (Vascular Endothelial Growth Factor) to form new blood vessels. A drug against VEGF was developed with the monoclonal antibody bevacizumab , which is effective against colon cancer , breast cancer , lung cancer and kidney cancer .

Stimulation of programmed cell death (apoptosis)

Certain active substances or the introduction of genes could trigger programmed cell death ( apoptosis ) in cancer cells . One approach is the introduction of the so-called “suicide receptor ” TRAIL into the cancer cells, although no effective method for this gene transfer has yet been available.

Fight against cancer stem cells

According to recent theories, so-called cancer stem cells are responsible for the recurrence of cancer after an apparent cure, the so-called recurrence . In some types of cancer or hemoblastosis , such as chronic myeloid leukemia (CML) , these stem cells have been identified. This makes new targets available for cancer therapy; However, corresponding therapy concepts are still in an early phase of research.

literature

• MA Green: Targeting Targeted Therapy . In: New England Journal of Medicine . No. 350 (21) , 2004, pp. 2191-2193 , PMID 15118072 .
• BJ Druker : Molecularly targeted therapy: have the floodgates opened? In: Oncologist . No. 9 (4) , 2004, pp. 357-360 , PMID 15266089 ( Article ).

Individual evidence

1. ↑ P. McLaughlin, AJ Grillo-Lopez et al: Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma: half of patients respond to a four-dose treatment program . In: J Clin Oncol . No. 16 (8) , 1998, pp. 2825-2833 , PMID 9704735 .
2. ↑ CG Willett, Y. Boucher et al .: Direct evidence that the VEGF-specific antibody bevacizumab has antivascular effects in human rectal cancer . In: Nature Medicine . No. 10 (2) , 2004, pp. 145-147 , PMID 14745444 .
3. ↑ BJ Klencke et al .: Independent review of E2100 progression-free survival (PFS) with the addition of bevacizumab (B) to paclitaxel (P) as initial chemotherapy for metastatic breast cancer (MBC). (Poster presented at ASCO Annual Meeting 2008, IL Poster 1036) In: J Clin Oncol. 2008; 26 (May 20) suppl: abstr 1036.
4. ↑ A. Sandler et al .: Paclitaxel-carboplatin alone or with bevacizumab for non-small-cell lung cancer. In: N Engl J Med. 255, 2006, pp. 2542-2550.
5. ↑ B. Escudier et al .: Bevacizumab plus interferon alfa2a for treatment of metastatic renal cell carcinoma: a randomized, double-blind phase III trial (AVOREN). In: The Lancet . 370, 2007, pp. 2103-2111.
6. ^ Y. Kim, DW Seol: TRAIL, a mighty apoptosis inducer. In: Molecules and Cells . No. 15 (3) , 2003, p. 283-293 , PMID 12872982 .
7. ↑ LJ Elric, HG Joergensen et al .: Punish the parent not the progeny . In: Blood . No. 105 (5) , 2005, pp. 1862-1866 , PMID 15528314 ( article ).

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