I certainly agree that this is a myeloproliferative disorder.The patient is anemic and thrombcytopenic. BMB shows moderate reticulinfibrosis, hyperplasia and leftshift of myelopoiesis, no icrease in blasts (CD117 is pending). Erythropoiesis is diminished. Megakaryopoiesis shows marked atypia with very large forms.  
Based on the morphology and the peripheral blood I would favour the diagnosis of chronic idiopathic myelofibrosis. Thrombocytosis is usually found in CIMF, but a minority of the cases may present with thrombocytopenia.

I agree this is originally a Myeloproliferstive disorder (MPD), but now with 16% blasts in the blood, it is either in accelerated phase or has transformed to Acute Leukaemia. In some of the sections there is an increase in blast cells, and the negative CD34 does not exclude myeloblasts, which are not infrequently negative in AML. Hopefully CD117 will confirm increased myeloblasts, but a small proprotion of MPD's may transform to ALL.  
Progression from Chronic Idiopathic Myelofibrosis (CIM) seems most likely, although the reticulin is only mildly increased, so the transformation would be from the cellular rather than the fibrotic stage of CIM. It would be helpful to know if there were other features of CIM such as spenomegaly, red cell taer drop formation and leucoerythroblastosis.  
The presence of large, dysplastic megakaryocytes makes CML as the original MPD unlikely, as the megakaryocytes are either normal in size or small in CML.  
My diagnosis would thus be AML following transformation from CIM.

Another possibility: it could be primary AL and megas are reactive. There are sheets of blasts, hyatus leukaemicus, neither typical clusters nor intrasinusoidal growth of megas.  
 
In any case we need two things:  
 
1. Clinical features, most notably - degree of hyperplastic syndrome (particularly hepatosplenomegaly). Anamnesis is crucial; if this is CIMF in transformation there should have been some complaints in the past.  
 
2. Blast cells have monocytoid nuclei, so I second the thought that CD34 may be not so informative. But other myelomonocytic markers besides CD117 could be helpful.  
 
And, well, if there are 16% of blasts in blood, they could be typed by flow. Though it is not easy, I know. And cytogenetics from bone marrow should be done in any case.  
 

The patient presented with weight loss and sweats. He had a history of abnormal differential of only a few months and a normal blood count 1 year ago. There was no evidence of splenomegaly on ultrasound. PBC: WBC 12x109/l, blasts 7% (16% in another hospital), myelo 9%, metamyelo 3%, bands 7%, segm 34%, eos 1%, lymph 35%, monoc 4%, plt 36 x 109/l, hb 89 g/l, normoblats 3/100. PB blasts by flow (10%) pos for: cMPO 50%, CD117 88%, CD34 29%, CD33 85%, CD11c 75%, CD7 36%.  
Molecular genetics: bcr/abl -, PML-RARA -, AMAL1-ETO -, CBFB-MYH11 -, JAK2V617F pending, cytogenetics pending.  
BM - dry tap.  
There is no evidence of chronic disease (no splenomegaly, short history, rapidly evolving disease (decreasing Hb and PLTs).  
Diff diagnosis: acute panmyelosis with MF, MP/MDS unclassfiable with transformation, RAEB-2.  
The patient is currenly undergoing AML type induction with SCT planed in the future.

Considering the age of the patient I would favor the diagnosis of AML with fibrosis - if imprints from the biopsy were done it would be easier to confirm AML by counting the blasts in the bone marrow. However, sheets of blasts shown in the photos (called "immature") can be enough to establish AML diagnosis. Considering the results of immunophenotyping from PB these would probably come out positive in CD 117 immunostaining.

Unfortunately, BM imprints have not been performed since the patient underwent the BM biopsy at another hospital. Having considered age, the rate of disease progression, PB cytology and FC data, we beleive that the patient has AML. However, not a clearcut BM picture casts some doubts on the diagnosis.

I have to apologize for not having included in my comment the fact that 16% blasts were present in the pb. It is not a good idea to comment on such complex cases at midnight.  
Ugnius, thanks for submitting this case. It is a classical example to demonstrate the importance of integration of clinical and laboratory data for bone marrow diagnosis.  
I agree with Dr.Grisevicius' differential diagnosis. The morphology of megakaryocytes, many pathologic small non lobated forms and some very large ones with hypolobated nuclei as well, are an argument in favour of acute panmyelosis, but not an absolute one.  
Let's wait for the results of the pending investigations.

Thank you for comments. New IH photos and somments will be appended as soon as possible.

Just thinking:  
 
Well, normal spleen and short anamnesis could exclude CIMF in transformation more or less safely.  
 
It looks like that on the given images blast count is well above 20%. But other fields should be examined to decide if the cryteria for bona fide AL are met.  
 
Changes in blood for several months are rather more suggestive for AML pos-MDS than for APMF or de-novo AML. By the way, were peripheral neutrophils and red cells morphologically normal? Atypical leucocytes could point to APMF or post-MDS AL; in contrast, red cells morphology should be normal in APMF.  
 
Another thought: WHO cryteria for APMF include pancytopenia. The patient had WBC count 12.000 - leukocytosis even if blasts are excluded.  
 
Finally, other mega markers besides CD61 could help if there is a suspiscion of AML-M7.

Dear Collegues: some new stains arrived. Unfortunatelly CD117+ only single cells (nonmastocytic) <5% population. But it's obvious that immature "blastic" NASDE cells are MPO+ and dim Bcl2+ and constitute abou 60% of population. Some of them CD68+ but majority is negative (M5 usually shows more extensive reactions). Can we postulate  
AML with CD34- CD117- MPO+ Bcl2+ CD68-/+ CD117-/+ imunophenotype (histologically)? M2,M3,M4 (appologies- I have only parafin block)? Thank you for the further comments.

For the time being, we have the diagnosis of AML with fibrosis, on flow: myeloid markers+ and CD117+; on IHC MPO+. Acute panmyelosis with myelofibrosis, seems still an option.  
AML secondary to other preceeding hematologic disease, seems less likely because of the extremely short history.  
I wonder if cytogentics will give us more insight.

Cytogenetics showed isolated loss of chromosome Y. This is a nonspecific but not an uncommon finding in AML.

Are there overt dysplastic features in peripheral blood?