Outcomes of subsequent antilymphoma therapies after second-line axicabtagene ciloleucel or standard of care in ZUMA-7.

The optimal management of patients with relapsed/refractory large B-cell lymphoma (LBCL) after disease progression or lack of response to second-line (2L) therapy remains unclear. Here, we report outcomes among patients who received subsequent antilymphoma therapy per investigator discretion separately by their randomized 2L arm in ZUMA-7, namely axicabtagene ciloleucel (axi-cel) vs standard of care (SOC). Progression-free survival (PFS) and overall survival (OS) were calculated from 3L therapy initiation.

Safety and Efficacy of Axicabtagene Ciloleucel versus Standard of Care in Patients 65 Years of Age or Older with Relapsed/Refractory Large B-Cell Lymphoma.

Purpose: Older patients with relapsed/refractory (R/R) large B-cell lymphoma (LBCL) may be considered ineligible for curative-intent therapy including high-dose chemotherapy with autologous stem-cell transplantation (HDT-ASCT). Here, we report outcomes of a preplanned subgroup analysis of patients ≥65 years in ZUMA-7.

Patients And Methods: Patients with LBCL refractory to or relapsed ≤12 months after first-line chemoimmunotherapy were randomized 1:1 to axicabtagene ciloleucel [axi-cel; autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy] or standard of care (SOC; 2-3 cycles of chemoimmunotherapy followed by HDT-ASCT).

Two-year follow-up of KTE-X19 in patients with relapsed or refractory adult B-cell acute lymphoblastic leukemia in ZUMA-3 and its contextualization with SCHOLAR-3, an external historical control study.

Background: Brexucabtagene autoleucel (KTE-X19) is an autologous anti-CD19 CAR T-cell therapy approved in the USA to treat adult patients with relapsed or refractory B-precursor acute lymphoblastic leukemia (R/R B-ALL) based on ZUMA-3 study results. We report updated ZUMA-3 outcomes with longer follow-up and an extended data set along with contextualization of outcomes to historical standard of care.

Methods: Adults with R/R B-ALL received a single infusion of KTE-X19 (1 × 10 CAR T cells/kg).

Neurological adverse effects associated with anti-PD1 antibodies alone or in combination with ipilimumab: a multicenter case series.

Anti-programmed cell death protein 1 (PD1) antibodies, pembrolizumab and nivolumab, alone or in combination with ipilimumab, have become standard treatment for melanoma and multiple other malignancies. Neurological adverse effects are rare and have not been well characterized to date. Patients who developed neurological adverse effects while being treated with PD1, alone or in combination with ipilimumab, were retrospectively identified from 10 cancer centers.

Paclitaxel, 5-fluorouracil, and leucovorin (TFL) in the treatment of metastatic breast cancer.

To assess the activity of paclitaxel in combination with 5-fluorouracil (5-FU) and leucovorin in breast cancer, a phase II trial was conducted in women with metastatic disease. Toxicity, response rate, median survival, median duration of response, and median time to disease progression were measured. Between January 1994 and May 1996, 47 patients with metastatic breast cancer and an Eastern Cooperative Oncology Group (ECOG) performance status (PS) < or = 2 who had previously been treated with chemotherapy received 175 mg/m2 paclitaxel over 3 hours on day 1.

Mitogen-activated protein kinase kinase 2 activation is essential for progression through the G2/M checkpoint arrest in cells exposed to ionizing radiation.

An increasing body of evidence suggests that mitogen-induced activation of the RAF/ERK signaling pathway is functionally separate from the stress-induced activation of the SEK/JNK/p38 signaling pathway. In general, stress stimuli strongly activate the p38s and the JNKs while only weakly activating ERK1 and ERK2. However, a number of independent groups have now shown that the RAF/ERK signaling pathway is strongly activated by ionizing radiation.

Paclitaxel by either 1-hour or 24-hour infusion in combination with carboplatin in advanced non-small cell lung cancer: preliminary results comparing sequential phase II trials.

Our group previously described the activity of carboplatin plus paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) (given as a 24-hour infusion) in 51 patients with advanced non-small cell lung cancer. To facilitate outpatient administration, the regimen was modified to infuse paclitaxel over 1 hour. Between February 1995 and August 1996, 63 patients with advanced non-small cell lung cancer were accrued by the Vanderbilt Cancer Center and its affiliate network.

Intranuclear distribution of the human myeloid cell nuclear differentiation antigen in HL-60 cells.

Based on solubility properties, the human myeloid cell nuclear differentiation antigen exists as at least two distinct populations. Most is easily extracted from isolated nuclei in 0.35 M NaCl, while 20 percent resists such treatment.

In vivo crosslinking of nuclear proteins to DNA by cis-diamminedichloroplatinum (II) in differentiating rat myoblasts.

When cells are briefly exposed to cis-diamminedichloroplatinum (II) before lysis in high sodium dodecyl sulfate-urea solutions, the high molecular-weight nucleic acids pelleted by ultracentrifugation contain an increased level of bound proteins when compared to a similar fraction from untreated cells. Subsequent shearing of the pelleted DNA followed by treatment with DNase permits electrophoretic and immunoblot analysis of the crosslinked proteins. In the present study such experiments were carried out with reference to nuclear envelope pore complex proteins in the differentiating L8 rat skeletal muscle cells.

Production and use of rat monoclonal antibodies to the human myeloid cell nuclear differentiation antigen.

A dot immunoblot screening assay was used to identify rat monoclonal antibodies to a human myeloid cell differentiation-specific nuclear antigen (MNDA). The selection was based on the positive reaction of hybridoma cell supernatants with a concentrated nuclear protein extract prepared from late stage human myeloid leukemia cells that express MNDA (HL-60) coincident with a negative reaction with the same extract prepared from a non-expressing more immature human myeloid leukemia cell line. The approach provided an efficient method for obtaining monoclonal antibodies to a specific low abundance nuclear antigen that has not been purified.

Characterization of chromium effects on a rat liver epithelial cell line and their relevance to in vitro transformation.

Chronic exposure to low concentrations or brief exposures to high concentrations of hexavalent chromium (K2CrO4) transformed a rat liver epithelial cell line as assessed by anchorage-independent growth. A clone of the transformed cells produced tumors in syngeneic animals, all of which were determined to be high grade carcinomas. The effects of various doses of chromium on cytotoxicity and cell cycle were established and related to ultimate numbers of transformants in the population.

A nuclear cAMP binding protein in retinoic acid-treated HL-60 cells.

A cAMP binding protein was detected in HL-60 cells using photoaffinity labeling with 8-azido [32P]cAMP. The binding protein was found in a 0.35 M NaCl nuclear protein extract from untreated HL-60 cells and from the HL-60 cells induced to mature with retinoic acid.

Lectin-binding proteins in nuclear preparations from rat liver and malignant tumors.

Lectin binding [concanavalin A, biotinylated ricinus communis agglutinin, and biotinylated succinylated wheat germ agglutinin (B-SWGA)] was used to detect the glycosylated proteins associated with a residual protein fraction [insoluble in 4% sodium dodecyl sulfate and termed the nuclear residual fraction (NRF)] or with nuclear matrix preparations from normal rat liver, azo dye (3'-MeDAB)-induced rat hepatoma, and Walker 256 transplantable carcinosarcoma. One- and two-dimensional gel electrophoresis were used with lectins, polyclonal antisera, and monoclonal antibody binding to characterize some of the glycoconjugates. Two polypeptide bands with approximate molecular weights of 95,000 and 55,000, shown previously to be present only in the induced tumor cells and the Walker 256 tumor, were reactive with lectins.