pilldoc

I HATE the version of the All Star ice capades.... I despise and refuse to watch it. Bring back the version from 20+ years ago.... I do like the skills competition but trash every thing else...

LOL ... post of the day! OMG that is too funny BUT true! Well played my friend!

has there been a HJ sighting .....someone better check that he is ok...

Yeah, I thought I read that somewhere. It makes perfect sense. Based on how he has been playing in Hartford, it really is a no-brainer for the Rangers to give him a few games. The kid has talent and at this point really has nothing else to prove in the AHL. At this point in time, I absolutely agree shop Georgiev around and see what you can get. Hence the reason I plucked Shesterkin off the FA list as fast as I could in NAHANA. It would be foolish for me to think he will see a lot of playing time for the rest of the year, but there is absolutely no reason he couldn't get the start in 30-35 games next year as the Rangers back-up. For that reason alone he is a Keeper for me.

Grubauer has struggled of late. See game log of Dec/Jan listed below. So yeah ....goaltending has been a recent issue. You have to factor in that the Rangers defense wanted to give a little extra in from of Shesterkin's rookie debut. Shesterkin gave up 2 early goals which I would attribute to nerves, but then he settled down. This kid is the real deal ......

So what do the Rangers do now? With the call up of Shesterkin ( Shestyorkin) the Rangers now have 3 netminders on the the roster. Shesterkin is no slouch. He has been touted for the past 2 years now as a potential top 5 goalie when he hits the NHL. He has been nothing short of spectacular with the Rangers AHL team in Hartford. "The thing is, the timing of this maneuver is a bit curious. Henrik Lundqvist and Alexandar Georgiev remain on the roster and are in good health. Lundqvist isn’t going anywhere. Georgiev’s waivers-exempt status expired on Dec. 20, when he played the 60th game of his NHL career. And though Georgiev has been erratic over the last two weeks, while Lundqvist has hit some high notes but missed on others, the team’s goaltending is the least of its problems." [Hidden Content] I am under no pretense that Shesterkin is all of a sudden going to get the bulk of the starts in NY. I am sure that come next year there is a 0.000001% chance that Shesterkin remains in the AHL. I would expect about 30-35 starts for him next year and one Lundqvist moves on he will be the starter the year after that. So what do the Rangers do with Georgiev the rest of the year? Do they try to move him? There is a distinct and real possibility that Shesterkin goes back to the AHL after a few games. He certainly did not look out of place last night earning his first career NHL win. He certainly deserves a chance for a few games and then re-evaluate the situation. It kind of reminds a little bit of the Flyers situation last year when then brought up Hart. though at the time, the Flyers had multiple goalie injury issues too. This kid is the real deal. Drafted at #114 in the 4th round, the Rangers may have gotten the steal of the draft. Shestyorkin has been dynamite as an AHL rookie. The recently turned 24-year-old sits top-five in all the major metrics and is looks more than ready for an NHL shot. He’s been superb at every level and appears destined to grow around the exciting young core in New York ....

LOL.... that means Eichel plays for the Flyers..... HJ’s head would explode! (fixed it for ya!)

Thanks @hf101...Late to party.... totally agree here. To @Hockey-78The report button is your friend. If you ever have a concern please use this tool and one of us will address as soon as possible....

Late to the party here.... my simple answer..... In stereo

No .... I primarily work in the surgical unit in the OR. We have a separate oncology department with pharmacist's who do this all the time. So no ...I'm sorry I don't have much experience. I can read the journals and protocols and give an educated opinion, but I have zero interaction with these patients on a daily basis, unless they come to the OR for a mediport or power port placement for their chemo.

I just thought everyone should be as informed as possible ....... hope you don't mind. Full transparency ..... I am not as strong in updated cancer chemotherapy treatments... I just don't do enough of it on a daily basis.

TREATMENT FOR LOCALIZED DISEASE Chemotherapy — Most modern treatment plans utilize initial (induction or neoadjuvant) chemotherapy followed by local treatment and additional chemotherapy. Reduction of local tumor volume is accomplished in the majority of patients, and this can facilitate resection. This is particularly important with regard to limb-sparing procedures for extremity lesions, but it may also be important for rib, chest wall, and vertebral primaries [31-33]. Initially, chemotherapy was used in the adjuvant setting to control metastatic disease, but it is now administered prior to local therapy (neoadjuvant therapy) to improve local control as well [34]. Since most treatment failures are attributable to systemic metastatic disease, local therapy considerations should never compromise the administration of effective systemic therapy. (See "Bone sarcomas: Preoperative evaluation, histologic classification, and principles of surgical management".) Chemotherapy treatment has evolved, largely due to the efforts of several cooperative groups [34]: ●In the first Intergroup Ewing sarcoma study (IESS-I), the combination of vincristine, doxorubicin, cyclophosphamide, and dactinomycin (VDCA or VACA) was associated with a significantly better five-year relapse-free survival than vincristine, dactinomycin, and cyclophosphamide (VAC) alone or VAC plus adjuvant bilateral pulmonary irradiation (60 versus 24 versus 44 percent, respectively) [9]. ●Increasing the doxorubicin dose intensity during the early months of therapy further improved response, and in the second Intergroup study (IESS-II), the five-year relapse-free survival rates using intermittent high-dose four-drug therapy improved to 73 percent for non-pelvic lesions [40]. Because of concerns about limiting the dose intensity of doxorubicin in regimens containing dactinomycin [41], dactinomycin was omitted from most trials thereafter, with no adverse impact on long-term outcome. ●Adding alternating cycles of ifosfamide and etoposide (I/E) to a vincristine, doxorubicin, and cyclophosphamide(VDC) backbone (VDC/IE) provides further benefit [14,42-44]. In a randomized phase III clinical trial (the IESS-III study), the addition of I/E to VDCA was associated with significantly better five-year relapse-free survival compared with VDCA alone (69 versus 54 percent, respectively) in patients with localized (nonmetastatic) disease but not in those with metastatic EFT or PNET [42]. As a result of these data, current standard chemotherapy for EFT in the United States includes VDC/IE [42]. Typically, four to six cycles of chemotherapy are given before local therapy in the absence of disease progression followed by local treatment, and then additional cycles of the same treatments are given postoperatively for a total of 14 to 17 cycles. Relief of pain, decrease in tumor size, fall in lactate dehydrogenase (LDH) level, radiologic improvement, and evidence of necrosis in the resected specimen are all evidence of the antitumor effect of the prescribed regimen.

SUMMARYEwing sarcoma (ES) and peripheral primitive neuroectodermal tumors (PNETs) comprise the same spectrum of neoplastic diseases known as the Ewing sarcoma family of tumors (EFT), which also includes malignant small-cell tumors of the chest wall (Askin tumor). Because of their similar histologic and immunohistochemical characteristics and shared nonrandom chromosomal translocations, these tumors are considered to be derived from a common cell of origin, although their histogenetic origin is debated. (See 'Introduction' above.) EFT most often arises in the long bones of the extremities (predominantly the femur, but also the tibia, fibula, and humerus) and the bones of the pelvis. The spine, hands, and feet are affected considerably less often. (See 'Primary sites' above.) Patients with EFT typically present with localized pain or swelling of a few weeks' or months' duration. Trauma, often minor, may be the initiating event that calls attention to the lesion. Constitutional symptoms or signs, such as fever, fatigue, weight loss, or anemia, are present in approximately 10 to 20 percent of patients at presentation. (See 'Signs and symptoms' above.) The goals of the initial evaluation are to establish the diagnosis, evaluate local disease extent, and determine the presence and sites of metastatic spread. (See 'Staging evaluation' above.) The diagnostic work-up is usually initiated with a plain radiograph of the affected area. EFT involving bone typically presents as a poorly marginated destructive lesion with a permeative or "moth-eaten" appearance, most often associated with a soft tissue mass. While computed tomography (CT) scan better delineates the extent of cortical destruction and soft tissue disease, definition of tumor size, local intraosseous and extraosseous extent, and the relationship of the tumor to fascial planes, vessels, nerves, and organs is best achieved by magnetic resonance imaging (MRI). (See 'Radiographic studies' above.) The metastatic work-up includes a CT scan of the chest to evaluate the thorax for metastatic disease and a radionuclide bone scan to evaluate the entire skeleton for the presence of multiple lesions. Positron emission tomography (PET) or PET/CT is increasingly used for the initial staging and response assessment of EFT and may be able to replace radionuclide bone scan for detection of bone metastases in selected patients with lytic disease. Some clinicians advocate bone marrow biopsy (at least unilateral) in all patients to exclude widespread metastatic disease. (See 'Metastatic work-up' above and 'Bone marrow aspirate and biopsy' above.) A biopsy should be carefully planned to obtain adequate diagnostic tissue without compromising a later operation, particularly the opportunity for limb salvage. (See 'Tumor biopsy' above.) Several clinical and biologic characteristics can assist in defining prognosis and directing the intensity of therapy. These include the presence or absence of metastases, the primary tumor location and size, age, response to therapy, and the presence of certain chromosomal translocations. (See 'Prognostic factors' above.)

PROGNOSTIC FACTORSSeveral clinical and biologic characteristics can assist in defining prognosis and directing the intensity of therapy [49]. These include the presence or absence of metastases, the primary tumor location and size, age, response to therapy, and the presence of certain chromosomal translocations. Disease extent — The key prognostic factor in Ewing sarcoma is the presence or absence of metastases. Approximate five-year survival rates for patients with localized disease are 70 percent, while they average 33 percent for those who have overt metastases at diagnosis. (See "Treatment of the Ewing sarcoma family of tumors", section on 'Treatment for localized disease' and "Treatment of the Ewing sarcoma family of tumors", section on 'Treatment for metastatic disease'.) The location of distant disease also impacts outcomes. In the European Intergroup experience, the five-year relapse-free survival rates for patients with localized and metastatic disease at presentation were 55 and 21 percent, respectively [9]. Patients with bone and lung metastases fared significantly worse than those with bone metastases alone, who in turn, fared worse than those with isolated lung metastases. Approximately 30 percent of patients with metastases limited to the lungs will survive five years, as compared with only 10 percent of those with bone or bone marrow involvement. Patients with limited pulmonary metastases who are candidates for resection may have a reasonable opportunity for cure. (See "Treatment of the Ewing sarcoma family of tumors", section on 'Pulmonary metastases'.) Tumor site and size — For patients presenting with localized disease, those with axial primary tumors (ie, pelvis, rib, spine, scapula, skull, clavicle, sternum) have a worse treatment outcome than those with extremity lesions [9,50]. In one series, the five-year relapse-free survival rates were 40 versus 61 percent [9]. In addition, patients with small primary tumors (<100 mL) fare better than those with larger tumors [9,51]. Fever, anemia, and elevated serum lactate dehydrogenase (LDH) all correlate with a greater volume of disease and a poorer prognosis [9,20,46,47]. The poorer prognosis of large primary tumors, and those involving the pelvis and spine, is at least partly attributable to the difficulty in achieving wide negative resection margins and to higher rates of local failure after radiation therapy for large lesions. (See "Bone sarcomas: Preoperative evaluation, histologic classification, and principles of surgical management", section on 'Non-extremity lesions' and "Radiation therapy for Ewing sarcoma family of tumors".) Extraosseous, as compared with osseous, origin does not have an adverse influence on survival [11,52,53]. In fact, tumors that arise in skin or subcutaneous sites have a generally favorable prognosis [53-55]. Response to therapy — Patients with apparently localized disease have only a 10 to 20 percent likelihood of cure if treated with surgery or radiation therapy alone; this is improved dramatically when chemotherapy is added to treatment (see "Treatment of the Ewing sarcoma family of tumors"). Both the completeness of surgical resection and the response to induction therapy are important prognostic factors. Patients who are left with significant amounts of viable tumor in the resected specimen following neoadjuvant chemotherapy do worse than those with minimal or no residual tumor [9,56-60]. These topics are discussed in detail elsewhere. (See "Bone sarcomas: Preoperative evaluation, histologic classification, and principles of surgical management", section on 'Neoadjuvant chemotherapy'and "Radiation therapy for Ewing sarcoma family of tumors", section on 'Adjuvant radiation therapy'.)