Histiocytic sarcoma (HS) is an extremely rare non-Langerhans cell disorder with an aggressive course and limited treatment options. Recent advances in molecular/genetic sequencing have suggested a common clonal origin between various hematolymphoid disorders and cases of secondary HS. Deriving conclusions from previously reported cases of HS arising secondarily to certain hematolymphoid disorders, here we have tried to provide insight into the mechanisms influencing this evolution. We also discuss a clinical case of a 72-year-old man with a diagnosis of chronic myeloid leukemia (CML), presenting subsequently with a heterogeneous liver mass positive with a diagnosis of HS. The liver mass showed a retained BCR-ABL1 translocation suggesting clonality between the CML and HS. As seen in our case and other reported cases of HS derived secondarily, the concurrent expression of immunoglobulin heavy (IGH)-/lightchain rearrangements or cytogenetic markers common to the primary malignancy suggests an evolutionary mechanism involving lineage switching that could potentially be influenced by genetic or epigenetic cues which may occur at the level of a progenitor or the malignant cell itself. Clinical caseA 72-year-old male was brought to the emergency room with a one-month history of progressively worsening bilateral lower extremity swelling, more than 10 lbs. of weight loss, lack of appetite, and rapidly declining performance status. His past medical history was notable for CML, which was diagnosed 30 months prior to presentation (Fig. 1). The patient was treated on a protocol with imatinib (400 mg daily) and demonstrated a complete molecular response to tyrosine kinase inhibitor (TKI) therapy. Focused physical examination demonstrated an emaciated male in mild distress from abdominal pain, right upper quadrant tenderness on deep palpation, and abdominal distension without any signs of an acute abdomen.His peripheral blood smear revealed normochromic, normocytic anemia with hemoglobin of 7.6 g/dL (normal range, 12.5-16.3 g/dL), a white blood count of 7 730/lL (normal range, 3 600-11 200/lL), a red blood cell count of 2.78 M/lL (normal range 4.06-5.63 M/lL), and a platelet count of 114 000/lL (normal range, 159 000-386 000/lL). Serum iron was low (21 lg/dL) with a low TIBC (216 lg/dL), which was attributed to anemia of chronic disease. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed the absence of the BCR/ABL transcript in the peripheral blood.Computed tomography scan of the chest and abdomen revealed a large, complex, heterogeneous, hypodense mass involving nearly all of the caudate and left lobes of the liver. These lesions were not present in the previous examination carried out 1 year before.Biopsy of the liver mass revealed diffuse infiltration of large and irregular pleomorphic cells with lobulated nuclei with some binucleated and trinucleated cells containing
IntroductionImmunotherapy in the form of immune checkpoint inhibitors has changed the landscape of cancer treatment. Newer monoclonal antibodies are coming up and are being tested in various cancers during different stages of treatment. With the increasing use of immune checkpoint inhibitors in the management of various types of cancers, the question is raised as to what next can be offered to a patient who has progressed on this newer treatment. Does Sequence matter? There have been reports of improved responses to chemotherapy after immunotherapy in the form of vaccines. Here we present a case series of 6 patients who progressed on immunotherapy with immune checkpoint inhibitors after initial modality of treatment (chemotherapy/radiation), subsequently received chemotherapy with excellent response.MethodsWe have a cohort of six patients who had disease progression on second line Immunotherapy for solid or hematological malignancies and had ECOG < 2. All these patients received third line salvage chemotherapy. Three patients had metastatic head and neck cancer, 2 had non-small cell lung cancer (NSCLC), and one had T -cell rich B- cell lymphoma. Prior review and approval were obtained from our institutional review board.ResultsAll patients had an excellent response to chemotherapy in third line setting, after immune checkpoint inhibitors and most of them achieved a complete response.ConclusionTargeting cancer with chemotherapy after failure of immunotherapy is a valid option and can lead to better response rates and PFS which may lead to OS. This effect may be secondary to immunotherapy removing the inhibition exerted by tumor cells or other immune cells initially followed by cytotoxic chemotherapy mediated killing of tumor cells.
Eltrombopag is a thrombopoietin agonist and has been used in aplastic anemia and post-transplantation thrombocytopenia. The c-MPL receptor is present on hematopoietic stem cells. There are no reports of eltrombopag utilization for improving poor graft function in the post-transplant setting. Here were report a case of a young female with post-transplant poor graft function as evident from the low absolute neutrophil count, anemia, and thrombocytopenia on day 60. Eltrombopag was started on day 72 and resulted in improvement in all 3 cell lines. The counts continued to be stable even after eltrombopag was discontinued. The patient tolerated the drug without significant side effects for 1 year.
We observed that payer status has a statistically significant relationship with overall survival from AML.
Anthracycline‐based chemotherapy is widely used in the management of breast cancer. Despite the lack of clinical evidence, obtaining prechemotherapy left ventricular ejection fraction (LVEF) by echocardiogram or multigated acquisition scan is a widely adopted practice throughout the world. We present here the results of a retrospective analysis of breast cancer patients who had LVEF measurements in anticipation of an anthracycline chemotherapy to determine whether predefined cardiac risk factors predicted for poor cardiac function. Retrospective data were analyzed from 482 female breast cancer patients in whom LVEF was measured before starting anthracycline‐based chemotherapy. Baseline demographics and multiple risk factors associated with congestive heart failure were collected. Twenty‐six possible risk factors for CHF were defined, and the frequency of finding an abnormal LVEF as a function of total risk factors was assessed. Statistical tests include chi‐squared and logistic regression analysis. The median age of the study population was 52 years. The original chemotherapy plan was changed in 7 patients (1.45%) based on LVEF findings, all of which had asymptomatic LV dysfunction (LVEF ranging 40%‐50%). In 32 patients, despite normal LVEF results, anthracyclines were omitted secondary to prior cardiac issues. In 17 patients where LVEF was reported normal, anthracyclines were skipped based on patient's preference, tumor characteristics, or upstaging of the cancer based on imaging studies. No patient with ≤2 risk factors had an abnormal LVEF (N = 350). The probability of finding an abnormal LVEF in patients without any cardiac risk factors is extremely rare. Skipping baseline LVEF assessment may be an option in some patients with no cardiac risk factors undergoing anthracycline‐based chemotherapy.
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