Mohamed Jalloh

Panobinostat: A surprising approval for the treatment of multiple myeloma

The National Cancer Institute has estimated that multiple myeloma, a form of cancer derived from plasma cells that accumulate in the bone marrow, takes the lives of more than 10,000 Americans annually. Panobinostat is a first-in-class medication that inhibits the activity of histone deacetylase enzymes. This inhibition may restore cell function by slowing the overproliferation of plasma cells in patients with multiple myeloma.

Lenvatinib: Another agent to fight refractory thyroid cancer

More than 500,000 patients are estimated to be living with thyroid cancer in the United States. More than 1,800 Americans died from it in 2014. While treatment is possible, few options are available for patients once the thyroid cancer has progressed. “The incidence of thyroid cancer has been increasing globally over the last 50 years, and for patients with thyroid cancer that progresses following surgery and radioactive iodine treat-

Isavuconazonium sulfate: A new azole for life-threatening fungal infections

Isavuconazonium sulfate (Cresemba—Astellas) has received FDA approval to treat invasive aspergillosis and invasive mucormycosis (also known as zygomycosis). Aspergillosis and mucormycosis are fungal infections caused by the Aspergillus species and by the Mucorales order of fungi, respectively. Both infections are seen predominantly in immunocompromised patients and are life-threatening.

ASCO 2015: Key cancer studies bring hope to patients

Highly anticipated cancer research was presented recently at the 2015 American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago. The most intriguing research presented addressed the cost of new oncology immunotherapy—one of the new immunotherapies could cost more than

Dinutuximab: First and only agent for treating a rare pediatric cancer

1 million per patient annually.

Olaparib: A new option for patientswith advanced ovarian cancer

Dinutuximab (Unitixin—United Therapeutics) has received FDA approval as part of a multimodality regimen for pediatric patients with high-risk neuroblastoma. Dinutuximab was also granted priority review and orphan product designation.

Nivolumab: New PD-1 inhibitor for most dangerous form of melanoma

Abstract Olaparib (Lynparza—AstraZeneca), a new medication to treatwomen with advanced ovarian cancer associated with mutatedBRCA (BReast CAncer) genes, has received accelerated FDA approval.Targeted to patients who have had repeated treatment failures withchemotherapy, olaparib was approved in conjunction with the BRACAnalysis Cdx, a genetic test used to detect mutated BRCA genes.

Catridecacog: First drug to treat rare genetic blood clotting disorder

Abstract Nivolumab (Opdivo—Bristol Meyers-Squibb) received accelerated FDA approval to treat patients with unresectable or metastatic melanoma who no longer respond to other therapies and for patients with melanoma whose tumors express a gene mutation called BRAF V600, for use after treatment with ipilimumab (Yervoy—Bristol– Myers Squibb) and a BRAF inhibitor. Nivolumab is the seventh new medication approved for treating melanoma since 2011, joining ipilimumab, vemurafenib (Zelboraf—Daiichi-Sankyo, Genentech), dabrafenib (Tafinlar—GlaxoSmithKline), and others.

Palbociclib: A new breakthrough for advanced breast cancer

Pathophysiology of the disorder Factor XIII is a terminal enzyme in the blood coagulation cascade that stimulates cross-linking of fi brin and other proteins in the fi brin clot to promote hemostasis. In human plasma, factor XIII circulates as a heterotetramer of two functional subunit proteins—two factor XIII A-subunits and two factor XIII B-subunits. The factor XIII A-subunit acts as the enzyme, while factor XIII B-subunit acts as a carrier for the factor XIII A-subunit. During coagulation, the factor XIII is activated by thrombin and calcium; the factor XIII A-subunit dissociates from the factor XIII B-subunit to become active and help cross-link fi brin to enhance platelet and clot adhesion to injured tissue. Patients with the factor XIII A-subunit defi ciency have a signifi cantly lower level of the active subunit, thus resulting in less stable clotting for injured tissue. Catridecacog binds to the free human factor XIII B-subunit, as factor XIII A-subunit, to strengthen fi brin clots, impede fi binolysis, and enhance platelet adhesion to the injury site.