Breast Cancer: Network

In their article, Patrone et al. use a modified version of Collins ' right to estimate the age of colorectal cancer, lung and breast cancer. Bill Collins, who claims that the likelihood of recurrence of a tumor is equal to the patient's age at diagnosis more than 9 months, has been applied mainly to pediatric cancers, tumours in particular embryonic.[1.2] the results of applying the law of Collins ' of these tumors were reasonable, although exceptions have been reported and the law is not applicable to all types of cancer.[3.4] its use in adults as used in this document is therefore unique.

The current study is based on the assumption of a constant growth of the cancer after surgery, that the authors admit is a potential limitation. Bias may also have been introduced into the patient selection "only surgery", especially those from retrospective studies, although the impact of this probably is diminished by the fact that older studies used were in most cases (probably from a time when there was less use of multimodal therapy that currently there is no). Finally, there is heterogeneity in tumor recurrence time based on the remaining burden after resection and intensity of follow-up. Some of these concerns are addressed by the use of mainly authors and prospective studies finding no difference between the rate of recurrence in retrospective studies and saw that in future studies, despite the differences in absolute terms.

Despite these limitations, the study concept is novel and extremely interesting. Still, the application of the results remains unclear. From the point of view of medical care, knowing the "age" of a tumor is unlikely to change management. The patient receives a new diagnosis of cancer, while this knowledge may relieve the anxiety about the emergency treatment, it may exacerbate the anxiety of the variety "what if". For example, a patient who has just said that his cancer is probably 5 to 6 years may berate herself with thoughts along the lines of "if only he had or hadn't done x then it would be in this situation right now."

One potential application of the results of the study, from the medical point of view is that you can perform a retrospective review of patient's contact with the health system during the period of the estimated age of his tumor. There were subtle physical exam or imaging findings that could be attributed to the patient's tumor reliably and applied to future patients to facilitate earlier diagnoses and, hopefully, a more favourable outcome? However, a less positive side of this potential application in our current environment of medicolegal is the possibility of increased risk of litigation due to perceived negligence (e.g., "Doctor X lost my Cancer 3 years ago").

As stated earlier, the conclusions of this article are based on the assumption of a constant growth rate of breast cancer after surgery and as a result, patients treated with chemotherapy, hormonal therapy, or radiation were excluded because of the potential of these therapies to alter the kinetics of growth. While the need for internal validity study estimating the age of a given cancer, this patient population limitation makes it difficult to use the results to determine the prognosis or longevity of postoperative follow-up after resection except in patients treated with surgery only. For all three cancers selected for this study (breast, lung and colon-rectum), a significant number of patients being treated with hormone therapy, radiation or chemotherapy adjuvant or neoadjuvant chemotherapy. It would be interesting to know the growth rates in these settings, and be able to provide a reasonable interval after which the recurrence is highly unlikely. We can then adapt the intensity of our follow-up accordingly. However, I imagine that these would be difficult to estimate given responses varied multimodal therapy of tumours.

Patrone et al. conclude that "age" typical of a tumor at diagnosis is about 5-6 years, while for lung and rectal cancer is 3-4 years, based on the time of occurrence in most patients. For these and many other types of cancer, the current standard is run fairly intensive clinical follow-up to the first 5 years after the first round of treatment. Subsequently, if there is no evidence of the disease recurring, cautiously consider the patient recovered and decrease the intensity of our vigilance. This period of five years neatly aligns with the time observed in this study. While this is reassuring, does not change the current paradigm.

Finally, the authors cite perhaps lead a similar analysis resected metastatic lesions and make inferences about their "age" than for the primary tumor. This knowledge would be extremely valuable to guide clinical decision making, especially now when increasingly aggressive metastasectomies are executed. Once again, however, this analysis would be difficult to interpret given our current multimodal therapeutic and unpredictable effects on tumor growth kinetics.

Overall, this book presents a concept interesting, exciting, but it is uncertain how the authors best results can be exploited.

financial reporting : the author has no significant financial interests or other relationships with producers of goods or supplier of any of the services referred to in this article.

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ONCOLOGY.Vol. 25No. 1COMMENTARY Breast Cancer Stem Cell TargetsThe Federici et al Article Reviewed [READ ARTICLE]By Wendy A. Woodward, MD, PhD1 |January 22, 20111 Department of Radiation Oncology, M. D. Anderson Cancer Center, Houston, Texas

The publication of the landmark paper by Al-Hajj et al, which demonstrated that breast cancer cells capable of tumor outgrowth when transplanted into the cleared mammary fatpad of immunocompromised mice could be prospectively identified using cell surface markers,[1] galvanized the cancer stem cell debate among breast cancer researchers and launched an exponential increase in papers exploring “breast cancer stem cells.” In this issue of ONCOLOGY, Federici et al review this explosion of literature in a clear and concise article that, like all broad reviews of rapidly expanding, highly debated fields, is greatly constrained by the need for brevity.

The dramatic discourse that was launched by Al-Hajj’s work, which suggested that solid tumors such as breast cancer could be completely recapitulated by only a small fraction of the tumor cells, was initially dominated by the stem cell purists’ demand for clear and rigorous definitions of cancer stem cells. Ideally, in every report, each system, surrogate, tissue, or cell line studied was to be interrogated for the hallmarks of cancer stem cells: self-renewal, multipotency, and quiescence. Inevitably, however, the demonstration, in a small number of reports adhering to these standards, that markers and culture techniques can identify or enrich for self-renewing “cancer stem cells,”[2, 3] has led to surrogates, such as those described by Federici et al—eg, mammosphere formation or aldehyde dehydrogenase activity—being equated to cancer stem cells in the absence of functional studies to complement this work. In addition, properties well studied in normal hematopoietic stem cell biology and in hematologic cancer stem cell biology have been assumed to be relevant to solid tumor stem cells, in many cases in the absence of comparable solid tumor data. Thus, perhaps the greatest omissions in the breast cancer stem cell reviews to date, including those by this author (WAW) have been the failure to separate the rigorous work incorporating functional cancer stem cell assays from those relying primarily on marker studies, and the failure to fairly reflect the limitations and complexities of the current literature.

It is clear that the percentage of cancer stem cells identified in a tumor can be highly variable—a function of the technique used to transplant the cells[4]—and it is conceivable that the absence of appropriate microenvironmental signals from the host limits tumor initiation to only a few cells in this artificial condition.[5] While some studies in syngeneic mouse models in which the host microenvironment is intact have demonstrated that the capacity to re-initiate the tumor is indeed limited to a small population of prospectively identifiable cells,[6] it remains to be seen whether this is true across all syngeneic mammary tumor models—and even harder to prove, across any or all in situ human tumors. Concordance between findings in syngeneic mouse models and human tumor xenografts is reassuring, however. In a novel study with parallel findings in both systems, Atkinson et al have recently demonstrated the proof in principle that sub-lethal radiation alone can shrink the tumors but enrich for the resistant tumor-initiating cells in both p53 null mammary tumors and triple negative human xenografts. In contrast, the combination of hyperthermia and radiation simultaneously decreases both the tumor bulk and the tumor-initiating capacity.[7] Rigorous therapy-based studies in multiple models, such as this report by Atkinson et al, suggest that the potential caveats regarding anti–cancer stem cell therapies, including the possibility of dedifferentiation by differentiated cells to replace targeted cancer stem cells, may not be insurmountable obstacles.

Ultimately, proving the value of cancer stem cell studies will require clinical data demonstrating that targeting cancer stem cells improves breast cancer survival. If the biology of normal stem cells teaches us something about the biology of cancer that leads to more cures, it will not matter whether the cells are stem cells, progenitors, tumor-initiators, or self-renewing cells. For now, though, it remains unclear whether breast cancer stem cell targets represent the heart of the beast or just something at which to aim.

Financial Disclosure: The author has no significant financial interest or other relationship with the manufacturers of any products or providers of any service mentioned in this article.

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This commentary refers to the following articleBreast Cancer Stem Cells: A New Target for Therapy

References

1. Al-Hajj M, Wicha MS, Benito-Hernandez A, et al. Prospective identification of tumorigenic breast cancer cells. Proc Natl Acad Sci U S A. 2003;100:3983-8.

2. Dontu G, Abdallah WM, Foley JM, et al. In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells. Genes Dev. 2003;17:1253-70.

3. Ginestier C, Hur MH, Charafe-Jauffret E, et al. ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome. Cell Stem Cell. 2007;1:555-67.

4. Quintana E, Shackleton M, Sabel MS, et al. Efficient tumour formation by single human melanoma cells. Nature. 2008;456:593-8.

5. Rosen JM, Jordan CT. The increasing complexity of the cancer stem cell paradigm. Science. 2009;324:1670-3.

6. Zhang M, Behbod F, Atkinson RL, et al. Identification of tumor-initiating cells in a p53-null mouse model of breast cancer. Cancer Res. 2008;68:4674-82.

7. Atkinson RL, Zhang M, Diagaradjane P, et al. Thermal enhancement with optically activated gold nanoshells sensitizes breast cancer stem cells to radiation therapy. Sci Transl Med.2:55ra79.

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Breast Cancer

Saturday, January 29, 2011

Age of cancer: we can reliably estimate and apply this knowledge? -Cancer Network

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