I think scientific collaboration but not scientific competition can drive progress in the field promptly. Sometimes, collaboration is the only way to resolve a controversy, especially coming from “ping-pong studies“.

Imagine - 2 or more very respectful labs running experiments in order to answer the same scientific question, but using different models and techniques, finally getting different contradictory results. Whom should we trust and where is the truth? In this case investigators should talk, collaborate, set the same protocol to find the truth and give the answer to the community. Unfortunately we don’t see a lot of collaborations like this in stem cell research - the field is currently full of controversies.

I was happy to find a collaborative effort from leading scientists, resolving some controversy and providing us a showcase, in the most recent issue of Cell Stem Cell journal. Leonard Zon came up with a great idea of collaboration in order to answer a very controversial question about the role of N-cadherin (dispensable or indispensable) in hematopoietic stem cells (HSC). As result you can read consensus paper, coordinated by Len Zon and Cell Stem Cell editor - Deborah Sweet.

The discrepancies described above were generating confusion in the published literature and thus in the field. With the aim of resolving the controversy and providing clarification of the issues involved, we embarked on an interactive discussion approach. At our (L.I.Z.) request, the principal investigators from the two groups that have generated the majority of the conflicting published data, Linheng Li and Sean Morrison, participated in a telephone conference in which each investigator presented and discussed pertinent data slides. This meeting also included another investigator, Toshio Suda, who has published work suggesting a positive role for N-cadherin in the bone marrow, and the editor of Cell Stem Cell, Deborah Sweet.

Points of discussion under moderation of Len Zon:

This joint discussion was followed by a series of one-on-one phone meetings and two other telephone conferences with L.I.Z. During the discussion, it became clear that the disagreement centered on three major questions: (1) Do HSCs express N-cadherin? (2) Is the MNCD2 monoclonal antibody specific for N-cadherin? (3) Does N-cadherin play a role in HSC maintenance and regulation? Involving the groups who had previously come to differing conclusions in a joint discussion provided an efficient mechanism for critical analysis of key experimental data and honest expression of opinion about the relevant issues.

Collaboration set up was following:

With the available information, some conclusions about the first two issues became clear, and these will be outlined below. However, we were not able to reach an agreement on the third question on the basis of the available data. Upon the senior scientist’s suggestion, the Li and Morrison labs agreed to independently perform a limiting dilution competitive transplantation with the exact same experimental conditions and N-cadherin conditional knockout mice, with a view to comparing data and coming to a consensus conclusion. Several emails between the groups outlined in detail the methods, doses of cells, and mechanism of conditional inactivation of N-cadherin. Six months later, we set up a phone call to examine the data from the two laboratories.

The results of this collaboration effort you can get from the paper.

I think this example is remarkable. It shows how collaboration can lead and be done in order to solve important controversies in HSC research. The main lesson to learn from this first showcase - collaboration is possible and it is productive.

Who should initiate and lead such collaborations? My obvious answer - principal investigators, leading scientists and journal editors under independent expert’s moderation. I hope more PI’s and editors will read this post and get the message. All we (postdocs, PhD students) can do ourselves in this case - just spread the word.

What platforms and tools could be used for such collaboration? My obvious answer - any available to date. Letters and emails for editors of journals, phone- and video- conferences, teleconferences, internet with a variety of web tools. Unfortunately PI’s are too rigid in terms of using internet and collaborative web tools.

Quote from Deborah Sweet editorial:

From the perspective of a journal such as Cell Stem Cell, it seems to me that the only fair approach is to remain neutral in any conflict and to publish studies that meet editorial criteria and peer reviewer standards even if they seem to conflict with previous work. However, there comes a time in many scientific disagreements where additional experiments along similar lines to those published previously do not provide significant new insights.

I encourage all of you, as our readers, to use this feature and provide your perspective on articles that we have published. More informal online venues such as blogs, society-sponsored networks such as the ISSCR groups on LinkedIn and Facebook, and even Twitter, also provide mechanisms for scientific discussion about published work and its interpretation that can help highlight issues for the benefit of the field overall.

But controversy initially is a good thing which could be correlated with scientific progress and assays/ models development.

Controversies prompt everyone to rethink their assumptions and devise new experiments to address outstanding issues. Ultimately, therefore, disagreements help drive progress.

Until it become too much. In case of N-cadherin in HSC, for example. And when controversy persist too long, collaboration is the only way to solve it and drive scientific progress further. We should do it all the time and make results available immediately for community and public.

I’d like to summarize a little the recent progress in understanding of the hematopoietic niche.

normal niche and stem cell quiescence
There is a common assumption, based upon experimental data, that a normal niche is required for maintain normal function of adult stem cells, hematopoietic (HSC) for instance, including one of the most important qualities - quiescence. Turns out that in embryonic development, the HSC niche doesn’t play so big a role as in adult, because needs of the growing embryo. In postnatal period of life hematopoietic system needs some “insurance” or protection in case of disasters (injuries). That’s where bone marrow niche comes up as an ideal place to keep HSC dormant or quiescent. Ideal, but not the only one. Splenic HSC and even adipose-derived HSC can also save lethally irradiated mice. But quiescence of splenic HSC is much inferior compared to bone marrow counterparts.

However, niche-HSC-quiescence relationships are not “completely mutual”. HSC spontaneously leaves the niches daily and egress in circulation without entering into cell cycle. So, it turns out that specific type of niche is not absolutely required to keep HSC quiescent. HSC can stay in G-0 phase of cell cycle in circulation (blood or lymph) and in different tissue-specific niches (spleen, bone marrow).

aged niche
It was shown before that aging phenomena of HSC explained mostly their intrinsic qualities. Now it turns out that it also, at least in part, could be explained by aged bone marrow niche (extrinsic mechanism). Very nice paper came up recently from Amy Wagers group at Harvard Stem Cell Institute, which showed that the aged niche is what really matters in aging of HSC. At least one component of the niche - osteoblasts increased in number with age in similar manner to HSC. The authors showed that old bone marrow niche can be rejuvenated by magic circulating factors in young blood.

niche-based diseases
Currently there is mounting evidence that niche abnormalities can be very important in hematological diseases development. For example, myeloproliferative disorders (MPD), myelofibrosis, myeloma and myelodysplastic syndrome. More evidences should come this year. The question also should be addressed whether transfer of abnormal niche is capable of transfering disease.

niche and cancer
There is no doubt right now that the bone marrow niche is largely involved in development of hematological malignancies and solid metastatic tumors. Cancer cells can migrate in bone marrow and hijack a niche, modifying it in order to serve disease progression. In leukemia, we can see another way of niche involvement in disease development. For example, human mesenchymal stromal progenitor cells, derived from acute myelogenous and acute lymphoblastic leukemic bone marrow samples, have clonal genetic abnormalities.

This scheme that I drew represents a simplistic view of hematopoietic bone marrow niche interaction and significance.

(adapted from David Scadden (2010), modified. Dotted lines represent possible transition from one state to another that needs to be validated in future research.)

The recent review by Linheng Li and Hans Clevers, published in Science, proposed the model of co-existence of quiescent and active adult stem cells in mammals. I’d like to point out that they didn’t propose it initially - it was done 2-3 years ago by Andreas Trumpp group for hematopoietic stem cells (HSC), but rather extrapolate it to other adult stem cell populations, such as hair and intestinal stem cells. Furthermore, they nicely shaped this model in the concept of stem cell niche and extrinsic signals, regulating cell divisions and fate.

I pooled some data from Andreas Trumpp’s model for HSC, some thoughts from this review, and and from Marieke Essers paper and made a table. This table summarize the main model points for HSC.

The new - dormancy model of coexistence of quiescent adult stem cell subpopulations, proposed by Andreas Trumpp group:

(Adapted from Marieke Essers and Andreas Trumpp, 2008-2009)

It is maybe too early to accept this model completely, but it look very nice and logical to me. Nevertheless, some things remain unclear. For example, what can make an active HSC become a dormant HSC during homeostasis? Also, I think it’s premature to divide them by bone marrow niche: dormant in endosteal, active in vascular (central marrow). This review convince me more that there is some kind of universal pattern in organization of adult stem cell populations across different tissues. What do you think?

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Also read:
Mapping quiescence of hematopoietic stem cells

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this is a guest post by James Trosko

These comments continue to add to the debate on the two hypotheses of the origin of cancers (adult stem cell versus the de-differentiation or “re-programming” of a somatic differentiated cell). Isn’t it interesting that those who claim cancers are the result of the re-programming during the multi-stage, multi-mechanism process of carcinogenesis fail to mention that no one has successfully neoplastically transformed a primary culture of human fibroblasts or epithelial cell, which ,under normal culture conditions, contain few, if any, adult stem cells. However, when “immortalizing viruses” ( SV40 or HPV-e6-e7)are added to early primary cultures, a few “immortalized” , but non-tumorigenic clones, are obtained, which, then, can be subsequently neoplastically transformed.

Might it explained more easily that these viruses entered all cells ( the few adult stem cells; the transit-amplifying and terminally differentiated cells) but only blocked the “mortalization” of the adult stem cells [one does not immortalize an already normal immortal adult stem cell? The fact that only a few such “immortalized” cells are recovered from a primary culture is equivalent to the few rare adult stem cells in the primary culture. Also, the frequency of “iPS” cells is about what one would expect from the number of adult stem cells in a primary culture.

In effect, those who still believe that “iPS” cells are really reprogrammed somatic differentiated fibroblast must believe that carcinogenesis starts with the induction of an “iPS” cell during the single “hit” of the initiation process, such as what happens when the skin is exposed to UV light. Yet those “initiated” skin cells do not form teratomas but, only after chronic exposure to non-mutagenic tumor promoters, such as TPA, does one see papillomas and later , carcinomas.

The real problem is that no one has produced “iPS” cells from differentiated skin keratinocytes or mature hepatocytes, yet our lab has easily produced human breast carcinomas from a normal human breast adult stem cell. Moreover, no one has compared the frequency of “iPS” cells from a primary culture of human cells versus that from a pure culture of human adult stem cells. I find it interesting that almost every day, new ways of producing “reprogramming” cells are reported( i.e., mouse skin cells directly, without the need for vector transmission of embryonic stem cell genes).

Ultimately, while this forum allows for academic freedom of thought in science, the current atmosphere of science, as is evidenced in trying to get grants or papers published, has not allowed easy access to challenge prevailing paradigms. When one views the power of the “iPS” story, via its publications in very influencing scientific journals ( and even the public media), and the absence of any challenge ( not to the reality of the production of the “iPS” but of the interpretation of the origin of these cells), one can see how science and the public are not well served.

In my own case, all my grants have been “trashed” or “triaged” and all of my publication, those that ultimately did get published, were rejected by the same journals that can’t publish the “iPS” stories fast enough.

It seems that science ( peer reviewers of grant proposals and manuscripts), while trying to assure quality, rigorous methodology, and ethical standards, should let the individual with “crazy” ideas or their own unique interpretations of their own data, make a fool” of themselves by allowing them to interpret their own data. In my case, I know I might not be correct…but then again, I’m sitting on my experience (of over 20 years of working with human adult stem cells and 44 years of studying all phases of carcinogenesis). With this experience as my guide to understand the “iPS” interpretation and the “re-programming” of differentiated somatic cells makes no sense to me. It does not help me rationalize all my research experience. If someone can demonstrate to me with new experiments ( not all those published as of yesterday), I will immediately be “converted”. I’m not so stupid as to hold onto a scientific idea that no longer has validity.

If one has not read my ideas , see: Tai, M.H. et. al, “Oct4 expression in adult human stem cells: evidence in support of the stem cell theory of carcinogenesis”. Carcinogenesis 20: 495-502, 2005; Trosko, J.E., “Cancer stem cells and cancer nonstem cells: From adult stem cells or reprogramming of differentiated somatic cells”. Vet. Pathol. 46: 176-193, 2009; Trosko, J.E. “Reprogramming or selecting adult stem cells?” Stem Cell Rev.4:81-88, 2008).

Clinical oncologists and cancer biologists spend a significant amount of time to investigate “genome-wide” signatures of tumors. This knowledge should help to diagnose, predict cancer development, make a prognosis for outcome and personalize a patient’s treatment. However, if the cancer stem cell (CSC) hypothesis is correct, we should not extrapolate those signatures to all tumor, but rather separate cancer-initiating cells population from non-tumorigenic cells. If you start to compare them, you can came up with quite interesting findings.

Correlation between embryonic stem cell (ESC)-like gene signature and poor clinical prognosis

The positive correlation between ESC-like genetic signature and tumor aggressiveness and poor clinical prognosis has been demonstrated for a number of cancers. For example, in leukemia and epithelial cancers activation of “ESC-like program” was identified. But some of these studies compared only bulk tumor cells versus normal tissue cells, but not cancer-initiating cells versus non-tumorigenic cells. Also, ESC-like signature was not consistently associated with tumor-initiating cells. It’s not surprising for me that poor patient prognosis, which is directly correlated with histologically poorly differentiated cancers (was shown many years ago), is associated with activation of ESC-like “gene module” expression. Most of so called “stemness genes” is also cancer-associate genes”.

Excerpt from the commentary:

Thus, the eSC-like signature in cancers is more likely the results of re-activation of an eSC-like phenotype during the course of tumor progression rather than an inherited phenotype from a cell-of-origin.

Correlation between adult tissue stem cell (TSC)-like gene signature and poor clinical prognosis

A recent study by Thomas Hussenet compared ESC-like and adult TSC-like gene signatures in tumorigenic (aka cancer stem cell (CSC)-enrich) versus non-tumorigenic cancer cells. They showed that TSC-like gene program is specifically activated in breast cancer-initiating cells (dissected by CD24-/CD44+ phenotype) in contrast to ESC-like program, which is activated in both - tumorogenic and non-tumorigenic cancer cells and bulk tumors. This trait was similar among a few murine and human epithelial cancers. Confirming the previous study by Michael Clarke group, they showed that activation of TSC-like gene signature was associated with poor clinical outcome in breast and lung cancer patients.
These findings could be interesting, if surface phenotype of breast CSC is a valid marker.

High level of stem cell markers correlate with poor clinical prognosis

Sometimes you don’t need to look at global or a partial gene expression profile of a tumor to predict an outcome. You can just look at commonly used ” normal stem cell markers” and find a correlation. It was very well shown for CD44+/CD24low and breast cancer, ALDH and breast cancer and leukemia, Bmi-1 and colon cancer, CD133 and colorectal cancer, and others. Interestingly, many of these studies were challenged later and the significance of these markers is still controversial. I guess it happened because different groups used different cohorts of patients and performed different sets of assays.

I also wonder if for each type or malignancy this possible correlation could be so different. For example, for leukemia, prognostic irrelevence of common human hematopoitic progenitor/stem cell marker CD34 was shown in 1992. But also it could depends on how further you can dissect the stem cell phenotype.

Will CSC gene expression signatures be useful in the clinic?

Well, cancer genome studies by microarrays is not a new thing, so what did we learn from it? Serge Koscielnyin his essay wrote:

Gene microarrays have brought little progress to the clinical management of cancer since Shena et al.’s 1995 publication. Van’t Veer et al. gave us a proof-of-concept when they showed that the gene microarray information could be used to predict the prognosis. Unfortunately, these predictions of prognosis are not very accurate and have not improved since 2002. This state of affairs is extremely disappointing given the potential of the technology.

So, do we have any hope about CSC gene expression signatures? I think, at this point in time, it is important to study gene expression signatures of CSC, because first of all we need to answer the question: Are CSCs clinically relevant? And if the answer is YES, overlapping of gene modules will allow us to identify new molecular therapeutic targets. Many researchers (not sure about clinicians) hope that defined CSC molecular signatures will allow us make a clinical prognosis and design personalized treatment.

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also read cancer stem cell category
twitter hashtag: #cancerSC
Connotea tags: cancer SC; gene expression profile

This lecture was given in 2007 on 49th Annual ASH meeting as esteemed E. Donnall Thomas Lecture and Prize.

(click picture to watch)

Even this lecture was recorded 3 years ago, I got to know so many things and most importantly - the history. I made a screenshot of this moment of the lecture because there are 3 heroes on the picture: Hangoc Giao, Hal Broxmeyer and Scott Cooper. In 1988 they took 2 liquid nitrogen tanks with cord blood samples and only through special connections with “PanAmerican” airlines moved them to Paris where Eliane Gluckman did the first transplant of cord blood. Very brave people!

I’d highly recommend you to watch this lecture.

Authors were not only able to expand cord blood HSC drastically, but also performed phase I of clinical trial, which appear to be safe and preliminary data demonstrated earlier rapid myeloid engraftment in 10 patients.

HSC expansion - from lab to the clinic

If you follow the progress in the field you know that many HSC expansion protocols were published, but only a few of them attempted to enter to clinical trials. I suspect it happened because the vast majority of them didn’t pass all of validation tests, such as functional assessment of HSC function in xenotransplant models after ex vivo expansion. But some protocols entered into the clinical trials phase. Most of them were done on bone marrow or mobilized blood HSC, but some with cord blood (CB). Some trials didn’t move from phase I (safety and feasibility) to phase II (efficacy).

There is a huge demand for HSC expansion from cord blood particularly, because this is the main disadvantage for wide CB transplantation as an alternative to bone marrow and mobilized blood. Currently, a few CB HSC expansion protocols are undergoing clinical trials. But Bernstain’s study we can consider as more solid and successful at this point. Companies are also actively involved in developing CB HSC expansion protocols and supervise the clinical trials. For example, Fate Therapeutics licensed the “small molecule - HSC expander” from Children’s Hospital Boston and started a clinical trial.

Is it possible to keep expanded HSC in undifferentiated state?

Unfortunately, more likely the answer is NO. Even if you can detect the difference of expansion within long-term HSC subset by flow cytometry, these guys already primed to be actively dividing but not quiescent after the transplant. It could sound like a speculation, but nobody has proven the opposite so far. Almost all studies calculate HSC expansion difference based on CD34+ total expression or CD34+/CD38-. But even the last mentioned population does not represent HSC, because most of CD34+/CD38- are progenitors and you need to go way further (Lin-/CD34+/CD38-/CD45RA-/CD90+) in order to conclude something about long-term HSC. Most of the in vivo studies do not assess multilineage engraftent long enough to conclude confidently about superior repopulation of expanded HSC.

That’s why earlier trials didn’t show advantage in neutrophil and platelet recovery time - they expand something withing CD34+ total population, but not that we need.

Citation from the review:

Initial efforts to expand UCB progenitors ex vivo have resulted in expansion of mature rather than immature HSC, confounded by the inability to accurately and reliably measure long-term reconstituting cells. Ex vivo expansion of UCB HSC has failed to improve engraftment because of resulting defects that promote apoptosis, disrupt marrow homing and initiate cell cycling.

Double unit CB competition for engraftment

As you can notice from Bernstein’s study, they didn’t transplant just expanded CB sample but rather mixed with competing second - unmanipulated unit. For the phase I of clinical trial this sounds reasonable and safe. As we know, in double unit CB transplant only the one sample will win engraftment eventually, but another sample will act as a helper. In the case of this trial, expanded CB sample was a helper and unmanipulated CB unit was a winner. Why so? Because virtually all expanded CD34+/CD38- cells were multipotent and myeloid primed progenitors with very very few true HSC. Those very few expanded HSC, the authors were not able to detect a few months after transplant in 8 out of 10 patients. 2 patients with some signs of expanded long-term HSC engraftment were under observation for 240 and 180 days. But in one of them they were not able to detect signs of multilineage engraftment at the time point of 1 year and second patient didn’t possess engraftment in T-cells.

Numbers game

So, even though they transplanted 6 millions per kg of expanded CB CD34+ cells with only 0.24 millions (25 times less!) per kg unmanipulated CD34+, the second unit won engraftment in all 10 patients by 1 year of observation period. Why so?

2-7 millions per kg of CD34+ cells we need for clinically significant engraftment in adults. Magically, in pediatrics, 0.1-0.3 millions per kg of CD34+ CB cells is enough for sufficient blood lineage recovery. Average CB sample can provide the dosage only below 1 million per kg for adults. So we need to at least expand CD34+ cells twice to make the patients happy. Why are researchers shooting 50-150 fold expansion then? Because in reality almost none of long-term HSC expanded, but primed to progenitors in vitro, as I mentioned above. So, when we are talking about twice more expansion, we should achieve it naturally and proportionally in all HSC and progenitor subsets, without “cell culture artifacts”, such as “progenitors skewing”.

Do we really need HSC expansion for clinical success?

It seems like expansion of common myeloid (CMP) or multipotent progenitors (MPP) is good enough to achieve earlier and rapid neutrophil recovery. Maybe we even don’t need to chase robust expansion of long-term quiescent HSC in experiment and pre-clinical setup. I would not, just because if I see 30-100 times expansion of long-term HSC my “cancer caution” alarm starts beeping. Total number of CD34+ or CD34+/CD38- game could be efficient for good clinical outcome, as this study showed. I wonder what would happen if transplant was just expanded CB sample alone? No, better not to take such a risk, but keep mixing with unmanipulated unit.

In 2008 the Harvard Stem Cell Institute (HSCI) began working with Amy and E.W. Steptoe, local sibling filmmakers, who were in search of the next interesting topic for a documentary. Together we decided to tell the story of the effect that stem cell research is having now on the lives of leukemia patients and the challenges that lie ahead, both in fighting leukemia and in advancing stem cell research. This documentary was produced with the valuable input of HSCI Faculty members Scott Armstrong, MD, PhD, George Daley, MD, PhD, and Corey Cutler, MD; Toni Dubeau, RN, and Harvard graduate student, Sean Buchanan; and with the generous cooperation of Children’s Hospital Boston and the Joslin Diabetes Center.

(picture is clickable)

The study give us more clue about how aging and stem cells are connected. Can we play with longevity through stem cells?

The current status of our knowledge I’d like to illustrate by quote from Sean Morrison’s review:

On the one hand, the changes in stem cell function that occur during aging would be expected to contribute to age-related morbidity by reducing tissue regenerative capacity. Moreover, the accumulation of genetic damage in stem cells likely contributes to increased cancer incidence during aging (Rossi et al. 2008, Sharpless & DePinho 2007). On the other hand, the effects of aging on fully differentiated cells are likely a major and independent contributor to age-related morbidity, cancer incidence, and degenerative disease. It remains unclear whether the changes that occur in stem cells are a major or minor contributor to age-related morbidity and life span.

You can find and download this presentation on Google Docs and Slideshare

How many lives could CB potentially save?

According to van Rood and Oudshoorn (2008), between 2000 and 2006, 151 000 patients qualified for an HLA unrelated donor transplant but, of these, only 64 720 actually received a transplant. [link]



Overall, 38% of patients for whom a search was started were actually transplanted. 28% of patients waited 6 months before failing the search procedure, 33% of patients were not transplanted despite a donor being found within 4 months, and finally, unrelated transplants were performed 2 months later than sibling transplants for the same indications. [link]

…timely CB access could benefit about one third of the patients requesting an unrelated donor. [link]

Public CB effectiveness

At a registry size of 10 million [bone marrow] donors, approximately 7 million additional donors are needed to increase the chance of matching by only 1%. [link]




…over 400,000 cord blood units donated and stored worldwide for unrelated use. Approximately, 14,000 unrelated cord blood transplants have been performed to date… [link]

… you can only donate your child’s cord blood if the baby is delivered in a hospital associated with a collection program. There are less than 200 collection centers in the US, mostly at large hospitals which deliver thousands of babies per year. [link]

The study showed that 50,000 donors would be required to provide at least one donor for 98% of the patients with at least a 4 out of 6 HLA match, to 80% with a 5 out of 6 match, and to 34% with a 6 out of 6 match. [link]

…estimate on the clinically useful size of a public CB bank to provide a suitable match for the UK population of 61 million people - 50 000 CB units. [link]

A non-biased bank of 50 000 would have around 15% of minority ethnic groups (about 7500 donors) and give a 36% chance of match for this group, and 80% for the whole population. If we bias collection towards the minority groups (i.e. doubling their representation to 30% of the inventory) the predicted figures are 74% for the whole population but 52% for the non-predominant ethnic groups. [link]

…the inventory should reach 150 000 donors to offer an 80% chance to the minority groups using the whole population… [link]

Private CB effectiveness

… about 900,000 cord blood units have been stored privately for personal use, with about 100 autologous transplants performed. [link]




Baseline assumptions included a cost of $3,620 for umbilical cord blood banking and storage for 20 years, a 0.04% chance of requiring an autologous stem cell transplant, a 0.07% chance of a sibling requiring an allogenic stem cell transplant, and a 50% reduction in risk of graft-versus-host disease if a sibling uses banked umbilical cord blood. [link]

Private cord blood banking is not cost-effective because it cost an additional $1,374,246 per life-year gained.

if the cost of umbilical cord blood banking is less than $262 or the likelihood of a child needing a stem cell transplant is greater than 1 in 110, private umbilical cord blood banking becomes cost-effective. [link]

None of the 93 US and Canadian physicians surveyed recommended private cord blood banking if there were no ill siblings and parents were of Northern European descent. [link]

There is no data on long-term viability of cord blood cells after 10-15 years. [link]

An analysis of 52 transplantation cases from cord blood units stored in private cord blood banks in the period 1994 to 2004 showed that of these 46 cases were actually allogeneic transplantation to siblings. Allogeneic transplantation is clearly the most common use of privately stored cord blood units. [link]

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Please discuss your thoughts in comments. I would like to join discussion.

Also read: Private cord blood banking - worth your money?