• Kirk Hartley

Molecular Biologists and Mathematicians Continue Progress in Tracing Cancer Cell Lineage

The annual ASCO national conference is in Chicago this weekend (and more). It’s a massive conference of oncologists working on treatments, research and answers. So, it’s an appropriate week for writing about cancer, research and the growing prevalence of cancer litigation.

One reason that asbestos litigation is prevalent is that the source of mesothelioma cancer is reasonably traceable to inhalation of asbestos fibers, especially amphibole fibers. Against that background, consider the implications of the increasing focus on and success in tracing cancer cell lineages for many forms of cancer. The work is underway as researchers seek to find out why some cancers "come back" or stop responding to treatment.

The cell lineage research also has implications for litigation. Consider, for example,that today’s cutting edge researchers can compare "before" and "after" cells, and see/model what changed, and when the changes were transpiring. Consider also the possible consequences of comparison of cells derived after cancer strikes a worker to cells in blood taken and bio-banked before starting work at a job involving suspected or known carcinogens. "Fingerprints" may be found.

On tracing lineage of cells, consider the following passage from ScienceDaily’s summary of a new paper on leukemias:

"To reconstruct the cancer cell lineage tree, the team used two sets of blood samples: the first taken from leukemia patients right after the disease was diagnosed, and the second from those patients who had undergone chemotherapy and in whom the cancer had returned. The researchers could then trace the relationships of the recurring cancer cells back to see if they descended from the original cancer cells. The lineage tree showed that, at least in some of the patients, the source of the renewed cancer was not in the rapidly proliferating cancer cells, but rather in cells that were close to the root of the tree. These cells had only divided a few times. In other words, the cancer arose from cells that divide very slowly, making them resistant to the attacks of chemotherapy drugs."

The article is in Blood – its abstract states the same principles in denser and more nuanced words that further highlight the increasing ability to work and learn at very specific levels:

"Human cancers display substantial intra-tumoral genetic heterogeneity, which facilitates tumor survival under changing microenvironmental conditions. Tumor substructure and its impact on disease progression and relapse are incompletely understood. In the current study, a high-throughput method that utilizes neutral somatic mutations accumulated in individual cells to reconstruct cell lineage trees was applied to hundreds of cells of human acute leukemia harvested from multiple patients at diagnosis and at relapse. The reconstructed cell lineage trees of acute myeloid leukemia (AML) patients demonstrated that leukemia cells at relapse were shallow (divide rarely) compared to cells at diagnosis and were closely related to their stem cell subpopulation, implying that in these instances relapse might have originated from rarely-dividing stem cells. In contrast, among acute lymphoid leukemia (ALL) patients, no differences in cell depth were observed between diagnosis and relapse. In one case of chronic myeloid leukemia (CML), at blast crisis, most of the cells at relapse were mismatch-repair deficient. In almost all leukemia cases, more than one lineage was observed at relapse, indicating that diverse mechanisms can promote relapse in the same patient. In conclusion, diverse relapse mechanisms can be observed by systematic reconstruction of cell lineage trees of leukemia patients."


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