Full Answer
What is Tam and why is it important?
When investors or board members are evaluating a company or product’s prospects, TAM is inevitably one of the most important data points they will ask for as it provides a relative value for the opportunity size compared to other investment opportunities they may be considering.
What is TMS used to treat?
It’s a noninvasive treatment that uses electromagnetic pulses to stimulate nerve cells, which may improve symptoms of neurological or mental health disorders. TMS is mainly used to treat depression. It’s had success helping people who don’t respond to antidepressant medication and psychotherapy.
What is tamsulosin used to treat?
Last updated on Dec 28, 2020. What is tamsulosin? Tamsulosin (Flomax) is an alpha-blocker that relaxes the muscles in the prostate and bladder neck, making it easier to urinate. Tamsulosin is used to improve urination in men with benign prostatic hyperplasia (enlarged prostate). Tamsulosin is not FDA approved for use in women or children.
How should we design clinical trials for Tam kinase inhibitors?
Clinical trial designs should use high-resolution clinical endpoints and proper control arms to determine the synergistic effects of combining TAM inhibition with immune checkpoint blockade. Keywords: TAM kinase inhibitors; cabozantinib; combination therapy; immune checkpoint inhibitors; sitravatinib.
What does tamoxifen do to the body?
Tamoxifen is a type of hormonal therapy known as a selective estrogen receptor modulator (SERM). The drug attaches to hormone receptors (specific proteins) in breast cancer cells. Once the medication is inside the cells, it stops the cancer from accessing the hormones they need to multiply and grow.
What is a medicine that starts of Tam?
Tamoxifen (TAM) is commonly used as an adjuvant treatment for breast cancer. Although patients taking TAM are often taking medications for comorbidities, data regarding the interaction of TAM with other medications are limited.
Is tamoxifen chemo in pill form?
Tamoxifen is usually prescribed as a pill taken once a day by mouth. For breast cancer risk reduction, tamoxifen is typically taken for a total of five years. The risk reduction benefit continues for five additional years after you stop taking tamoxifen. In total, you could receive up to 10 years of benefit.
What type of breast cancer is tamoxifen used for?
Tamoxifen is used mainly to treat hormone receptor-positive breast cancer (breast cancer with cells that have estrogen and/or progesterone receptors on them). Raloxifene is used mostly to prevent and treat osteoporosis (very weak bones) in post-menopausal women.
What is the best medication for enlarged prostate?
Alpha-blockers, such as tamsulosin (Flomax) or terazosin (Hytrin), which relax muscle tissue. 5-alpha reductase inhibitors, such as dutasteride (Avodart) and finasteride (Proscar), which shrink the prostate. A combination of the two, which, when used long-term, may help your symptoms more than either medicine alone.
What are the long term effects of taking alfuzosin?
Alfuzosin 10 mg was well tolerated; the most common adverse event related to vasodilatation was dizziness/postural dizziness (3.1%). Ejaculatory disorders were uncommon (0.3%). Changes in blood pressure remained marginal, including in elderly men and those receiving antihypertensive agents.
Do you lose hair with tamoxifen?
No one goes bald from Tamoxifen, but some people do experience thinning hair. Like hair thinning, a lowered libido is common postmenopause and in the setting of reduce estrogen. Some women also attribute weight gain to Tamoxifen.
Does tamoxifen make you gain weight?
Some even call it the "backbone" of breast cancer treatment. Even with all that fanfare, tamoxifen has been loosely associated with weight gain. Studies have tracked weight gain and other side effects of the drug for years. Some resources even list weight gain as a possible side effect.
How much weight do you gain on tamoxifen?
Many women will gain weight after diagnosis. In fact, according to an article published in the World Journal of Clinical Oncology, you can expect to gain anywhere from 2 to 11 pounds.
Can breast cancer come back while on tamoxifen?
While tamoxifen can lower the chance of hormone receptor-positive breast cancer coming back (as well as the risk of getting a second breast cancer), it can increase the risk of uterine cancer (endometrial cancer and uterine sarcoma).
What is the success rate of tamoxifen?
The absolute increased risk of death from endometrial cancer in women who took tamoxifen for 10 years versus 5 years was 0.2 percent....Ten Years of Tamoxifen Reduces Breast Cancer Recurrences, Improves Survival.5 Years10 YearsRisk of Death from Breast Cancer15.0 percent12.2 percent1 more row•Mar 20, 2013
What type breast cancer has the highest recurrence rate?
Research suggests that estrogen receptor-positive breast cancer is more likely to come back more than five years after diagnosis. In this study, the researchers looked at the risk of late breast cancer recurrence, meaning the breast cancer came back 10 or more years after diagnosis.
Why is TAM important?
The Total Addressable Market is the first ingredient in almost every business case and the essential information to consider when pondering any business opportunity. Without a sense of how many people or companies could potentially purchase a product, it can be difficult to validate any subsequent assumptions about revenue, growth, or usage.
Why is it important to calculate TAM?
When an organization considers building a new product, entering a new vertical market, or even adding a new feature, it is critical to understand the revenue impact of that strategic move. Calculating TAM may reveal that an opportunity isn’t as attractive as initially thought, or it could show an even larger market than originally considered. With this information in hand, companies can make more informed decisions about where to invest their time and money for maximum ROI, even discarding their plans when the TAM is too small.
What is Total Addressable Market (TAM)?
Total Addressable Market (TAM) refers to the maximum size of the opportunity for a particular product or solution. In other words, if every single person who could potentially find value in a product or solution purchased/started using it (i.e. 100% market share), how big would that market be?
How to calculate TAM?
The fundamental math equation for calculating TAM is a very simple multiplication problem: Average revenue per user (ARPU) times the total number of potential customers in the target market. ARPU is pretty straightforward and can be adjusted as part of the business planning process, but the second part of the equation is trickier.
Is TAM a snapshot?
While TAM may be calculated for a snapshot in time, it will change. Markets shrink and grow all the time based on demographic changes, business cycles, and technology adoption, so when used as part of a forecast those macroeconomic elements should also be considered and calculations should be revisited regularly.
Is TAM a measure of revenue?
TAM is not a measure of actual future customers or revenue as competitors and alternative solutions can address the TAM as well—but it gives stakeholders a sense of how large the total pie is before it gets divvied up among the company, its various competitors, and those potential customers who choose to sit on the sidelines and not use or purchase anything at all.
What is a TAM?
TAM is characterised by increased circulating blast cells that harbour acquired N-terminal truncating mutations in the key haematopoietic transcription factor gene GATA1[5–10]. Around 10–15 % of neonates with Down syndrome have a diagnosis of TAM with blasts >10 % and typical clinical features that require close monitoring in the neonatal period since the mortality rate may be up to 20 %. A further 10–15 % of neonates with Down syndrome have one or more acquired GATA1mutations in association with a low number of circulating blast cells (<10 %) and have clinically and haematologically silent disease (silent TAM) [11••]. In the majority of cases of TAM and silent TAM, the GATA1mutant clone goes into complete and permanent remission without the need for chemotherapy. However, 10–20 % of neonates with TAM and silent TAM subsequently develop ML-DS in the first 5 years of life when persistent GATA1mutant cells acquire additional oncogenic mutations, most often in cohesin or epigenetic regulator genes [12••, 13]. This review article discusses the recent clinical and biological advances in TAM and ML-DS and how these may impact on clinical management.
What are the clinical features of tam?
blasts >10 %) will have one or more of the well recognised clinical features of TAM which are summarised in Table Table1.1. Amongst these features, hepatomegaly, splenomegaly, pericardial/pleural effusions and skin rash are seen more frequently in neonates with TAM compared with neonates without any GATA1mutations. Jaundice, on the other hand, is common in neonates with Down syndrome with or without TAM [11••, 30–32]. Importantly, however, as no single clinical feature is specific for TAM, it is essential to review the blood film of all neonates with Down syndrome to avoid missing cases of TAM and to assess the significance of the clinical features shown in Table Table11[11••]. This is also important in the setting of delayed onset or prolonged hyperbilirubinaemia in neonates with Down syndrome as this may be the presenting feature of progressive TAM-associated liver fibrosis that may be fatal. Although the majority of cases of TAM present within the first few days of life, TAM may also present in fetal life either with hydrops fetalis or with features similar to those presenting postnatally [34•].
What is the cellular and molecular events involved in initiation and evolution of TAM and ML-DS?
The cellular and molecular events involved in initiation and evolution of TAM and ML-DS can best be understood as a three-step model which requires the presence within a fetal liver-derived haematopoietic stem or progenitor cell of (i) trisomy 21, (ii) an acquired GATA1mutation, and (iii) at least one additional oncogenic mutation (Fig. 1).
What is TAM and ML-DS?
Schematic representation of molecular, biological and clinical data, indicating that transient abnormal myelopoiesis (TAM) and myeloid leukaemia of Down syndrome (ML-DS) are initiated before birth when fetal liver haematopoietic stem and progenitor cells (HSPC) trisomic for chromosome 21 demonstrate perturbed haematopoiesis with an expansion of megakaryocyte-erythroid progenitors (MEP) and megakaryocytes. These cells subsequently acquire N-terminal truncating GATA1mutations resulting in TAM in late fetal or early neonatal life. Although most cases of TAM spontaneously and permanently remit (∼90 %) by the age of 6 months, in ∼10 % of cases, additional genetic/epigenetic events lead to further clonal expansion resulting in ML-DS before the age of 5 years
What is bsilent tam?
bSilent TAM: Peripheral blood blasts ≤10 % and one or more acquired GATA1mutations
Is ML-DS a type of AML?
ML-DS is classified as a specific subtype of AML in the World Health Organisation (WHO) classification [42]. This leukaemia is unique to Down syndrome and has several distinct features. Firstly, ML-DS presents at a median age of 1–1.8 years and is rare after the age of 4 years [43, 44]. Secondly, most cases of ML-DS have a clinical history consistent with preceding TAM in the neonatal period, and for those that have no such history, the most likely reason is the absence of appropriate diagnostic tests at birth [11••]. Consistent with this, GATA1mutations are found on neonatal bloodspots from neonates with ML-DS even in the absence of an antecedent history of TAM [9]. ML-DS often shows an indolent presentation with myelodysplasia and progressive pancytopenia, in particular thrombocytopenia and leucopenia, with a low percentage of circulating blasts for many months before the development of ML-DS [43, 45, 46]. Since the circulating blast count is often low in ML-DS and the predominant haematological picture may be of slowly progressive pancytopenia, a bone marrow aspirate is usually essential for the diagnosis of ML-DS. However, this is often associated with a ‘dry tap’ secondary to marked bone marrow fibrosis and a bone marrow trephine may be necessary to confirm ML-DS—it is not clear that the conventional bone marrow blast threshold used in acute myeloid leukaemia is of value in ML-DS in view of the natural history of the condition and the difficulty in obtaining a representative sample.
