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Diagnostic Technologies
Results of using the CellSearch System indicate that monitoring of circulating tumor cells (CTC's) can contribute to the understanding of tumor-blood interactions and may provide a valuable tool for therapy monitoring in solid tumors like breast, colorectal or prostate cancer. With cells being alive in circulation, it may mean that a patient would need additional treatment.
These ciculating tumor cells can detach from solid tumors and enter the blood stream, thus beginning the process of metastasis, the most life-threatening aspect of cancer. To metastasize, or spread cancer to other sites in the body, circulating tumor cells travel through the blood and can take root in another tissue or organ (like the lungs, bones, liver, adrenals and even the brain).
Immunicon's founder/scientist (immunologist) Paul Liberti's Immunicon team developed all the technology to help researchers and oncologists monitor CTC's. Immunicon licensed their technology to Johnson & Johnson who formed a new unit called Veridex to market Immunicon's CellSearch technology. The technology gives the patient and oncology community a great method to monitor treatment.
The CellSearch system can be very complimentary to an array of tools that oncologists should be using to counsel their patients. The technique can be done earlier than other currently approved diagnostic modalities like CT, MRI or PET imaging. CellSearch is basically what is going on with functional profiling, showing what patients are benefiting from what drug agents "before" introducing them into the patient.
Anti-cancer treatments often effectively shrink the size of tumors, but some might have an opposite effect, actually expanding the small population of cancer stem cells believed to drive the disease. Some treatments could be producing more cancer stem cells which are then capable of metastasizing, because these cells are trying to find a way to survive the therapy. The tumor escapes from chemotherapy by induction of stem cell marker expression. The small number of cells that survive the treatment could then generate another tumor that metastasizes.
This may help explain why the expression of stem cell markers has been associated with resistance to chemotherapy and radiation treatments and poor outcome for patients with cancers including prostate, breast and lung cancers. That tells us that understanding how to target these markers and these cells could prove useful in treating these cancers.
Analysis of stem cell expression before and after treatment reveals that even as some anti-cancer treatments shrank tumors, they increased expression of stem cell markers (of which contibute to stem cells' defining ability to renew themselves and differentiate into different cell types). Some treatments are not enough to completely inhibit tumor growth, and the cancer stem cell markers are still present.
Even if one or more chemotherapy regimen is identified as being likely to work on a particular cancer, has the science advanced to tell us whether application of the chosen chemotherapy regimen will not cause other changes that also cause cancer to later return and perhaps be even harder to treat? Is it a case of chemotherapy being bad, in cases where it apparently works? Chemotherapy can be mutagenic (changes in form). It might kill off a whole lot of cancer, only to cause a mutation in the remaining cancer, such that the remaining cancer behaves in a more aggressive fashion.
Much more work needs to be done, and oncologists need to adapt treatment to the patient. There are hundreds of chemotherapeutic agents, all of which have approximately the same probability of working. The tumors of different patients have different responses to chemotherapy. It requires individualized treatment based on testing individual properties of each patient's cancer.
Sources:
BMJ2007;334(suppl 1):s1(6January),doi:10.1136/bmj.39034.719942.94
The European Science Foundation
Cell Function Analysis
journal Molecular Biology of the Cell
American Assoication for Cancer Research
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