Background. Multiple articles discuss the rare incidence and potential causes of second hematologic disorders arising after treatment of Chronic Myelogenous Leukemia (CML), leading to the theory of imatinib, the current treatment regimen for CML, as a possible trigger for the development of secondary neoplasms. Our case eliminates the possibility of imatinib as the sole cause since our patient received a diagnosis of simultaneous plasma cell myeloma, CML, and a Jak2 mutation positive myeloproliferative disorder (MPD) arising de novo, prior to any treatment. We will further investigate into alternative theories as potential causes for multiple hematopathologic disorders. Case Report. There are currently no reported cases with the diagnosis of simultaneous plasma cell myeloma, chronic myelogenous leukemia, and Jak2 positive myeloproliferative disorder. We present a case of a 77-year-old male who was discovered to have these three concurring hematopathologic diagnoses. Our review of the literature includes a look at potential associations linking the three coexisting hematologic entities. Conclusion. The mechanism resulting in simultaneous malignancies is most likely multifactorial and potentially includes factors specific to the host, continuous stimulation of the immune system, previous chemotherapy or radiation, a potential common pluripotent stem cell, or, lastly, preexisting myeloma which may increase the susceptibility of additional malignancies.

Giant cell tumor of bone is a benign, locally aggressive neoplasm that is composed of sheets of neoplastic mononuclear cells interspersed amongst non-neoplastic, uniformly distributed, osteoclast-like giant cells. They represent approximately 4-5% of primary bone tumors. Rarely, bone tumors have been noted to produce human chorionic gonadotropin, a finding most often reported in osteosarcoma. We present the case of a young woman who presented with a low-level human chorionic gonadotropin level which, after resection of her recurrent giant cell tumor of bone with secondary aneurysmal bone cyst-like change, became undetectable in her blood. Furthermore, cells within the aneurysmal bone cyst component were immunohistochemically positive for β-human chorionic gonadotropin. This is the first report of such a finding in the literature.

Background: Coexistence of Chronic lymphocytic lymphoma (CLL) to Acute lymphoblastic leukemia is extremely rare with only a few reported cases [1-5]. Chronic lymphocytic leukemia is a neoplasm of small monomorphic round to irregularly shaped lymphocytes of B-cell lineage. Adverse prognostic factors in CLL include flow cytometric expression of ZAP-70 and CD38 which are surrogate markers for the mutational status of IVIg. T-cell acute lymphoblastic leukemia (T-ALL) is a neoplasm of lymphoblasts that are of T-cell lineage and are small to medium-sized cells. Case Report: We present a case of a 62-year-old man, diagnosed with B-Chronic Lymphocytic Leukemia who was treated successfully twice. A year following an allogeneic stem cell transplantation (SCT), the CLL returned for a third time along with a secondary diagnosis of T-cell acute lymphoblastic leukemia. Our review of literature explores the potential pathophysiologic mechanisms of the coexistence of these two diagnoses. Conclusion: Chronic lymphocytic leukemia has been known to evolve into various lymphoid transformations, including diffuse large b-cell lymphoma, and prolymphocytic leukemia, however the coexistence and transformation of CLL to T-cell acute lymphoblastic lymphoma is extremely rare. Potential mechanisms of this phenomemon may include a common genetic predisposition, a malignant transformation of a common progenitor cell, immune deregulation, chronic stimulation of T-cells by the B-CLL cells, adverse effects of chemotherapy exposure, increased T-cell resistance to apoptosis, or to the slight occurrence of pure chance. Numerous hypotheses exist, however the precise relation of the two entities coexisting is unknown due to limited research and only a few known cases.

Pseudoangiomatous stromal hyperplasia is a lesion of breast tissue but can occur in anogenital mammary-like glands. It must be distinguished from low-grade angiosarcoma.

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