Derived from 2 yr of deliberations and community engagement, Medical Physics 3.0 (MP3.0) is an effort commissioned by the American Association of Physicists in Medicine (AAPM) to devise a framework of strategies by which medical physicists can maintain and improve their integral roles in, and contributions to, health care and its innovation under conditions of rapid change and uncertainty. Toward that goal, MP3.0 advocates a broadened and refreshed model of sustainable excellence by which medical physicists can and should contribute to health care. The overarching conviction of MP3.0 is that every healthcare facility can benefit from medical physics and every patient's care can be improved by a medical physicist. This large and expansive challenge necessitates a range of strategies specific to each area of medical physics: clinical practice, research, product development, and education. The present paper offers a summary of the Phase 1 deliberations of the MP3.0 initiative pertaining to strategic directions of the discipline primarily but not exclusively oriented toward the clinical practice of medical physics in the United States.
In our series, prior external beam radiotherapy, tumor volume, and tumor grade are risk factors for PRS, while pretreatment edema approached statistical significance. Peritumoral edema is the predominant mechanism of significant PRS, and skull base tumors have a lower risk of posttreatment edema.
C olorectal carcinoma (CRC) is rare in pediatrics, with an incidence of approximately 1 per million in children and adolescent patients (1). Risk factors include inherited diseases such as familial adenomatous polyposis (FAP), Lynch syndrome/hereditary nonpolyposis colon cancer, genetic microsatellite instability (1), and pediatric ulcerative colitis. Gastrointestinal (GI) cancer carries a dire prognosis in children, with high rates of mucinous pathology and metastatic spread at diagnosis. The 10-year cumulative local recurrence rate is 48.2% (2).
Introduction/RationaleFollowing exposure to thoracic radiation (RT), subjects exposed to thoracic radiation (RT) often develop acute inflammatory radiation pneumonitis (RTP) 4–5‐weeks (wks) post‐RT, followed months later by pulmonary fibrosis (RTPF).RT leads to RTP in ~20% of lung cancer patients, many of whom develop RTPF. Our laboratory is studying a novel early host response whereby oxidative stress triggers secretion of gastrin‐releasing peptide (GRP) by oxygen (O2)‐chemosensory pulmonary neuroendocrine cells (PNECs) within 24 hours after RT (post‐RT). In premature baboons exposed to hyperoxia, GRP‐blocking MoAb 2A11 treatment twice a week for 2 weeks abrogated chronic lung disease with fibrosis 10–14d later. In radiation‐sensitive C57L/J mice (L/J), we recently observed that a single dose of moAb 2A11 given IP 24h post‐RT (RT+2A11) abrogates development of RTPF 15 wks later.MethodsTo determine human relevance of GRP blockade to prevent RTPF, we collaborated with Dr. Mark Cline at Wake Forest University to test MoAb 2A11 in their established rhesus macaque (NHP) model of RTPF, giving a single dose of MoAb 2A11 (~5 mg/kg) IV 24h post‐RT.ResultsWe observed several effects of the single dose: First, there was earlier onset of RTP (3–5 wks post‐RT+2A11), compared to RT+PBS (5–8 wks post‐RT+PBS). Second, RT+2A11 NHP had prolonged survival (Fig. 1A): Of 9 RT+PBS animals, 4 died between 2–3 months post‐RT, for an overall survival of 56% to 9 months. Of 3 RT+2A11 NHP, all survived to 9 months. At necropsy, RT+2A11 animals had markedly reduced interstitial collagen deposition assessed by using blinded slides stained with Masson's trichrome (6–8 lung slides per animal, from all 5 lobes): All surviving RT+PBS NHP had advanced interstitial fibrosis (modified Ashcroft score ~7.8/8.0), whereas the 3 RT+2A11 survivors had mild to moderate fibrosis (modified Ashcroft score of 4/8.0) (Fig. 1B, P<0.01). There was no difference between the groups in lesions on CT scans, in total body weight, or in respiratory rate.ConclusionsOne dose of MoAb 2A11 given 24h post‐RT increases animal survival and abrogates interstitial pulmonary fibrosis, supporting potential human relevance of GRP blockade as a treatment to mitigate RTPF following RT exposure, either therapeutic or accidental.Support or Funding Information2016–2019 NIH Centers for Medical Countermeasures Against Radiation (CMCR, RadCCOR). Pilot Project: Sunday M (PI) “Oxygen, Gastrin‐Releasing Peptide, and Radiation‐Induced Pulmonary Fibrosis” to test anti‐GRP mAb 2A11 in a well‐characterized rhesus monkey model of radiation‐induced pulmonary fibrosis. (Duke Program Director: Dr. Nelson Chao)Fig. 1A and 1B as described in abstractThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Molecular Imaging in Oncology. Pomper Martin G. and Gelovani Juri G. Informa Healthcare USA, Inc., 2008. Hardcover 744 pp. Price: $399.95. ISBN 9780849374173.
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