Skip to main content

Concise Reviews from the Literature Relevant to Hematology Oncology Pharmacy

JHOP - September 2011, Vol 1, No 3 - From the Literature
Robert J. Ignoffo, PharmD, FASHP, FCSHP, FHOPA
Clinical Professor Emeritus
University of California, San Francisco
Professor of Pharmacy
College of Pharmacy, Touro University–California
Mare Island, Vallejo, CA
Download PDF

Exemestane Effective for the Prevention of Invasive Breast Cancer in Postmenopausal Women

Background: Estrogen is a known risk factor for breast cancer in women with a high level of circulating plasma estrogen. Therefore, chemoprevention of breast cancer has centered on the selective estrogen-receptor modulators (SERMs) tamoxifen and raloxifene. However, the majority of postmenopausal women who are at increased risk for breast cancer have not accepted the 2 SERMs for chemoprevention, primarily because of their toxic effects. In patients with early-stage breast cancer, aromatase inhibitors have been shown more effective than tamoxifen in preventing contralateral breast cancer and with fewer side effects. A recent international clinical trial was designed to investigate the benefit of the aromatase inhibitor exemestane for the prevention of invasive breast cancer in postmenopausal women.

Design: This international, randomized, placebo-controlled, double-blind clinical trial enrolled 4560 postmenopausal (ie, no menses for 12 months) women (aged ≥35 years; median age, 62.5 years) from Canada, the United States, Spain, and France between February 2004 and March 2010. Postmenopausal women had to have 1 of these eligibility criteria—a 5-year risk for breast cancer (Gail risk score >1.66%); age ≥60 years; or previous atypical ductal or lobular hyperplasia or lobular carcinoma in situ, or ductal carcinoma in situ (DCIS) with mastectomy. The women were randomized to receive exemestane (N = 2285) or placebo (N = 2275) in 1 of 3 groups—exemestane 25 mg plus placebo, exemestane 25 mg plus celecoxib, or placebo—for 5 years or until an unacceptable adverse event occurred, including breast cancer, neoplastic disease, or a serious cardiovascular event. The primary end point was the incidence of invasive breast cancer. The secondary end points included the incidence of DCIS breast cancer; combined incidence of invasive breast cancer and DCIS; and the combined incidence of atypical ductal hyperplasia, atypical lobular hyperplasia, and lobular carcinoma in situ.

Summary: At a median 35 months of follow-up, a total of 43 women were diagnosed with invasive breast cancer—11 women in the exemestane groups and 32 women in the placebo group. This translates to an annual breast cancer incidence of 0.19% with exemestane compared with a 0.55% incidence rate with placebo, for a 65% relative risk reduction with exemestane (hazard ratio [HR], 0.35; 95% confidence interval [CI], 0.18- 0.70; P <.002). Exemestane was also associated with a lower incidence of invasive breast cancer plus DCIS (0.35%) compared with a 0.77% incidence rate with placebo (HR, 0.47; 95% CI, 0.27-0.79; P = .004). The majority of the tumors were estrogen receptor (ER)-positive, HER2/neu-negative, and node-negative. Adverse event rates were 88% with exemestane and 85% with placebo (P = .003). There were no significant differences in the rates of skeletal fractures, cardiovascular events, other cancers, and treatment-related deaths between the placebo and the active drug groups, and the differences in quality of life were minimal.

Takeaway: For postmenopausal women with ER-positive, HER2/neu-negative, node-negative breast cancer who are at moderate risk for future invasive breast cancer, the use of exemestane prophylaxis reduces the annual risk of recurrent invasive breast cancer by 65%, as well as invasive DCIS by 35%. The antiestrogens tamoxifen and raloxifene have been used to also decrease invasive breast cancer, but their acceptance is poor (only 0.08% of women aged 40-79 years currently use these agents), probably because both are associated with rare endometrial cancers and thromboemboli (Ropka ME, et al. J Clin Oncol. 2010;28:3090-3095). With 3 years of follow-up, the absence of serious adverse effects, including bone fractures, is reassuring and may improve the acceptance of this agent for breast cancer chemoprevention. Bone mineral loss was prevented with oral bisphosphonate therapy.

Goss PE, Ingle JN, Alés-Martínez JE, et al. Exemestane for breastcancer prevention in postmenopausal women. N Engl J Med. 2011;364:2381-2390.

Genotype-Based Dosing of Tamoxifen Improves Therapeutic Response in Invasive Breast Cancer

Background: A majority of women diagnosed with invasive breast cancer are estrogen receptor (ER)-positive and therefore are candidates for tamoxifen treatment. However, approximately 50% of them do not derive full benefit from the drug, because genetic variations in the cytochrome P450 2D6 (CYP2D6) limit the ability of the enzyme to convert tamoxifen into its primary active metabolite, endoxifen. In a new study, researchers have investigated whether CYP2D6 genotyping could help guide the dosing of tamoxifen to increase the concentration of endoxifen in women who are intermediate or poor metabolizers of the CYP2D6 allele.

Design: A total of 119 women (25 black women) aged ≥18 years were enrolled in the study, but only 89 were included in the final analysis of tamoxifen dose intervention. The women had been taking tamoxifen 20 mg daily ≥4 months and no strong CYP2D6- inhibiting medications, and were evaluated for the CYP2D6 genotype and for plasma concentration of tamoxifen metabolites. Patients were divided into 3 genotype groups based on their endoxifen concentration— extensive metabolizers, intermediate metabolizers, and poor metabolizers. Patients who were extensive metabolizers of endoxifen continued to take the 20-mg dose of tamoxifen, and those who were intermediate or poor metabolizers had the tamoxifen dose increased to 40 mg daily. After 4 months, patients were measured again for their tamoxifen metabolites. The study primary end point was a change in plasma endoxifen concentration after 4 months of increased tamoxifen dosing for patients who were intermediate metabolizers of the drug.

Summary: Among the study population, an unexpectedly high percentage of patients (72%) had one of the CYP450 alleles indicative of intermediate or poor metabolism of tamoxifen. African American women were approximately twice as likely as other women to have the CYP2D6 allele, which has been found to be associated with reduced tamoxifen metabolism (odds ratio, 2.26; 95% confidence interval, 1.17-4.37). Among the 89 patients who completed the study, the median baseline endoxifen concentration was higher in the 32 extensive metabolizers than in the 74 intermediate metabolizers (34.3 ng/mL vs 18.5 ng/mL;P = .004) or in the 11 poor metabolizers (4.2 ng/mL; P <.001). After 4 months of therapy with an increased tamoxifen dose from 20 mg to 40 mg, the median endoxifen concentration increased significantly in the intermediate metabolizers to 21.8 ng/mL (P <.001) and among poor metabolizers to 12.9 ng/mL (P = .020). Of note, after the 4 months, no significant difference was seen between the intermediate and extensive metabolizers in endoxifen concentrations, despite the almost twice as high concentration levels at baseline; in the poor metabolizers, the endoxifen concentration level remained significantly lower than both groups.

Takeaway: This study demonstrates that adjusting tamoxifen dosing based on genotyping of CYP2D6 in women with ER-positive breast cancer may lead to endoxifen concentrations similar to those in extensive metabolizers. Increasing the dose from 20 to 40 mg in both poor and intermediate metabolizers of tamoxifen was effective and safe in raising endoxifen levels. However, this study was not designed to show whether clinical outcomes were improved with higher endoxifen levels. It may be that the efficacy of tamoxifen is not mediated solely through endoxifen. Until endoxifen concentrations are shown to be strongly associated with improved clinical outcomes in response and survival, the use of CYP2D6 genotyping will remain investigational. Of note is a recent study by Goetz and colleagues from the National Surgical Adjuvant Breast and Bowel Project’s Breast Cancer Prevention Trial (BCPT)-P1 and BCPT-P2 that showed alterations in CYP2D6 metabolism were not associated with either tamoxifen or raloxifene efficacy (Goetz MP, et al. Clin Cancer Res. 2011 Aug 31. Epub ahead of print). As suggested above, there may be other cytochrome alterations that may impact the use of genotyping. A recent study by van Schaik and colleagues from the Netherlands has shown that CYP2C19*2 genotype predicts tamoxifen treatment outcomes in patients with advanced breast cancer (van Schaik RH, et al. Pharmacogenomics. 2011;12:1137-1146). The time to treatment failure was improved by 28% in those who were heterozygous or homozygous for the CYP2C19*2 enzyme.

Irvin WJ Jr, Walko CM, Weck KE, et al. Genotype-guided tamoxifen dosing increases active metabolite exposure in women with reduced CYP2D6 metabolism. J Clin Oncol. 2011;29:3232-3239.

Vemurafenib Improves Survival in Metastatic Melanoma with BRAF V600E Mutation

Background: The prognosis for patients with metastatic melanoma is poor, ranging from 8 to 18 months, and the only chemotherapeutic agent currently approved by the US Food and Drug Administration (FDA) for the treatment of this disease is dacarbazine. A large percentage of cutaneous melanomas involve mutations in the BRAF gene that can activate tumor growth through the mitogen-activated protein kinase pathway. Previous studies have suggested that mela - nomas with the BRAF V600E mutation are more aggressive and less sensitive to chemotherapy than those with the BRAF wild-type mutation. In earlyphase clinical trials, the investigational agent vemurafenib, a BRAF kinase inhibitor that targets the BRAF V600E mutation, was associated with response rates of >50% in patients with BRAF V600E mutation melanoma. In a recent study, researchers compared the efficacy of dacarbazine and vemurafenib in this patient population.

Design: In this phase 3 clinical trial, a total of 675 patients with previously untreated, unresectable stage IIIC or stage IV melanoma with the BRAF V600E mutation were randomly assigned to oral vemurafenib (N = 337) 960 mg twice daily or to dacarbazine (N = 338) 1000 mg/m2 infused every 3 weeks. With each drug, intolerable grade 2 toxic effects required dose reduction. Vemurafenib administration was halted until the toxic effect was reduced to grade 1 at least and was resumed at a dosing of 720 mg twice daily; the dose was reduced to 480 mg twice daily if the toxic effect recurred. If the 480-mg dose did not reduce the toxic effect to grade 1 or if the effect recurred, the treatment was stopped permanently. Dacarbazine administration was interrupted if grade 3 or 4 events occurred and was resumed within 1 week of grade 1 or 2, or resumed at a dosing of 75% for grade 4 neutropenia or febrile neutropenia. The primary end points were the rates of overall survival (OS) and progression-free survival (PFS). Secondary end points included the response rate, response duration, and safety.

Summary: Patients were examined every 3 weeks and tumors assessed at baseline and at weeks 6, 12, and then every 9 weeks. Response to treatment was assessed with the Response Evaluation Criteria in Solid Tumors, version 1.1. The response rate with vemurafenib was 48% versus 5% with dacarbazine. The hazard ratio for death was 0.37 (95% confidence interval [CI], 0.26- 0.55) with vemurafenib versus dacarbazine (P <.001). At 6 months, the OS was 84% (95% CI, 78-89) among patients receiving vemurafenib compared with 64% (95% CI, 56-73) among those receiving dacarbazine. The estimated median PFS was 5.3 months with vemurafenib and 1.6 months with dacarbazine. Compared with dacarbazine, vemurafenib was associated with a 63% relative risk reduction for death and a 74% risk reduction for either death or disease progression. The data and safety monitoring board recommended that patients in the dacarbazine group be allowed to cross over to receive vemurafenib based on the significant survival benefit with the latter. The most common adverse events associated with vemurafenib were arthralgia, rash, fatigue, alopecia, secondary neoplasia (keratoacanthoma or squamous-cell carcinoma), photosensitivity, nausea, and diarrhea. In all cases of secondary neoplasia (18%) associated with vemurafenib, the lesions were removed by simple excision, and no modifications in drug dose were necessary.

Takeaway: The approval of vemurafenib marks the second new drug for metastatic cancer approved by the FDA in the past 13 years. This study showed a significant improvement over dacarbazine in OS. It also provides a strong case for the use of pharmacogenomic testing using the cobas 4800 BRAF V600 Mutation Test. Approximately 40% to 60% of cutaneous melanomas carry mutations in BRAF that lead to constitutive activation of downstream signaling through the MAPK pathway. Vemurafenib is an oral agent that is a moderate CYP1A2 inhibitor, a weak CYP2D6 inhibitor, and a CYP3A4 inducer and substrate. Increased monitoring is therefore advised for patients receiving warfarin therapy. Furthermore, strong CYP3A4 inhibitors and inducers may increase or decrease vemurafenib’s effects. The role of vemurafenib is still being investigated. Further studies are needed to determine if combinations with chemotherapy or other new agents (eg, ipilimumab) will improve on these results.

Chapman PB, Hauschild A, Robert C, et al. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med. 2011;364:2507-2516.

PARP Inhibitor Olaparib a Promising Treatment for Ovarian Cancer

Background: In phase 1 and 2 clinical trials, olaparib, a small-molecule poly(ADP-ribose) polymerase (PARP) inhibitor, has demonstrated objective responses in the treatment of tumors with BRCA1 and BRCA2 mutations in women with breast or ovarian cancer. Researchers have set out to assess the impact of BRCA mutations on the benefit of oral olaparib in patients with advanced triple-negative breast cancer or in those with high-grade ovarian cancer.

Design: This open-label, nonrandomized phase 2 clinical study was conducted in 6 centers in Canada. A total of 91 women (aged ≥18 years) with advanced high-grade serous and/or undifferentiated ovarian carcinoma (N = 65) or triple-negative breast cancer (N = 26) were stratified according to BRCA mutation or lack of mutation; all the patients received oral olaparib 400 mg twice daily. The primary end point was the objective complete or partial response rate, based on the Response Evaluation Criteria in Solid Tumors. Secondary end points were the rate of disease control, percent change from baseline in tumor size, progression- free survival, and for those with ovarian cancer, evaluation of CA-125.

Summary: All patients with measurable lesions were included in the objective response analysis, and all patients who received at least 1 dose of olaparib were included in the safety analysis. Of the 91 patients enrolled, 90 were treated between July 8, 2008, and September 24, 2009. Objective responses were not reported in patients with breast cancer. Among the 64 patients with ovarian cancer who received treatment, 63 were evaluable, and objective responses were confirmed in 7 (41%; 95% confidence interval [CI], 22-64) of the 17 women with BRCA1 or BRCA2 mutations and in 11 (24%; 95% CI, 14-38) of the 46 patients without BRCA mutations. A total of 13 of the 65 (20%) patients with ovarian cancer discontinued the study early because of worsening disease (N = 3), adverse event (N = 3), voluntary discontinuation (N = 2), and other reasons (N = 5). In addition, 1 of the patients with breast cancer discontinued early because of an adverse event. At study end, 13 of the 65 patients with ovarian cancer and 26 of those with breast cancer were still receiving olaparib. Drug-related adverse events occurred in 56 of 64 (88%) patients with ovarian cancer. The most common adverse events reported were fatigue (70% of patients with ovarian cancer and 50% of patients with breast cancer); nausea (66% and 62%, respectively); vomiting (39% and 35%, respectively); and decreased appetite (36% and 27%, respectively).

Takeaway: This is the first study to show that the PARP inhibitor olaparib has activity in a heavily pretreated cohort of patients with high-grade serous ovarian cancer. It was active in patients whether they had germline BRCA mutations or not; it produced responses in 24% to 41% of the patients, which is similar to outcomes observed with the cytotoxic drugs pegylated doxorubicin and topotecan. This study was limited by the small number of patients (ie, 63), but it suggests that additional clinical trials with olaparib in patients with serous ovarian cancer are warranted. Olaparib was very well tolerated in this heavily pretreated group and may be an appropriate option for this aggressive form of ovarian cancer, in which treatment is usually limited to toxic chemotherapies. At the 2009 ASCO annual meeting, Tutt and colleagues reported that single-agent olaparib was active in BRCA-deficient triple-negative breast cancer (Tutt A. J Clin Oncol. 2009;27[suppl]). In that study, however, olaparib had no activity in triplenegative breast cancer, regardless of BRCA status. This may have been because of the small number of patients (ie, 23) in this cohort.

Gelmon KA, Tischkowitz M, Mackay H, et al. Olaparib in patients with recurrent high-graded serous or poorly differentiated ovarian carcinoma or triple-negative breast cancer. Lancet Oncol. 2011;12:852-861.

Nilotinib Sustains Efficacy Superior to Imatinib for 24 Months in Chronic Myeloid Leukemia

Background: Nilotinib is a BCR-ABL inhibitor that was developed as a potent and selective treatment for patients with chronic myeloid leukemia (CML) in whom imatinib therapy has not shown appropriate efficacy. The US Food and Drug Administration approved the use of nilotinib 300 mg twice daily for the treatment of patients with newly diagnosed Philadelphia chromosome (Ph)-positive CML in the chronic phase based on results from the Evaluating Nilotinib Efficacy and Safety in Clinical Trials–Newly Diagnosed Patients (ENESTnd) study, which showed superior efficacy for nilotinib over imatinib for up to 12 months. Now researchers from the ENESTnd study published the results of a new 12-month follow-up to the ENESTnd study.

Methods: In this phase 3, multicenter, open-label, randomized study, 847 adult patients with chronic phase, Ph-positive CML were randomized (1:1:1) to receive oral therapy with nilotinib 300 mg twice daily (N = 282), nilotinib 400 mg twice daily (N = 281), or imatinib 400 mg once daily (N = 283). The efficacy results are based on the intention-to-treat population of patients. The primary end point was the major molecular response at 12 months, defined as BCR-ABL transcript levels on the International Scale of ≤0.1% by real-time quantitative polymerase chain reaction in peripheral blood.

Summary: At 24 months, a major molecular response was seen in 201 (71%) patients receiving nilotinib 300 mg twice daily, in 187 (67%) patients receiving nilotinib 400 mg twice daily, and in only 124 (44%) patients receiving imatinib 400 mg once daily—a significant difference for both comparisons (P <.001). In addition, a complete molecular response was observed significantly more often in both nilotinib groups than in the imatinib group—74 (26%) patients receiving 300 mg nilotinib and 59 (21%) patients receiving 400 mg nilotinib compared with 29 (10%) of patients receiving 300 mg once P <.001 for nilotinib 300 mg twice daily vs imatinib; P = .004 for nilotinib 400 mg twice daily vs imatinib). Progression to accelerated or blast phase CML during treatment, including clonal evolution, occurred in 7 patients in the nilotinib groups and in 17 patients in the imatinib group. At 24 months, survival was comparable in all treatment groups, but there were fewer CMLrelated deaths with nilotinib (N = 8) than with imatinib (N = 10). In addition, the only grade 3 or 4 nonhematologic adverse effects occurring more frequently with nilotinib were headache and rash. However, in the second 12-month follow-up study, 8 additional serious adverse events were reported—7 in the nilotinib group and 1 in the imatinib group.

Takeaway: This is an updated report of the ENESTnd trial, the international phase 3 clinical trial of nilotinib versus imatinib in CML with a minimum follow-up of 2 years. More than 90% of patients treated with nilotinib who had achieved major molecular response at 12 months were maintained at 24 months. Furthermore, BCR-ABL transcript levels were decreased below the threshold of <0.1% about 1 year earlier with nilotinib than with imatinib. This study demonstrated nilotinib’s superiority over imatinib, with faster, deeper, and more durable molecular responses and a significantly decreased risk of disease progression. In addition, emerging mutations of BCR-ABL in the nilotinib group were half that reported in those treated with imatinib. Nilotinib should be considered a first-line therapy for CML in chronic phase. Kantarijian HM, Hochhaus A, Saglio G, et al. Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome–positive, chronic myeloid leukemia. Lancet Oncol. 2011;12:841-851.

Radiotherapy plus Short-Term Androgen Deprivation Extend Survival in Men with Intermediate-Risk, Early-Stage Prostate Cancer

Background: In patients with locally advanced pros - tate cancer, radiotherapy added to long-term hormone therapy, or androgen-deprivation therapy (ADT), improves survival but also increases adverse events. Whether short-term ADT used before and during radiotherapy could improve survival in patients with early-stage, localized prostate cancer has not been known. Previous studies have shown that short-term ADT improves survival among patients with later-stage prostate cancer. In a new large clinical trial funded by the National Cancer Institute, researchers investigated the best approach to therapy for men with intermediate- risk, early-stage prostate cancer.

Method: This 212-center study included 1979 men with early-stage prostate cancer. All patients had localized prostate cancer and prostate-specific antigen (PSA) levels ≤20 ng/mL. Among the patients, 395 were black men, who are known to have greater rates of prostate cancer than other men. Patients were randomly assigned to treatment with radiotherapy alone (N = 992; 197 black men) or to radiotherapy plus 4 months of ADT that consisted of drugs that block the natural production of testosterone (N = 987; 198 black men).

Summary: The median follow-up in this study was 9.1 years. Results showed that short-term ADT plus radiotherapy significantly improved the 10-year overall survival (OS) compared with radiation therapy alone (62% vs 57%, respectively). The addition of short-term ADT to radiation therapy led to significantly fewer prostate cancer–related deaths (4% vs 8%, respectively; P = .001). The benefits of short-term ADT seen true for white and for black men. In a later analysis looking at the patients by disease risk, participants were divided into 3 groups— high, intermediate, and low risk, using various variables, including PSA levels, tumor grade, and disease stage. The patients with intermediate risk benefited from the combination therapy, unlike those with low or high risk. In those with intermediate risk, the 10-year OS rate significantly increased from 54% with radiotherapy alone to 61% with the combination of short-term ADT plus radiotherapy, and disease-specific death rate was reduced from 10% to 3%. The researchers noted that for now, because of potential side effects with ADT (eg, erectile dysfunction, hot flashes), the evidence does not support longer follow-up therapy for men with low-risk disease.

Takeaway: This study of almost 2000 patients shows that men with intermediate-risk prostate cancer (Gleason score of 7 or a Gleason score of ≤6 with a PSA level of >10 and ≤20 ng/mL or clinical stage T2b) benefit from combination ADT and radiotherapy. With 12 years of follow-up, there were more than 60% fewer deaths with combination ADT and radiotherapy. However, in their discussion, the authors noted that this study was performed with a traditional method of radiation therapy. New radiation techniques such as intensity-modulated radiation therapy, intensity-guided radiation therapy, and low-dose-rate and high-dose-rate brachytherapy have resulted in safe delivery of higher doses of radiation than was possible when this study was conducted. Furthermore, they warned that it is uncertain if the addition of ADT to these newer techniques would significantly add benefit to the new radiation methods. The Radiation Therapy Oncology Group has initiated a randomized study to answer this question, but it may be several years before we have the answer to whether combination ADT and radiotherapy is better than current radiation strategies.

Jones CU, Hunt D, McGowan DG, et al. Radiotherapy and short-term androgen deprivation for localized prostate cancer. N Engl J Med. 2011;365:107-118.

By Robert J. Ignoffo, PharmD, FASHP, FCSHP, Section Editor
Clinical Professor Emeritus, University of California, San Francisco Professor of Pharmacy,
College of Pharmacy, Touro University—California, Mare Island Vallejo, CA

Related Items
First-Line Nivolumab Combination Therapy Improves Survival in Patients with Advanced Esophageal Squamous-Cell Carcinoma: CheckMate-648
Robert J. Ignoffo, PharmD, FASHP, FCSHP, FHOPA
JHOP - April 2022 Vol 12, No 2 published on May 3, 2022 in From the Literature, Gastrointestinal Cancers, Checkpoint Inhibitors
Second-Line Axicabtagene Ciloleucel Therapy Improves Outcomes in Patients with Large B-Cell Lymphoma: ZUMA-7
Robert J. Ignoffo, PharmD, FASHP, FCSHP, FHOPA
JHOP - April 2022 Vol 12, No 2 published on May 3, 2022 in From the Literature, Lymphoma, CAR T-Cell Therapy
Pembrolizumab plus Chemotherapy for Neoadjuvant and Adjuvant Therapy in Early Triple-Negative Breast Cancer: KEYNOTE-522
Robert J. Ignoffo, PharmD, FASHP, FCSHP, FHOPA
JHOP - April 2022 Vol 12, No 2 published on May 3, 2022 in From the Literature, Breast Cancer, Checkpoint Inhibitors
Daily Aspirin Does Not Lower Colorectal Cancer Risk When Started After Age 70
JHOP - June 2021 Vol 11, No 3 published on June 16, 2021 in From the Literature
Adjuvant Nivolumab Therapy Prolongs Disease-Free Survival in Patients with Esophageal Cancer
JHOP - June 2021 Vol 11, No 3 published on June 16, 2021 in From the Literature
New Data Reveal Mismatched Need and Supply of Oncology Physicians and Pharmacists in America
JHOP - June 2021 Vol 11, No 3 published on June 16, 2021 in From the Literature
Low-Dose Capecitabine Maintenance Therapy Improves Survival in Patients with Triple-Negative Breast Cancer
Robert J. Ignoffo, PharmD, FASHP, FCSHP, FHOPA
JHOP - April 2021 Vol 11, No 2 published on April 27, 2021 in From the Literature, Breast Cancer, Dose Escalation/Reduction
Enfortumab Vedotin Superior to Chemotherapy in Urothelial Cancer
Robert J. Ignoffo, PharmD, FASHP, FCSHP, FHOPA
JHOP - April 2021 Vol 11, No 2 published on April 27, 2021 in From the Literature, Bladder Cancer
Oral Azacitidine Prolongs Survival in Patients with Acute Myeloid Leukemia
Robert J. Ignoffo, PharmD, FASHP, FCSHP, FHOPA
JHOP - April 2021 Vol 11, No 2 published on April 27, 2021 in From the Literature, Leukemia
Pembrolizumab Shows Long-Term Benefits in Patients with Metastatic Colorectal Cancer and MSI-H or dMMR
JHOP - February 2021 Vol 11, No 1 published on February 22, 2021 in From the Literature, Colorectal Cancer, Biomarkers