Special Issue "Personalized Cancer Therapy"

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A special issue of Journal of Personalized Medicine (ISSN 2075-4426).

Deadline for manuscript submissions: closed (31 March 2014)

Special Issue Editor

Guest Editor
Dr. Roy S. Herbst (Website)

Yale Cancer Center, Section of Medical Oncology, 33 Cedar Street, PO Box 208028, New Haven, CT, USA
Interests: early phase clinical trials; biomarker studies; personalized medicine for cancer treatment

Special Issue Information

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Personalized Medicine is an international peer-reviewed Open Access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

Published Papers (4 papers)

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Research

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Open AccessArticle Surveillance Recommendations in Reducing Risk of and Optimally Managing Breast Cancer-Related Lymphedema
J. Pers. Med. 2014, 4(3), 424-447; doi:10.3390/jpm4030424
Received: 1 April 2014 / Revised: 1 July 2014 / Accepted: 6 August 2014 / Published: 18 August 2014
Cited by 8 | PDF Full-text (626 KB) | HTML Full-text | XML Full-text
Abstract
Breast cancer survivors are at increased risk for the development of breast cancer-related lymphedema (BCRL), a chronic, debilitating, and disfiguring condition that is progressive and requires lifelong self-management of symptoms. It has been reported that over 40% of the 2.5 million breast [...] Read more.
Breast cancer survivors are at increased risk for the development of breast cancer-related lymphedema (BCRL), a chronic, debilitating, and disfiguring condition that is progressive and requires lifelong self-management of symptoms. It has been reported that over 40% of the 2.5 million breast cancer survivors in the United States may meet the criteria for BCRL during their lifetimes. Ongoing surveillance, beginning with pre-operative assessment, has been effective in identifying subclinical lymphedema (LE). A prospective model for surveillance is necessary in order to detect BCRL at an early stage when there is the best chance to reduce risk or slow progression. Physical methods for monitoring and assessment, such as circumferential arm measures, perometry, bioimpedance; exercise programs; prophylactic and early-intervention compression garments; and referral for complete decongestive therapy are all interventions to consider in the development of a BCRL surveillance program. In addition, supportive-educative programs and interactive engagement for symptom self-management should also be implemented. The importance of interdisciplinary collaboration is integral to the success of an effective personalized medicine program in breast cancer-related lymphedema surveillance. Full article
(This article belongs to the Special Issue Personalized Cancer Therapy)
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Open AccessArticle Differential Transcriptome Profile of Peripheral White Cells to Identify Biomarkers Involved in Oxaliplatin Induced Neuropathy
J. Pers. Med. 2014, 4(2), 282-296; doi:10.3390/jpm4020282
Received: 25 March 2014 / Revised: 21 May 2014 / Accepted: 28 May 2014 / Published: 5 June 2014
Cited by 1 | PDF Full-text (693 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Anticancer chemotherapy (CT) produces non-desirable effects on normal healthy cells and tissues. Oxaliplatin is widely used in the treatment of colorectal cancer and responsible for the development of sensory neuropathy in varying degrees, from complete tolerance to chronic neuropathic symptoms. We studied [...] Read more.
Anticancer chemotherapy (CT) produces non-desirable effects on normal healthy cells and tissues. Oxaliplatin is widely used in the treatment of colorectal cancer and responsible for the development of sensory neuropathy in varying degrees, from complete tolerance to chronic neuropathic symptoms. We studied the differential gene expression of peripheral leukocytes in patients receiving oxaliplatin-based chemotherapy to find genes and pathways involved in oxaliplatin-induced peripheral neuropathy. Circulating white cells were obtained prior and after three cycles of FOLFOX or CAPOX chemotherapy from two groups of patients: with or without neuropathy. RNA was purified, and transcriptomes were analyzed. Differential transcriptomics revealed a total of 502 genes, which were significantly up- or down-regulated as a result of chemotherapy treatment. Nine of those genes were expressed in only one of two situations: CSHL1, GH1, KCMF1, IL36G and EFCAB8 turned off after CT, and CSRP2, IQGAP1, GNRH2, SMIM1 and C5orf17 turned on after CT. These genes are likely to be associated with the onset of oxaliplatin-induced peripheral neuropathy. The quantification of their expression in peripheral white cells may help to predict non-desirable side effects and, consequently, allow a better, more personalized chemotherapy. Full article
(This article belongs to the Special Issue Personalized Cancer Therapy)
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Review

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Open AccessReview Non-Small Cell Lung Cancer beyond Biomarkers: The Evolving Landscape of Clinical Trial Design
J. Pers. Med. 2014, 4(3), 386-401; doi:10.3390/jpm4030386
Received: 26 March 2014 / Revised: 10 June 2014 / Accepted: 13 June 2014 / Published: 30 June 2014
Cited by 5 | PDF Full-text (467 KB) | HTML Full-text | XML Full-text
Abstract
The approval of EGFR and ALK directed tyrosine kinase inhibitors materialized the concept of tailoring therapy on the basis of specific biomarkers for treating patients with NSCLC. Research for other biologics, although demonstrating clinical benefit, has been less successful so far for [...] Read more.
The approval of EGFR and ALK directed tyrosine kinase inhibitors materialized the concept of tailoring therapy on the basis of specific biomarkers for treating patients with NSCLC. Research for other biologics, although demonstrating clinical benefit, has been less successful so far for producing biomarkers that predict response. Blocking angiogenesis is the prototype for the agents that belong in the latter group that target specific molecules, yet they are currently approved for relatively unselected groups of patients. In order to meet the goal of personalizing care in the various settings of NSCLC, a wealth of biologics and compounds are currently being tested in clinical trials in different phases of clinical development. In a subset of the relevant studies, a biomarker perspective is appreciated. This review summarizes the clinical rationale of the major ongoing phase II and III NSCLC studies that employ targeting specific molecules with novel agents, as well as innovative strategies, and includes a comparative discussion of the different designs. Full article
(This article belongs to the Special Issue Personalized Cancer Therapy)
Open AccessReview Re-Treatment with EGFR-TKIs in NSCLC Patients Who Developed Acquired Resistance
J. Pers. Med. 2014, 4(3), 297-310; doi:10.3390/jpm4030297
Received: 27 March 2014 / Revised: 15 April 2014 / Accepted: 4 June 2014 / Published: 25 June 2014
Cited by 5 | PDF Full-text (464 KB) | HTML Full-text | XML Full-text
Abstract
In the era of personalized medicine, epidermal growth factor receptor (EGFR) inhibition with tyrosine kinase inhibitor (TKI) has been a mainstay of treatment for non-small cell lung cancer (NSCLC) patients with an EGFR mutation. Acquired resistance, especially substitution of methionine for threonine [...] Read more.
In the era of personalized medicine, epidermal growth factor receptor (EGFR) inhibition with tyrosine kinase inhibitor (TKI) has been a mainstay of treatment for non-small cell lung cancer (NSCLC) patients with an EGFR mutation. Acquired resistance, especially substitution of methionine for threonine at position 790 (T790M), which has accounted for more than half of the cases, developed inevitably in patients who were previously treated with EGFR-TKI. At present, there is no standard treatment for patients who have developed a resistance to EGFR-TKI. Several strategies have been developed or suggested to treat such patients. This article aimsto review the EGFR-TKI re-treatment strategy and the efficacy of different generations of EGFR-TKIs in patients with acquired resistance to prior EGFR-TKI. Full article
(This article belongs to the Special Issue Personalized Cancer Therapy)

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

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