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  1. Molecular Genetics of Metastatic Breast Cancer
  2. Molecular subtypes and clinical complete response (CR)
  3. Transplant Drug May Improve Immunotherapy for Breast Cancer - National Cancer Institute
  4. Introduction

Thus, similarities between the microenvironment of primary tumors and that of the distant sites make the preselected metastatic seeds compatible with the target tissue and prime the development of organ-specific metastatic traits in primary tumors. In addition to this example, it has been widely shown that different stromal components in primary tumors play critical roles in promoting tumor growth, increasing their invasiveness, and inducing the EMT phenotype.

In summary, metastatic traits may arise from a combination of oncogenic forces, repurposing of intrinsic cellular properties, and stromal influences. An important lesson learned from the above findings is the relation of microenvironment similarity to the metastatic organ tropism. The distinction of distant sites from the primary sites has been long recognized and advocated.

Thus, what becomes critical is their chance to find a similar feature like their home from the vast sea of differences in the foreign tissue. The identification of metastasis gene mediators provides new potential targets for treating metastatic breast cancer. The promise of these discoveries for translational medicine will be clinically evaluated in the future. Here, we discuss some of the foreseeable conceptual challenges of pushing these therapies into the clinic. Often times, when a patient is diagnosed with breast cancer, the primary tumor will be surgically removed and the residual disease will be eradicated by hormone, chemo, or radiation therapies.

For patients who are at risk for developing metastasis, dissemination from primary tumors occurred prior to diagnosis and will cease with the radical surgery. Thus, it is futile to target the metastasis steps that already happened, including intravasation, circulation, and extravasation. These processes will be more meaningful targets for therapy within the context of multiple established metastases.

Molecular Genetics of Metastatic Breast Cancer

Via preventing metastatic lesions from cross-seeding, self-seeding, or re-seeding to a tertiary site, , these lesions can be locally confined and cytotoxic therapies can be more effectively applied one at a time. Owing to the transient nature of these processes, it may also be challenging to predict their occurrence and to develop corresponding therapeutic strategies.

Thus, the clinical value of identifying these targets remains to be demonstrated. The current systemic therapy and its extension to the adjuvant setting are designed exactly for this purpose. Despite recognition of the distinctions between metastases and their primary tumors, metastases are treated mainly based on their tumors of origin. This is based on the idea that metastases overall behave like their tissue of origin and many of the primary tumor characteristics, such as growth dependency and drug sensitivity, are maintained in metastases.

Indeed, any type of cancer treatment essentially aims to target a sensitivity window, within which cancer cells are selectively killed but normal tissues are spared. Based on such reasoning, targeting the oncogenic signaling in the case of anti-HER2 or the lineage peculiarity of growth demand in the case of anti-ER is an optimal treatment strategy. In line with this idea, many emerging targeted agents against other oncogenic signaling or pathways that were underappreciated in breast tumorigenesis are now being tested in multiple clinical trials.

Not all these inhibitors are necessarily based on rationales and insights from metastasis biology, but in one setting or another, they are proven to have the ability to inhibit breast tumor growth. However, it is also foreseeable that without considering the contextual specificity of distant organ environments for therapy, relapse and resistance may occur in many cases.

As cancer cells adapt to the distant environment and metastases form, their growth dependence may shift away from stringent addiction to the oncogenic drivers of primary tumor growth.

Molecular subtypes and clinical complete response (CR)

In the established bone metastases from breast cancer, a repertoire of various growth factors released from the dissolved bone matrix may compensate significantly for the growth stimulus and liberate cancer cells from reliance on the ER. The multilevels of interplay between cancer cells and stromal cells may render cancer cells such flexibility that when one proliferation signal is inhibited, another pathway can act on the cells and compensate.

This highlights the complexity of established metastases. The metastasis cascade is depicted as a delicate process that requires an intricate, coordinated action of multiple gene programs. If this is true, one may expect that it should be easy to disrupt the cascade and inhibit metastasis by abolishing any gene mediator of the process.

This view is largely true on a single-cell level. However, metastasis occurs at the level of cell populations. Intratumor heterogeneity that is intrinsic to most of the metastases renders the metastatic traits versatile, redundant and complicated for targeting. Analysis of single clones from the metastatic subpopulations toward a certain organ suggests that different clones within the aggressive subpopulation do not necessarily upregulate every metastatic gene, but rather harbor different subsets.

In analogy to the intertumor heterogeneity seen in breast tumorigenesis, there exist multiple evolutionary routes for the breast tumor to reach the metastatic phenotype. As a result, inhibiting one mediator may eliminate part of metastasis but cannot eradicate it entirely. Denosumab, an RANKL antibody, is in clinical trials to revert the osteolytic cycle of breast cancer bone metastasis and to inhibit bone resorption. Moreover, the same genes and pathways may be repeatedly utilized for different purposes, functioning in a pleiotropic, context-dependent manner.

The PI3K—Akt pathway is critical for cell survival in breast cancer metastasis to both bone and lung. Collectively, abolishing the metastatic traits requires concurrent targeting of multiple gene mediators that may play redundant roles and compensate each other at the population level. Because of the intratumor complexity and the plasticity of metastases, it is expected that many of the targeted agents Fig. TN cancer, in contrast, presents a more substantial challenge. There is no targeted therapy available, and cytotoxic chemotherapy is the mainstay for TN tumor treatment.

A special case where targeted therapy is available is the tumors with BRCA mutations, which show deficiency in one arm of the DNA repair pathways. Together, these findings demonstrate the potential of combination therapy and revive the hope of many targeted agents that previously were shown to be futile as single agents. Another layer of combination therapy is to target the metastasis cascade mediators and block cancer—stromal crosstalk. PI3K—Akt pathway inhibitors have gained increased interest for the TN subtype, partly because many of the cancer—stromal interactions converge on the activation of this pathway and it controls metastatic survival as a central hub.

Despite the many ongoing clinical trials, these inhibitors have proven only marginally effective as single agents. Therefore, what therapies these inhibitors should be combined with so that their potency could be leveraged becomes a major question for future research. A fundamental challenge for combination therapy is the side effects that each drug carries. As the treatment potency increases with the drug combination, the toxic effects to the host tissue also worsen. Thus, the compound effects of the drug toxicities significantly limit the numbers of drugs that can be combined as well as the dose that can be applied for each drug.

The success of combination therapy relies on a high therapeutic index and requires careful design of the combination regimen. As a result, to develop combination therapy with optimal efficacy, the therapy may have to be tailored from patient to patient, based on a more detailed understanding and more comprehensive characterizations of the metastasis lesions for each patient. With the advent of personal genomics and single-cell sequencing technologies and their wider application with patient biopsies in the clinic, precision medicine is no longer a farfetched idea and may be feasible in the future.

Because of the many existing challenges in targeting established metastases, adjuvant therapy is designed to prevent metastasis formation, where the treatment is given after surgery and before any signs of disease recurrence. This protracted temporal gap between the primary tumor diagnosis and the emergence of metastatic foci in distant organs is referred to as metastatic latency or metastatic dormancy Fig. At the cellular level, clinical latency may show as either solitary cancer cells or microlesions that are below the detection threshold in the clinic.

These micrometastases may adopt a cellular state either entering quiescence or abortive growth with cell proliferation counterbalanced by cell death. Occasional reports of transmitting cancer to immunosuppressed recipients by organ transplantation highlight that organs beyond the bone marrow can harbor latent metastases as sanctuary sites. Despite the clinical importance of the dormancy state, few experimental models exist, leaving its biology unknown. It is believed that metastatic latency results from delayed adaptation of disseminated cancer cells to the foreign microenvi-ronment.

Though this notion requires definitive proof, it prompts deeper thought about the targeting of latent tumor cells for improved metastasis prevention. Even though the detailed knowledge about latent metastasis is still lacking, some basic nature of these cells can be inferred based on the current clinical and experimental evidences. First, there exist robust cell survival mechanisms that can support these cells during the latent period, even up to decades. The inability of most antimitotic therapies to eliminate metastases indicates that the machinery supporting latent cancer survival is different from that of cancer proliferation.

Second, these latent cells maintain their proliferation potential and competence for cell cycling when the condition becomes congenial enough. Once they start proliferating, they may no longer depend on the latent survival mechanism. Thus, a drug effective against latent cancer cell survival may as well be futile against established, proliferating metastases. Such a possibility may let these targeted agents drop off the clinical trials easily, because most of these agents will be first tested in the advanced cancer settings in breast cancer clinical trials.

Systematic therapies, including hormonal therapy, anti-HER2 therapy, and chemotherapy, are approved for the adjuvant setting because of their demonstrated efficacies in shrinking established tumors or metastases. Thus, the existing therapeutic regimens set a high standard for the latency-targeting agents. Even if these inhibitors can be evaluated in the adjuvant trials, the readout of their clinical benefits remains obscure. Detection of CTCs, circulating tumor DNA, or circulating tumor transcripts remains not yet reliable enough for inferring disease progression, let alone predicting status of latent metastases.

If the eventual occurrence of metastasis and patient survival serves as the end readout, patients may need to be monitored for more than 10—20 years. Such long-term investments, expensive efforts, and high-demanding support deter the enthusiasm of pharmaceutical companies. As a result, even though it seems quite appealing to target latent metastasis, many practical concerns impede such therapy from entering clinical testing. To overcome these limitations, a deeper understanding of the latency biology and convincing preclinical evidence of such therapeutic value are imperative.

Metastasis remains the biggest hurdle for curing breast cancer. Recent findings have established a conceptual framework of cancer metastasis and provided deeper insights on the molecular basis of metastatic traits, their origins, and their evolution. How to incorporate this knowledge into the design of next-generation therapy is key to combating breast cancer metastasis. Different challenges exist for different breast cancer subtypes.

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TN breast cancers are the most aggressive and metastatic, with no effective targeted therapy available. Pursuing more potent and more specific therapies that reduce the first five-year recurrence rate is needed. How to combat drug resistance via developing novel combination therapy of chemotherapy, small molecule therapy, and immunotherapy is key to achieving durable therapeutic efficacies. A deeper molecular insight of organ-specific metastases may guide novel therapeutic designs. To conclude, the past half century witnessed significant advancements in effective therapies for breast cancer, and we anticipate amazing breakthroughs in targeting breast cancer metastasis within the next 50 years.

We thank members of the Golub laboratory for insightful discussions. We thank Elizabeth Hoover for editing the manuscript. XJ is a Susan G. Komen Fellow. Dimri, Editor in Chief. The authors confirm that the funder had no influence over the study design, content of the article, or selection of this journal. Paper subject to independent expert blind peer review. All editorial decisions made by independent academic editor.

Upon submission manuscript was subject to anti-plagiarism scanning. Prior to publication all authors have given signed confirmation of agreement to article publication and compliance with all applicable ethical and legal requirements, including the accuracy of author and contributor information, disclosure of competing interests and funding sources, compliance with ethical requirements relating to human and animal study participants, and compliance with any copyright requirements of third parties.

Author Contributions. Wrote the first draft of the manuscript: XJ. Contributed to the writing of the manuscript: XJ and PM. Agree with manuscript results and conclusions: XJ and PM. Made critical revisions and approved final version: XJ and PM. Both authors reviewed and approved of the final manuscript. National Center for Biotechnology Information , U. Journal List Breast Cancer Auckl v. Breast Cancer Auckl. Published online Sep 1. Xin Jin 1, 2 and Ping Mu 3.

Find articles by Xin Jin. Find articles by Ping Mu. Author information Article notes Copyright and License information Disclaimer. This article has been cited by other articles in PMC. Abstract Metastasis is the leading cause of breast cancer-associated deaths. Keywords: breast cancer, metastasis, metastatic traits, targeted therapy, precision medicine. Introduction Breast cancer is the most common cancer among females worldwide, with an incidence rate of over 1. Genomic Landscape of Breast Cancer A comprehensive portrait of the genomic makeup of breast cancer has now become available as a result of multiple high-throughput profiling efforts.

Metastatic Patterns of Breast Cancer It is well known from clinical observations that different tumor types display distinct organ tropisms in metastatic patterns. Metastasis Cascade Cancer cells need to undergo a series of steps in order to depart from the primary site and spread to various organs. Open in a separate window. Figure 1. Local Invasion To overcome the multiple organismal barriers, tumor cells have to gain an extra set of gene activities or characteristics, in addition to their ability to grow without restriction in the primary tumor.

Circulation To survive the transit in circulation, cancer cells need to resist anoikis, shear forces of the blood flow, and innate immune attack. Extravasation Extravasation and intravasation are, to some degree, mirrored processes. Survival After passing these steps, the disseminated tumor cells DTCs face the biggest hurdle toward their colonization, the foreign microenvironment. Outgrowth The surviving cancer cells then need to engage extra genes that could modify the distant stroma and extract signals that trigger their intrinsic oncogenic signaling for proliferation.

Evolution of Metastatic Traits How metastatic traits arise as the primary tumor evolves remains a poorly investigated question. Stroma The third principle is the contribution from tumor-associated stroma and the microenvironment they shape. Targeting Metastasis The identification of metastasis gene mediators provides new potential targets for treating metastatic breast cancer.

Targets for Therapy Often times, when a patient is diagnosed with breast cancer, the primary tumor will be surgically removed and the residual disease will be eradicated by hormone, chemo, or radiation therapies. Lessons from Hormonal Therapy and Anti-HER2 Therapy Despite recognition of the distinctions between metastases and their primary tumors, metastases are treated mainly based on their tumors of origin. Figure 2.

Transplant Drug May Improve Immunotherapy for Breast Cancer - National Cancer Institute

A schematic shows key pathways of breast tumorigenesis and their targeted agents. Intratumor Heterogeneity The metastasis cascade is depicted as a delicate process that requires an intricate, coordinated action of multiple gene programs. Combination Therapy and Precision Medicine Because of the intratumor complexity and the plasticity of metastases, it is expected that many of the targeted agents Fig.

Latent Metastasis Because of the many existing challenges in targeting established metastases, adjuvant therapy is designed to prevent metastasis formation, where the treatment is given after surgery and before any signs of disease recurrence. Concluding Remarks Metastasis remains the biggest hurdle for curing breast cancer. Acknowledgments We thank members of the Golub laboratory for insightful discussions. Author Contributions Wrote the first draft of the manuscript: XJ.

Thus, angiogenesis decreased in tumor cells, and metastasis ability of TEM8 significantly degraded with the deletion in cancer cells.

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  • Cancer cell proliferation, angiogenesis, and metastases are blocked with the prevention of cell cycle and the expression of the kinetochore-associated genes with the inhibition of TEM [ 15 ]. Cancer cells are known to secrete the pro-angiogenic signals such as VEGFA and open the angiogenic lock by affecting the tumor microenvironment.

    TEM8 is known to work in cooperation with other factors such as VEGF for promoting endothelial cell migration and angiogenesis. In conclusion, TEM8 expression is higher in tumor cells than in normal cells. All these studies reveal the potential of TEM8 as a therapeutic target for combating the disease; however, more clinical studies are required for developing the TEM8 -targeted therapies [ 15 ].

    In addition, this molecule in distant metastasis regions was demonstrated to be highly expressed than the levels in regional lymph node metastases. This showed that APOBEC3B not only in the primary tumor stage has a role in the development of different metastatic stages of breast cancer.

    Therefore, the identification of different expression levels of APOBEC3B suggests that it carries a biological marker feature that may show a different metastatic stage and may be used in the identification of the metastasis stages in future. Lymph node metastasis shows that distant metastasis risk is higher. The absence of lymph node metastases is associated with lower metastasis risk; however, the presence of more than four lymph node metastases is the precursor that distant metastasis risk is significantly higher.

    Distant tumor metastasis develops through axillary lymphoid nodes ALD and blood circulation. Therefore, lymph nodes are used as an indicator of the metastasis ability of tumor cells. There is an association between the tumor size and the rate of lymph node metastasis.

    Metastatic Breast Cancer Forum 2018: HER2-positive Breast Cancer - Dana-Farber Cancer Institute

    Higher CCN1 expression is associated with lymph node metastasis and poor prognosis in breast cancer patients. CCN1 increases the breast tumor vascularization and causes metastasis with Hg signaling [ 4 ]. In addition, CCN1 has a regulatory role in fibroblast production by affecting MMP-1 for increasing the breast cancer cell migration and invasion. CCN4 expression is associated with lymph node metastasis and poor prognosis.

    The common cause of morbidity and mortality in most advanced stage breast cancer patients is the development of osteolytic bone metastasis. Most bone metastases detected in breast cancer are associated with osteolytic-type metastatic lesions owing to the osteoclast-mediated bone resorption. Although all subtypes of breast cancer have a tendency of bone metastases, luminal subtype tumors develop higher bone metastases Tumor cells demonstrate different reactions in accordance with the environment in the new organ such as gene expression, growth ability, and response to treatment.

    Therefore, any of the breast cancer cell reaching to the bone may promote the excessive growth in molecular interaction with osteoblasts and osteoclasts. Cytokines, chemokines, and other growth factors support the development of bone metastasis. Some cancer cells in the primary tumor accumulate additional genetic changes which lead to bone metastasis. This causes invasion and colonization of tumor cells to the bone matrix. Another effective gene is the protein osteopontin OPN which has various functions including the stimulating ability of the bone matrix to attach to the osteoclast.

    This protein is continuously overexpressed in metastatic cells. The genes effective in bone metastasis affect the tumor microenvironment toward metastasis. The overexpression of these genes develops the osteolytic bone metastasis. IL11 is a strong osteoclast inducer which is synthesized by the progenitor cells in the bone marrow [ 4 ]. IL11 and OPN significantly increased the osteolytic bone metastasis by increasing the osteoclast function. The significantly overexpressed genes in bone metastasis encode the cell surface and secreting proteins which have functions that could possibly change the host tissue environment, each promoting the formation of osteolytic bone lesions.

    The molecular mechanisms that are mediated by the genes effective in breast cancer-associated bone metastasis. Primary breast tumor develops with the accumulation of oncogenic mutations from normal breast epithelium. The increased expression of gene classes that facilitate metastasis to different organs among tumor cells enables the invasion of the bone matrix, colonization of metastatic tumor cell, and destruction of the bone matrix [ 39 ].

    In addition, CCN proteins have roles in various pathological cases by organizing the extracellular signals in the cellular environment. CCN3 was demonstrated to increase the bone metastasis in the studies conducted in metastatic breast cancer cell line [ 29 ].

    This significant effect of CCN3 in metastasis was reported to deteriorate the osteoblast differentiation and provided a favorable environment for osteolytic breast cancer bone metastasis owing to supporting the osteoclastogenesis [ 29 ]. One of the overexpressed genes in bone-specific metastasis is the NAT1 N-acetyltransferase-1 and is a potential biological indicator for breast cancer. The liver is the most common metastatic region for cancers and represents the second organ where breast cancer metastasis occurs.

    The development of liver metastasis in breast cancer patients is associated with Wnt signal and Ki67 signal independent of beta-catenin and an indicator of poor prognosis. CXCR4 is the most common chemokine receptor that mediates the initiation of liver metastases. In addition, the dysregulation of cell adhesion molecules N-cadherin and E-cadherin was demonstrated to contribute to liver metastases in breast cancer Figure 4. Breast cancer cells with higher N-cadherin level develop liver metastasis.

    E-cadherin which inhibits the metastasis was found lower in breast cancer cells with liver metastasis [ 30 ]. Although N-cadherin increases the liver metastasis, in normal conditions E-cadherin suppresses the development of liver metastasis. In addition, IL-6 expression in liver metastasis of breast cancer facilitates the development of liver metastasis by inhibiting the E-cadherin expression [ 30 ].

    Metastasis is a multistep procedure which is responsible for most cancer-associated deaths and is affected by both cell-cell or cell-matrix interactions and tumor microenvironment vascularization, etc. Clinically, low oxygen level hypoxia is known to be associated with metastasis [ 17 ]. Lysyl oxidase LOX expression is both associated with tumor suppression and tumor progression, and its role in tumorigenesis changes in accordance with the cellular location, cell type, and transformation.

    Mostly distant metastasis is detected, and overall survival is poor in patients who have tumors which highly express the LOX. The LOX inhibition eliminates metastasis in breast cancer patients. LOX is required in metastatic growth to form a niche. LOX is required for hypoxia-associated metastasis.

    Although LOX inhibition has no significant effect on primary tumor growth, LOX was associated to significantly decrease the lung metastases and inhibited the liver metastasis [ 17 ]. LOX molecule is suggested to be a good therapeutic target in prevention and elimination of metastasis [ 17 ]. Brain metastasis BM is detected as a complication that generally develops in the late stages of disease. Brain metastases develop after systemic emergence of metastases in the lungs, liver, and bone [ 16 ]. Two main primary tumors that do metastasis to the brain are lung and breast adenocarcinomas [ 33 ].

    Brain metastases are associated with neurological disorders by affecting both the cognitive and sensory functions in addition to their association with highly poor prognosis. Breast cancer is the most common cancer type where brain metastasis develops after lung metastasis. Lung and breast cancer-associated brain metastasis is more frequently detected than the primary brain tumors.

    Brain metastasis incidence has gradually been increasing in breast cancer patients. Due to the development of systemic therapies, many breast cancer patients live longer, but still in a way brain metastases may develop. Various factors were described for increased brain metastasis risk in breast cancer patients. These factors may be reported as early age, poorly differentiated tumor histology high grade , hormone receptor negativity, and metastasis in more than four lymph nodes.

    These factors were associated with the brain metastasis risk [ 16 ]. However, brain metastasis in triple negative breast cancer patients develops in earlier periods. The development of brain metastasis in breast cancer was detected to be associated with Wnt, Notch, and EGFR pathways [ 36 ]. Breast cancer-associated metastasis shows poor prognosis due to the lack of molecular therapeutic targets. HER2 amplifications and mutations were frequently demonstrated in breast cancer and in breast cancers with brain metastasis [ 36 ]. There are no target-specific treatment options in the clinical practice generally in breast cancers that carry BRCA1 and BRCA2 gene mutation and triple negative brain metastasis.

    Brain metastasis is a multistep procedure with migration, intravasation, circulation, adhesion, extravasation, and brain microenvironment. Particularly the blood-brain barrier BBB is highly selective in the entrance of tumor cells and therapeutics to the brain microenvironment. In compliance with that, the cells to make a metastatic lesion in the brain have a specific clonal origin. This shows that a brain metastasis shared the common abnormalities with a metastasis ancestor cell, and the further abnormalities could only be present in only brain metastatic subclones.

    More frequent detection of TP53 mutations in breast cancer with brain metastasis compared with the other breast cancers is an example. In addition, the majority of snoRNAs and snRNAs have higher expression in breast cancer metastasizing to the brain [ 34 ]. Luminal breast tumors have the tendency to do metastasis to the bone; however, basal-like breast tumors mainly do metastasis to the lungs. We also have a number of clinical trials for advanced kidney cancer.

    She was in regular follow up with TMH Mumbai. Unfortunately in July'18 she diagnosed with Metastatic cancer spread in brain and lungs. Although she got radiotherapy and now taking chemotherapy, but hardly any improvement is showing. Plz suggest possible treatment to get rid of it or how to control it.


    Unfortunately, we are not able to make treatment recommendations on our blog. If she would like to consult with one of our doctors, including to arrange to have her medical records reviewed remotely, she can contact our International Center at international mskcc. Thank you for your comment and best wishes to you and your family. Primary neuro endocrine.. Secondary multiple liver tumor high grade Is it cureable MSK has a number of experts in treating neuroendocrine tumors. I would welcome a bit of help in understanding my recent pathology report from my surgery Dec.

    The initial tumor site is my left breast. Stage 1 1. The words metatastic carcinoma weren't mentioned by the doctor, but I saw them in the report. We must wait 2 weeks to order the Onco test. That will provide a I understand My question: Would a PET scan be advised to see if any other part of my body was already involved? Odd pains and memory issues have recently surfaced I'm just wondering if the PET scan would tell us lots more and really help with a plan.

    Thank you for your attention. I'm learning a lot, but this lymph node thing was a BIG surprise to even the doctors. I'm 70 and otherwise very healthy. Water skiing, jogging, eating responsibly and loving life. Trying to be responsible with my own care too. Thank you for your comment and best wishes to you. We are really mentally drained at all this news. Thank you for any advise you can give. You and your family members may find it helpful to read this blog post with tips for caregivers. You may also find it helpful to join Connections , our online community for patients and caregivers.

    We welcome your questions and comments. While we share many of them with our world-class doctors and researchers, we regret that in order to protect your privacy, we are not able to make personal medical recommendations on this forum, nor do we publish comments that contain your personal information. If you would like to consult with an MSK doctor, we encourage you to make an appointment at or request an appointment online.

    What is metastatic cancer? Metastatic cancer occurs when cancer cells break off from the tumor where they originated, spread through the bloodstream or lymph vessels to another part of body, and establish new tumors. Radiation oncologist Kathryn Beal completed a study in for people with melanoma that has spread to the brain. This is much better than the response to stereotactic radiosurgery alone.