F. H. Grand

Imatinib sensitivity as a consequence of a CSF1R-Y571D mutation and CSF1/CSF1R signaling abnormalities in the cell line GDM1 (2009)

Chase, A., Schultheis, B., Kreil, S., Baxter, J., Hidalgo-Curtis, C., Jones, A., ...

Imatinib is usually a highly effective treatment for myeloproliferative neoplasms (MPNs) associated with ABL, PDGFRA or PDGFRB gene fusions; however, occasional imatinib-responsive patients have been...

Imatinib sensitivity as a consequence of a CSF1R-Y571D mutation and CSF1/CSF1R signaling abnormalities in the cell line GDM1 (2009)

Chase, A., Schultheis, B., Kreil, S., Baxter, J., Hidalgo-Curtis, C., Jones, Alexander, ...

Imatinib is usually a highly effective treatment for myeloproliferative neoplasms (MPNs) associated with ABL, PDGFRA or PDGFRB gene fusions; however, occasional imatinib-responsive patients have been...

Imatinib sensitivity as a consequence of a CSF1R-Y571D mutation and CSF1/CSF1R signaling abnormalities in the cell line GDM1 (2009)

Chase, A., Schultheis, B., Kreil, S., Baxter, J., Hidalgo-Curtis, C., Jones, Alexander, ...

Imatinib is usually a highly effective treatment for myeloproliferative neoplasms (MPNs) associated with ABL, PDGFRA or PDGFRB gene fusions; however, occasional imatinib-responsive patients have been...

Two novel imatinib-responsive PDGFRA fusion genes in chronic eosinophilic leukaemia (2007)

Curtis, C.E., Grand, F.H., Musto, P., Clark, A., Murphy, J., Perla, G., ...

We identified two patients with a t(2;4)(p24;q12) and a t(4;12)(q2?3;p1?2), respectively, in association with BCR-ABL and FIP1L1-PDGFRA negative chronic eosinophilic leukaemia. Molecular analysis...

Acquired isodisomy is common in atypical myeloproliferative disorders (2007)

Curtis, C., Grand, F.H., Kreil, S., Oscier, D.G., Hall, A.G., Cross, N.C.P.

Analysis of T(9;22) breakpoints indicates that P210 and P190BCR-ABL are formed by distinct mechanisms (2007)

Score, J., Calasanz, M.J., Pane, F., Ottmann, O., Cross, N.C.P., Grand, F.H.

Acquired isodisomy is common in atypical myeloproliferative disorders (2007)

Curtis, C., Grand, F.H., Kreil, S., Oscier, D.G., Hall, A.G., Cross, N.C.P.

Analysis of T(9;22) breakpoints indicates that P210 and P190 BCR-ABL are formed by distinct mechanisms (2007)

Score, J., Calasanz, M.J., Pane, F., Ottmann, O., Grand, F.H., Cross, N.C.P.

A novel ETV6-PDGFRB fusion transcript missed by standard screening in a patient with an imatinib responsive chronic myeloproliferative disease (2007)

Curtis, C.E., Grand, F.H., Waghorn, K., Sahoo, T.P., George, J., Cross, N.C.P.

The platelet-derived growth factor receptor beta fuses to two distinct loci at 3p21 in imatinib responsive chronic eosinophilic leukaemia (2007)

Grand, F.H., Curtis, C., Score, J., Chase, A., Cross, N.C.P.

Identification of a novel imatinib responsive KIF5B-PDGFRA fusion gene following screening for PDGFRA overexpression in patients with hypereosinophilia (2006)

Score, J., Curtis, C., Waghorn, K., Stalder, M., Jotterand, M., Grand, F.H., ...

Idiopathic hypereosinophilic syndrome (IHES) is a disease that is difficult to classify, and diagnosis is one of exclusion. The identification of a cytogenetically invisible interstitial deletion...

The platelet-derived growth factor receptor beta fuses to two distinct loci at 3p21 in imatinib responsive chronic eosinophilic leukemia (2005)

Curtis, C., Apperley, J.F., Dang, R., Jeng, M., Gotlib, J., Cross, N.C.P., ...

We have identified three patients (2 adults, one infant) who presented with BCR-ABL negative eosinophilic myeloproliferative disorders. Cytogenetic analysis revealed a t(1;3;5)(p36;p21;q33) for case...

Disruption and aberrant expression of HMGA2 as a consequence of diverse chromosomal translocations in myeloid malignancies (2005)

Odero, M.D., Grand, F.H., Iqbal, S., Ross, F., Roman, J.P., Vizmanos, J.L., ...

Chromosomal translocations that target HMGA2 at chromosome band 12q14 are seen in a variety of malignancies, notably lipoma, pleomorphic salivary adenoma and uterine leiomyoma. Although some HMGA2...

Treatment with interferon-alpha preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors (CFU-GM) from patients with chronic myeloid leukemia but spares normal CFU-GM.

Gordon, M Y, Marley, S B, Lewis, J L, Davidson, R J, Nguyen, D X, Grand, F H, ...

The biological target for interferon (IFN)-alpha in chronic myeloid leukemia (CML) is unknown, but one possibility is that amplification of granulocyte-macrophage colony-forming cells (CFU-GM) is...

Treatment with interferon-alpha preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors (CFU-GM) from patients with chronic myeloid leukemia but spares normal CFU-GM.

Gordon, M Y, Marley, S B, Lewis, J L, Davidson, R J, Nguyen, D X, Grand, F H, ...

The biological target for interferon (IFN)-alpha in chronic myeloid leukemia (CML) is unknown, but one possibility is that amplification of granulocyte-macrophage colony-forming cells (CFU-GM) is...