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Prognostic value of survivin and EGFR protein expression in triple-negative breast cancer (TNBC) patients

Prognostic value of survivin and EGFR protein expression in triple-negative breast cancer (TNBC) patients | Metaplastic Breast Cancer | Scoop.it

"Zhang M, et al. – Triple–negative breast cancer (TNBC) is a particular type of breast cancer which is characterized by its biological aggressiveness, worse prognosis, and lack of prognostic markers or therapeutic targets in contrast with hormonal receptor–positive and human epidermal growth factor receptor 2–positive (HER2+) breast cancers. .

Methods

A total of 136 patients who had undergone a resection of primary TNBC were enrolled at the Third Affiliated Hospital of Harbin Medical University from March 2003 to September 2005.Expression of ER, PR, HER2, EGFR, and survivin was assessed by immunohistochemistry.The association of TNBC and other clinicopathological variables and the prognostic value of survivin and EGFR expression were evaluated.
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Maria Fowler's insight:

EGFR is commonly overexpressed in MpBC tumors as well. It is a potential target for future thearpies.

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Susan Zager's curator insight, December 5, 2013 12:02 PM

Conclusion: 

We draw a conclusion from the present study that survivin and EGFR expression are useful prognostic markers of TNBC and might be useful for molecular targeting therapy of TNBC treatment.

Metaplastic Breast Cancer
Breast cancer studies that may give insight to metaplastic breast cancer patients.
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Pain like 'skin being peeled'

Pain like 'skin being peeled' | Metaplastic Breast Cancer | Scoop.it

"My breast cancer went undiagnosed for eight weeks.

There is no blame to my GP at the time as I ended up with metaplastic breast cancer - and as with 0.02 per cent of women who have this deadly cancer, it presented like a cyst.

I owe my life to my breast surgeon who removed this fast-growing nightmare with deep, clear margins, however I ended up with severe nerve damage down the left side of my chest. This wonderful man even apologised but pffttt he saved my life, this pain is a small thing in comparison.

However, at times, it feels like my skin is being peeled off layer by layer. I am unable to bear even pure silk camisoles against my skin so I lie there bare-chested (in private of course!).

Chemotherapy didn't suit my body very well either, and I ended up for months enduring a mouth and throat full of abscesses. The pain was indescribable. "  


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A metaplastic breast cancer story

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Susan Zager's curator insight, October 10, 2014 2:55 PM

This article is about a Metaplastic breast cancer patient who discusses all of the incredible side effects and other things that happen as a result of the awful disease. 

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Vanderbilt-led study identifies genes linked to breast cancer in East Asian women

Vanderbilt-led study identifies genes linked to breast cancer in East Asian women | Metaplastic Breast Cancer | Scoop.it

"A new study in East Asian women has identified three genetic changes linked to an increased risk of breast cancer. The research, led by Vanderbilt University investigators, was published online July 20 in Nature Genetics.

While breast cancer is one of the most common malignancies among women worldwide, most studies of the genetic risk factors for the disease have focused on women of European ancestry.

Given the differences in genetic heritage and environmental exposures between East Asian women and those of European ancestry, the investigators decided to conduct a study in East Asians to search for genetic changes that are linked to breast cancer development. The current study was conducted as part of the Asia Breast Cancer Consortium led by Wei Zheng, M.D., Ph.D., MPH, Ingram Professor of Cancer Research at Vanderbilt.

First author Qiuyin Cai, M.D., Ph.D., associate professor of Medicine, and colleagues performed a genome-wide association study of 22,780 women with breast cancer, and 24,181 control subjects who were recruited in 14 studies in Asian countries, including China, Japan, Korea, Malaysia and Singapore.

DNA for the gene assays was obtained through blood samples or buccal cells from mouthwash.

"We found DNA sequence changes in two genes, PRC1 and ZC3H11A, and a change near the ARRDC3 gene were associated with breast cancer risk and we identified a possible association with a fourth gene locus," said Cai. "Two of those sequence changes are in parts of the genome that regulate the expression of nearby genes."


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Empowering Patients Is More Than Engagement

Empowering Patients Is More Than Engagement | Metaplastic Breast Cancer | Scoop.it

"I was invited to participate in the 2014 Rev Forum, a “big-tent” type of event sponsored by LiveSTRONG and Genentech, and featuring the participation of ASCO’s Conquer Cancer Foundation, who had extended the invitation to me. The Rev Forum brings together a diverse group of participants—from clinicians, to policymakers, artists, advocates, and most importantly, patients, to rethink cancer care. As I considered what issues we could address, one thought was first and foremost in my mind: how to engage and empower more patients in these types of discussion.

In the business community, distinctions are clearly made between engagement and empowerment. Engagement reflects one’s understanding of purpose and mission, and the shared commitment from all involved to seeing an organizational goal accomplished. In contrast, empowerment refers to the ability to do what one wants and/or feels necessary to accomplish a task. The best way to realize a mission or achieve a goal is to be both engaged and empowered.

As a clinician, I want my patients engaged. It is important to me that they understand their diagnosis, prognosis, and the treatments they are being asked to take. I want them to feel invested in their therapy and to understand their side effects and how they will be monitored. When my patients are engaged, I see myself as a partner in their care. Their treatment becomes a shared responsibility and the doctor-patient relationship is one of equals. To me, patient engagement lies at the heart of ethics in medicine and informed consent. Indeed, it is a reflection of good patient care."


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Susan Zager's curator insight, April 26, 2014 6:18 PM

It's so refreshing to read Dr. Don Dizon's words reflecting the importance of patients being engaged in their cases. When facing a cancer diagnosis patients and doctors have the shared responsibility to work together in decision making related to targeted treatments, financial issues, care guidelines, side effects and options related to each individual case.

Don Dizon will be speaking at Rev Forum, a conference in Washington DC, May 8-9, 2014, (with registration still open), where medical professionals,  patients and doctors can "connect with leaders in cancer treatment, advocacy, and policy to build a new paradigm in cancer care." For more information about Rev Forum go to: http://www.rev-forum.com/.


Susan Zager's curator insight, April 26, 2014 6:19 PM

It's so refreshing to read Dr. Don Dizon's words reflecting the importance of patients being engaged in their cases. When facing a cancer diagnosis patients and doctors have the shared responsibility to work together in decision making related to targeted treatments, financial issues, care guidelines, side effects and options related to each individual case.

Don Dizon will be speaking at Rev Forum, a conference in Washington DC, May 8-9, 2014, (with registration still open), where medical professionals,  patients and doctors can "connect with leaders in cancer treatment, advocacy, and policy to build a new paradigm in cancer care." For more information about Rev Forum go to: http://www.rev-forum.com/.

Tambre Leighn's curator insight, May 10, 2014 12:56 AM

Survivors do not have to leave it to fate that they may or may not end up with a physician who has the time and the consciousness to be their patients' "sherpa".  As much as I have great admiration for the sherpas I met in Kathmandu, we have guides who know how to navigate the path to empowerment right here at home. We are cancer survivorship coaches...and we have the tools and skills to help survivors not just engage in their experience but live in an empowered way.  To learn more about becoming a cancer survivorship coach, go to http://www.ipeccoaching.com/Becoming-a-Cancer-Survivorship-Coach

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New drug, molecular insight into triple negative breast cancers

New drug, molecular insight into triple negative breast cancers | Metaplastic Breast Cancer | Scoop.it

"Most breast cancers are treated by blocking their addictions, for example depriving estrogen-fueled tumors of estrogen. But what about breast cancers without these hormonal addictions? In so-called "triple negative" tumors the cancer's addiction remains a mystery, making this subtype difficult to treat. However, a University of Colorado Cancer Center study presented today at the American Association for Cancer Research (AACR) Annual Meeting 2014 showcased a new drug active against triple-negative breast cancer, and through analysis of the drug's mechanism of action, offers increased understanding of the biology of this very aggressive form of breast cancer.

"We developed the compound AMPI-109 in collaboration with Dr. Rahul Ray, a synthetic organic chemist at the Boston University School of Medicine, and showed its effectiveness in preliminary studies of renal and prostate cancers. But it seemed initially as if the drug was inactive against breast cancer," says James R. Lambert, PhD, investigator at the CU Cancer Center and assistant research professor at the CU School of Medicine.

However, the initial test of AMPI-109 had been performed against only one form of breast cancer and this disease is notoriously heterogeneous. Despite initial negative results, the group decided to investigate the drug's efficacy against a panel of all known breast cancer subtypes. Strikingly, Lambert and colleagues found the drug was especially effective in specifically one subtype: triple-negative breast cancer, in which the drug blocked the growth of cells by greater than 50 percent.

"This was exciting," Lambert says, "not only did we have a drug that potentially targeted triple-negative breast cancer, but we had a biochemical tool that could be used to dissect the molecular underpinnings of the disease. "

To begin to investigate the molecular mechanism of AMPI-109 action in triple negative breast cancer, the group performed a genome-wide functional genetic screen, individually turning off every gene in the cell while exposing the cells to the drug. Identification of the silenced genes in cells that survived drug treatment would show which genes are essential for the drug's cell-killing effect.


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Maria Fowler's insight:

Very early study which also does not indicate if any of the TNBC was Metaplastic

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Gene Implicated in Progression and Relapse of Deadly Breast Cancer

Gene Implicated in Progression and Relapse of Deadly Breast Cancer | Metaplastic Breast Cancer | Scoop.it

"NEW YORK — (March 24, 2014) — Scientists from Weill Cornell Medical College and Houston Methodist have found that a gene previously unassociated with breast cancer plays a pivotal role in the growth and progression of the triple negative form of the disease, a particularly deadly strain that often has few treatment options. Their research, published in this week'sNature, suggests that targeting the gene may be a new approach to treating the disease.

About 42,000 new cases of triple negative breast cancer (TNBC) are diagnosed in the United States each year, about 20 percent of all breast cancer diagnoses. Patients typically relapse within one to three years of being treated.

Senior author Dr. Laurie H. Glimcher, the Stephen and Suzanne Weiss Dean of Weill Cornell Medical College, wanted to know whether the gene — already understood from her prior work to be a critical regulator of immune and metabolic functions — was important to cancer's ability to adapt and thrive in the oxygen- and nutrient-deprived environments inside of tumors. Using cells taken from patients' tumors and transplanted into mice, Dr. Glimcher's team found that the gene, XBP1, is especially active in triple negative breast cancer, particularly in the progression of malignant cells and their resurgence after treatment.

"Patients with the triple negative form of breast cancer are those who most desperately need new approaches to treat their disease," said Dr. Glimcher, who is also a professor of medicine at Weill Cornell. "This pathway was activated in about two-thirds of patients with this type of breast cancer. Now that we better understand how this gene helps tumors proliferate and then return after a patient's initial treatment, we believe we can develop more effective therapies to shrink their growth and delay relapse."

The group, which included investigators from nine institutions, examined several types of breast cancer cell lines. They found that XBP1 was particularly active in basal- like breast cancer cells cultivated in the lab and in triple negative breast cancer cells from patients. When they suppressed the activity of the gene in laboratory cell cultures and animal models, however, the researchers were able to dramatically reduce the size of tumors and the likelihood of relapse, especially when these approaches were used in conjunction with the chemotherapy drugs doxorubicin or paclitexel. The finding suggests that XBP1 controls behaviors associated with tumor-initiating cells that have been implicated as the originators of tumors in a number of cancers, including that of the breast, supporting the hypothesis that combination therapy could be an effective treatment for triple negative breast cancer.

The scientists also found that interactions between XBP1 and another transcriptional regulator, HIF1-alpha, spurs the cancer-driving proteins. Silencing XBP1 in the TNBC cell lines reduced the tumor cells' growth and other behaviors typical of metastasis.

 


Via Susan Zager
Maria Fowler's insight:

MpBC of course is very often TNBC.

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Susan Zager's curator insight, March 26, 2014 2:17 PM

Although these findings are very early, when it comes to triple negative breast cancer we are always seeking as much information as possible because this aggressive type of breast cancer needs much more treatment options. To see the study go to: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13119.html


Maria Fowler's curator insight, March 26, 2014 8:49 PM

As always, studies of TNBC rarely give details as to whether any metaplastic tumor types were involved. This one specifically discusses tumors with basal-like characteristics, which we do not all share.

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Gene Implicated in Progression and Relapse of Deadly Breast Cancer

Gene Implicated in Progression and Relapse of Deadly Breast Cancer | Metaplastic Breast Cancer | Scoop.it

"NEW YORK — (March 24, 2014) — Scientists from Weill Cornell Medical College and Houston Methodist have found that a gene previously unassociated with breast cancer plays a pivotal role in the growth and progression of the triple negative form of the disease, a particularly deadly strain that often has few treatment options. Their research, published in this week'sNature, suggests that targeting the gene may be a new approach to treating the disease.

About 42,000 new cases of triple negative breast cancer (TNBC) are diagnosed in the United States each year, about 20 percent of all breast cancer diagnoses. Patients typically relapse within one to three years of being treated.

Senior author Dr. Laurie H. Glimcher, the Stephen and Suzanne Weiss Dean of Weill Cornell Medical College, wanted to know whether the gene — already understood from her prior work to be a critical regulator of immune and metabolic functions — was important to cancer's ability to adapt and thrive in the oxygen- and nutrient-deprived environments inside of tumors. Using cells taken from patients' tumors and transplanted into mice, Dr. Glimcher's team found that the gene, XBP1, is especially active in triple negative breast cancer, particularly in the progression of malignant cells and their resurgence after treatment.

"Patients with the triple negative form of breast cancer are those who most desperately need new approaches to treat their disease," said Dr. Glimcher, who is also a professor of medicine at Weill Cornell. "This pathway was activated in about two-thirds of patients with this type of breast cancer. Now that we better understand how this gene helps tumors proliferate and then return after a patient's initial treatment, we believe we can develop more effective therapies to shrink their growth and delay relapse."

The group, which included investigators from nine institutions, examined several types of breast cancer cell lines. They found that XBP1 was particularly active in basal- like breast cancer cells cultivated in the lab and in triple negative breast cancer cells from patients. When they suppressed the activity of the gene in laboratory cell cultures and animal models, however, the researchers were able to dramatically reduce the size of tumors and the likelihood of relapse, especially when these approaches were used in conjunction with the chemotherapy drugs doxorubicin or paclitexel. The finding suggests that XBP1 controls behaviors associated with tumor-initiating cells that have been implicated as the originators of tumors in a number of cancers, including that of the breast, supporting the hypothesis that combination therapy could be an effective treatment for triple negative breast cancer.

The scientists also found that interactions between XBP1 and another transcriptional regulator, HIF1-alpha, spurs the cancer-driving proteins. Silencing XBP1 in the TNBC cell lines reduced the tumor cells' growth and other behaviors typical of metastasis.

 


Via Susan Zager
Maria Fowler's insight:

As always, studies of TNBC rarely give details as to whether any metaplastic tumor types were involved. This one specifically discusses tumors with basal-like characteristics, which we do not all share.

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Susan Zager's curator insight, March 26, 2014 2:17 PM

Although these findings are very early, when it comes to triple negative breast cancer we are always seeking as much information as possible because this aggressive type of breast cancer needs much more treatment options. To see the study go to: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13119.html


Maria Fowler's curator insight, March 30, 2014 8:41 PM

MpBC of course is very often TNBC.

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PARP Inhibitor BMN 673 Advances in Breast Cancer Study

PARP Inhibitor BMN 673 Advances in Breast Cancer Study | Metaplastic Breast Cancer | Scoop.it

"As PARP inhibitors continue to emerge as a novel class of anticancer agents, BMN 673 has entered late-stage clinical development as a treatment for patients with locally advanced or metastatic breast cancer whose tumors test positive for germline BRCA1/2 mutations.1


The agent is being compared with treatment of physician’s choice in a phase III trial launched in October with a projected enrollment of 429 participants (Figure). Men and women are eligible. As a class, PARP inhibitors have received renewed attention recently, with several agents advancing in development in both breast and ovarian cancers. One of the first agents to “graduate” from the groundbreaking I-SPY 2 breast cancer clinical trial is veliparib (ABT-888), which also has entered a phase III study.

BMN 673 inhibits PARP 1/2, which are members of the nuclear enzyme poly(ADP-ribose) polymerase family that helps repair single-strand breaks in damaged DNA.2 The compound is an oral small molecule that selectively targets tumor cells with BRCA1, BRCA2, or PTEN gene mutations and is believed to be the most potent PARP inhibitor in development.2 Although the agent has been studied in ovarian cancer and other malignancies, the program is furthest along in breast cancer.

In updated phase I results presented at the 2013 San Antonio Breast Cancer Symposium in December, Mina LA et al3 reported that 13 of 18 patients (72%) with BRCA1/2-mutated breast cancer experienced a clinical benefit response from BMN 673 monotherapy, defined as complete response (CR), partial response (PR) or stable disease ≥24 weeks. The responders included 1 patient with a CR and 7 with a PR. The drug was generally well tolerated, with myelosuppression, fatigue, nausea, and alopecia among the most common adverse events, each occurring among less than onethird of patients."


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Maria Fowler's insight:

A PTEN mutation has been linked to Metaplastic breast cancer.

 

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Susan Zager's curator insight, February 19, 2014 3:56 PM

According to the article "PARP mediates single-strand break repair through the base excision repair pathway, and BRCA1 and BRCA2 proteins are crucial for homologous recombination for accurate DNA double-strand break repair,” said Blum. “In BRCA1 or BRCA2 mutation carriers, they have lost some of the ability to do this homologous recombination, and in their tumor, which we assume has lost a second copy, they really don’t have any functioning double-stranded, homologous recombination repair. If you knock out this single-strand base repair mechanism that PARP facilitates, by using the PARP inhibitor, then you are making it impossible for that cancer cell to repair DNA damage.”


For more information about participation in the clinical trial in the US go to the NBCC web site at: http://www.breastcancerdeadline2020.org/get-involved/take-action/MetsClinicalTrials.html


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New finding points to potential options for attacking stem cells in triple-negative breast cancer | Science Codex

New finding points to potential options for attacking stem cells in triple-negative breast cancer | Science Codex | Metaplastic Breast Cancer | Scoop.it

"ANN ARBOR, Mich. — New research from the University of Michigan Comprehensive Cancer Center and Georgia Regents University finds that a protein that fuels an inflammatory pathway does not turn off in breast cancer, resulting in an increase in cancer stem cells. This provides a potential target for treating triple negative breast cancer, the most aggressive form of the disease.

The researchers identified a protein, SOCS3, that is highly expressed in normal cells but undetectable in triple-negative breast cancer. They showed that this protein is degraded in cancers, blocking the cellular off-switch of a feedback loop involving the inflammatory protein interleukin 6, IL6. When the switch does not get turned off, it enables cancer stem cells to grow.

"We have known for a long time known that there are important links between inflammation and cancer, including similar pathways that regulate normal and cancer stem cells," says study author Max S. Wicha, M.D., distinguished professor of oncology and director of the U-M Comprehensive Cancer Center.

"This work helps explain why these pathways shut off in normal tissues after injury but remain active in cancers, resulting in an increase in cancer stem cells. Furthermore, they suggest that blocking these inflammatory loops may be a means of targeting cancer stem cells, improving patient outcome," he says."


Via Susan Zager
Maria Fowler's insight:

A study with promise. Let's hope that targeting inflammatory pathways is effective in more studies and trials. Being able to treat TNBC with drugs that already exist would be amazing.

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Susan Zager's curator insight, February 17, 2014 4:31 PM

Although this study is not yet in clinical trials, according to the article, the research team previously showed that" IL6 can stimulate breast cancer stem cells in HER2-positive breast cancers and they are designing a clinical trial which uses an IL6 blocker. The new research suggests that adding bortezomib to the IL6 inhibitor may be a way to target stem cells in triple-negative breast cancer." 

The study was published in Oncogene at : http://www.nature.com/onc/journal/v32/n5/full/onc201285a.html




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Patients may now get lab results without a doctor's help

Patients may now get lab results without a doctor's help | Metaplastic Breast Cancer | Scoop.it

"WASHINGTON — Patients or their representatives may now see their medical test results directly from the laboratory, rather than having to request them from a doctor's office, according to a new rule announced Monday.

"Information like lab results can empower patients to track their health progress, make decisions with their health care professionals and adhere to important treatment plans," Health and Human Services Secretary Kathleen Sebelius said.

Although people may still get their results from their doctors, the new rule changes the Health Insurance Portability and Accountability Act so they may also get personal health information from a laboratory. The new rule may open a door to quicker access through electronic records, though the HHS announcement stressed that a patient may need to pay for mail, copying or flash drives. In most cases, the announcement states, the information must be given within 30 days of a request.

However, the results could come much more quickly through an e-mail, a secure website or an application on the patient's phone.

In the past, a doctor's office often only notified patients if there were a problem with a lab result. However, a 2009 study in The Archives of Internal Medicine found that 1 out of 14 patients with negative test results never learned of the problem from their doctors. That may have been because the doctor was unable to reach the patient, or because of an oversight. But doctors have also raised concerns that patients would not be able to properly interpret their lab results without help, but diagnostic labs welcomed the change."


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Susan Zager's curator insight, February 5, 2014 3:13 PM

This makes lots of sense to be able to get test results directly from the lab instead of having to wait for the doctor. 

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Downregulation of Smurf2, a tumor-suppressive ubiquitin ligase, in triple-negative breast cancers: Involvement of the RB-microRNA axis

Downregulation of Smurf2, a tumor-suppressive ubiquitin ligase, in triple-negative breast cancers: Involvement of the RB-microRNA axis | Metaplastic Breast Cancer | Scoop.it

"The HECT family ubiquitin ligase Smurf2 regulates cell polarity, migration, division, differentiation and death, by targeting diverse substrates that are critical for receptor signaling, cytoskeleton, chromatin remodeling and transcription. Recent studies suggest that Smurf2 functions as a tumor suppressor in mice.

However, no inactivating mutation of SMURF2 has been reported in human, and information about Smurf2 expression in human cancer remains limited or complicated. Here we demonstrate that Smurf2 expression is downregulated in human breast cancer tissues, especially of the triple-negative subtype, and address the mechanism of Smurf2 downregulation in triple-negative breast cancer cells.

Methods: Human breast cancer tissues (47 samples expressing estrogen receptor (ER) and 43 samples with triple-negative status) were examined by immunohistochemistry for the expression of Smurf2.

Ten widely-studied human breastcancer cell lines were examined for the expression of Smurf2. Furthermore, microRNA-mediated regulation of Smurf2 was investigated in triple-negative cancer cell lines.

Results: Immunohistochemical analysis showed that benign mammary epithelial cells expressed high levels of Smurf2, so did cells in ductal carcinomas in situ.

In contrast, invasive ductal carcinomas showed focal or diffuse decrease in Smurf2 expression, which was observed more frequently in triple-negative tumors than in ER-positive tumors. Consistently, human triple-negative breast cancer cell lines such as BT549, MDA-MB-436, DU-4475 and MDA-MB-468 cells showed significantly lower expression of Smurf2 protein, compared to ER + or HER2+ cell lines."


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Comparative Proteome Analysis Revealing an 11-Protein Signature for Aggressive Triple-Negative Breast Cancer

Comparative Proteome Analysis Revealing an 11-Protein Signature for Aggressive Triple-Negative Breast Cancer | Metaplastic Breast Cancer | Scoop.it

Abstract


Background Clinical outcome of patients with triple-negative breast cancer (TNBC) is highly variable. This study aims to identify and validate a prognostic protein signature for TNBC patients to reduce unnecessary adjuvant systemic therapy.

Methods Frozen primary tumors were collected from 126 lymph node–negative and adjuvant therapy–naive TNBC patients. These samples were used for global proteome profiling in two series: an in-house training (n = 63) and a multicenter test (n = 63) set. Patients who remained free of distant metastasis for a minimum of 5 years after surgery were defined as having good prognosis. Cox regression analysis was performed to develop a prognostic signature, which was independently validated. All statistical tests were two-sided.

Results An 11-protein signature was developed in the training set (median follow-up for good-prognosis patients = 117 months) and subsequently validated in the test set (median follow-up for good-prognosis patients = 108 months) showing 89.5% sensitivity (95% confidence interval [CI] = 69.2% to 98.1%), 70.5% specificity (95% CI = 61.7% to 74.2%), 56.7% positive predictive value (95% CI = 43.8% to 62.1%), and 93.9% negative predictive value (95% CI = 82.3% to 98.9%) for poor-prognosis patients. The predicted poor-prognosis patients had higher risk to develop distant metastasis than the predicted good-prognosis patients in univariate (hazard ratio [HR] = 13.15; 95% CI = 3.03 to 57.07; P = .001) and multivariable (HR = 12.45; 95% CI = 2.67 to 58.11; P = .001) analysis. Furthermore, the predicted poor-prognosis group had statistically significantly more breast cancer–specific mortality. Using our signature as guidance, more than 60% of patients would have been exempted from unnecessary adjuvant chemotherapy compared with conventional prognostic guidelines.                      


Via Susan Zager
Maria Fowler's insight:

Metaplastic Breast Cancer paitents could greatly benefit from a better way to determine which tumors are chemo-resistant and which are primed for Metastasis .

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Susan Zager's curator insight, February 1, 2014 3:16 PM

Conclusions from the study:


Triple-negative breast cancer (TNBC) is one of the most aggressive breast cancer subtypes. To date, there is no clinically available targeted therapy for patients diagnosed with TNBC. Current guidelines for breast cancer treatment recommend that the majority of lymph node–negative (LNN) breast cancer patients, including TNBC patients, be treated with adjuvant chemotherapy.

Eventually approximately 30% of LNN TNBC patients develop distant metastasis and could thus potentially benefit from adjuvant chemotherapy; this indicates that the majority of patients are currently being overtreated. The lack of highly sensitive and specific prognostic markers is a major obstacle to predicting prognosis of TNBC patients. Moreover, there is an urgent need to identify potentially useful targets for therapy. Some commonly applied approaches for biomarker discovery, such as gene expression profiling, have not yet succeeded in identifying highly sensitive and specific markers related to disease progression of TNBC. Although a few publications have claimed to identify gene signatures that predict prognosis of TNBC, the reported signatures have limited clinical value because of their experimental design and lack of sufficient sensitivity and specificity. Therefore, it is desirable to identify a highly sensitive and specific prognostic signature for clinical application.

 In this study, we identified and independently validated a protein signature to predict 5-year metastasis-free survival of LNN patients who did not receive systemic adjuvant therapy, which would allow for the selection of TNBC patients that can be spared the toxicity of adjuvant chemotherapy.                

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Breast Cancer: Don't Delay Chemo

Breast Cancer: Don't Delay Chemo | Metaplastic Breast Cancer | Scoop.it

"Delaying adjuvant chemotherapy for breast cancer more than 60 days significantly increased the odds of premature death and distant metastasis, a review of almost 7,000 cases showed.

As compared with starting adjuvant therapy within 30 days of surgery, initiating chemotherapy at 61 days or later was associated with a 19% increase in the risk of premature death. In the subgroup of patients with stage III disease, the mortality risk increased by 76%. Relapse-free survival (RFS) and distant relapse-free survival (DRFS) worsened regardless of stage at diagnosis, according to Mariana Chavez-MacGregor, MD, of the University of Texas MD Anderson Cancer Center in Houston, and colleagues.

Patients with high-risk breast cancer (triple negative, HER2-positive, or stage III) seemed most susceptible to the adverse effects of delayed chemotherapy, as reported online in the Journal of Clinical Oncology."


Via Susan Zager
Maria Fowler's insight:

Metaplastic Breast Cancer grows so quickly... it is my personal beliefe that you shouldn't wait for any treatment both chemo and surgery.

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Research findings could lead to life-saving treatments to fight tumor metastasis

Research findings could lead to life-saving treatments to fight tumor metastasis | Metaplastic Breast Cancer | Scoop.it

"A team of researchers from the Cleveland Clinic and Case Western Reserve School of Medicine have identified critical complex mechanisms involved in the metastasis of deadly "triple negative" breast cancers (TNBC). These tumors are extremely difficult to treat, frequently return after remission, and are the most aggressive form of breast cancer in women. The discovery of this critical interaction of mechanisms could be used to develop new life saving treatments to kill metastatic tumors in TNBC.

"In previous findings published over the past 10 years, our teams have described key mechanisms in these critical proteins," said Khalid Sossey-Alaoui, PhD, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic. "A key component in the deadly metastatic potential of TNBC tumors is that they spread through tissues outside the breast very quickly. The two proteins that we studied, WAVE3 and TGF-β, when together, promote tumor aggressiveness."
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Maria Fowler's insight:

Another TNBC article... may be helpful for MpBC

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Gene Predicts Breast Cancer Relapse, Response to Chemo

Gene Predicts Breast Cancer Relapse, Response to Chemo | Metaplastic Breast Cancer | Scoop.it

"Scientists have made it easier to predict both breast cancer relapses and responses to chemotherapy, through the identification of a unique gene. The newly found marker could help doctors classify each breast cancer patient and customize a treatment regimen that is more effective. The discovery was a collaborative effort by scientists from A*STAR’s Institute of Molecular and Cell Biology (IMCB), and the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS).

 Despite advancements in cancer treatment, breast cancer remains the most common cancer among Singapore women. Thirty percent of early breast cancer patients in the world experience relapse due to metastasis, or the spread of cancer cells to other organs in the body. Some patients also do not respond well to chemotherapy. The inability to forecast relapses or the effectiveness of chemotherapy has led to a pressing need to identify predictive markers, which doctors can use to tailor appropriate treatment for each breast cancer patient at an early stage.     


Via Susan Zager
Maria Fowler's insight:

Biomarkers will be important to all of us.

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Susan Zager's curator insight, August 22, 2014 2:21 PM

To see the study published in the Journal of Clinical Investigation go to: http://www.jci.org/articles/view/73451


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Scientists ID New Drug Targets for Triple Negative Breast Cancer

Scientists ID New Drug Targets for Triple Negative Breast Cancer | Metaplastic Breast Cancer | Scoop.it

"The suppression of two genes reduce breast cancer tumor formation and metastasis by interfering with blood vessel formation and recruitment, report scientists from Houston Methodist and five other institutions in the Proceedings of the National Academy of Sciences (now online). The findings may help medical researchers identify effective drug targets for triple negative breast cancer, or TNBC.

 The genes, MLF2 (myeloid leukemia factor 2) and RPL39 (a ribosomal protein), were found to most profoundly impact the production of nitric oxide synthase, which helps regulate blood vessel behavior and could be crucial to the recruitment of new blood vessels to growing tumors. These genes impact the spread of TNBC throughout the body, and have not so far been linked with breast cancer.  "We have found two unique genes that may affect the most lethal type of breast cancer" said principal investigator and Houston Methodist Cancer Center Director Jenny Chang, "Most importantly, by knowing how these genes function, we have drugs that can block nitric oxide signaling and will begin a clinical trial in the Cancer Center in the near future" 
Via Susan Zager
Maria Fowler's insight:

As always this may apply to some of us and not others.

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Susan Zager's curator insight, May 27, 2014 7:07 PM

To see the abstract about the study go to: http://www.pnas.org/content/early/2014/05/01/1406655111.abstract


For more information about XPB1 go to: http://bms.ucsf.edu/sites/ucsf-bms.ixm.ca/files/20140501.adams_.christina.pdf


PJ's curator insight, May 28, 2014 9:40 AM
Susan Zager's insight (Breast Cancer News):
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AR Findings Highlight Detailed Tumor-Profiling Study

AR Findings Highlight Detailed Tumor-Profiling Study | Metaplastic Breast Cancer | Scoop.it

"A wide-ranging analysis of more than 5500 breast cancer tumors that combined genomic and protein expression testing has identified promising targets to explore for treating patients with poor prognoses, with particularly notable findings involving androgen receptor (AR) expression,1 according to Joyce A. O’Shaughnessy, MD. Nearly 36% of the samples were from patients with triple-negative breast cancer (TNBC), making the study the largest genomic analysis in that disease setting to date.


The clues yielded through the analysis confirm the utility of multiplatform molecular profiling in identifying targets that could help oncologists direct patients who have metastatic disease, or who are not responding to standard therapies, into clinical trials, said O’Shaughnessy. In some instances, drugs aimed at these targets already have been approved.

O’Shaughnessy, who is chair of Breast Cancer Research at Baylor Charles A. Sammons Cancer Center, Texas Oncology and US Oncology, presented findings from the analysis at the 2013 San Antonio Breast Cancer Symposium (SABCS).1

She discussed her research in an interview in advance of the 31st Annual Miami Breast Cancer Conference (MBCC) in March, where she served as a faculty member. O’Shaughnessy’s expertise includes using emerging technologies to explore novel therapies, particularly for TNBC. Her presentation was entitled “Human Subject Implications of Genomic Profiling of Tumors.”

The clinical utility of next-generation sequencing for managing patients with high-risk or metastatic breast cancer continues to progress with the development of gene expression assays, and genomic profiling of newly diagnosed patients in these settings “will increasingly allow for early intervention with rational targeted therapies that could very significantly improve patients’ outcomes,” O’Shaughnessy said in her MBCC presentation."


Via Susan Zager
Maria Fowler's insight:

Androgen Receptor status is a new area of study that could play a role in the treatment of MpBC.

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Susan Zager's curator insight, April 22, 2014 4:52 PM

O’Shaughnessy believes that the evidence is strong enough now for clinicians to consider AR-targeting agents may be appropriate for patients with metastatic breast cancer currently approved for patients with prostate cancer.


"She is participating in a phase II study of enzalutamide (Xtandi) in patients with advanced AR-positive TNBC.2 The primary outcome of the single-arm, open-label study will be the clinical benefit rate, defined as a combination of the best complete responses, partial responses, or stable disease for ≥16 weeks.

Bicalutamide, initially approved to treat men with metastatic prostate cancer in 1995, has demonstrated promising results in a study led by Memorial Sloan Kettering Cancer Center, O’Shaughnessy noted. The study screened 424 patients with ER- and PR-negative breast cancer and went on to treat the 12% who also were AR-positive.3 "
To follow the studies:
References
  1. O’Shaughnessy JA, Gatalica Z, Kimbrough JM, Millis SZ. Comparison of mutations and protein expression in potentially actionable targets in 5500 triple negative vs non-triple negative breast cancers. Presented at: 2013 San Antonio Breast Cancer Symposium; December 10-14, 2013; San Antonio, TX. Abstract PD4-1.
  2. Traina TA, O’Shaughnessy J, Kelly C, et al. A phase 2 single- arm study of the clinical activity and safety of enzalutamide in patients with advanced androgen receptor-positive triple-negative breast cancer. Presented at: 2013 San Antonio Breast Cancer Symposium; December 10-14, 2013; San Antonio, TX. Abstract OT3-2-08.
  3. Gucalp A, Tolaney S, Isakoff SJ, et al. Phase II trial of bicalutamide in patients with androgen receptor-positive, estrogen receptor-negative metastatic breast cancer [published online August 21, 2013]. Clin Cancer Res. 2013;19(19):5505-5512.
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AACR Annual Meeting 2014

AACR Annual Meeting 2014 | Metaplastic Breast Cancer | Scoop.it

 

"The 105th Annual Meeting of the American Association for Cancer Research will be held April 5-9, 2014, in San Diego, California. With about 18,000 researchers, patient advocates, and other professionals in the cancer field from around the world scheduled to be in attendance, the 2014 Annual Meeting continues the tradition of being the premier cancer research event where the latest and most exciting basic, translational, and clinical discoveries are presented. It provides a unique opportunity for members of the worldwide cancer research community to learn about cutting-edge advances, obtain feedback on their own research, and make connections that will foster future collaborations.

 

The theme for this year’s meeting, “Harnessing Breakthroughs – Targeting Cures,” reflects the fact that the translation of basic science into clinical advances for the benefit of cancer patients is occurring at an increasing pace and more seamlessly than ever before. Along with hundreds of invited talks from an elite roster of speakers, we will feature more than 6,000 proffered papers from the world’s top cancer researchers. As a new feature of this year’s meeting, we are providing five early-career investigators, called “NextGen Stars,” the chance to present their research during selected major symposia and current concepts sessions. We are very excited about this initiative because it is vital that we acknowledge the great work of these young investigators who will drive the remarkable progress against cancer going forward.

The annual meeting will also showcase pioneering clinical trials, many of which will highlight emerging approaches for personalizing cancer care. The therapeutics being evaluated in these clinical trials are underpinned by our knowledge of cancer biology, and this meeting provides a tremendous opportunity for basic and clinical researchers and clinicians to exchange ideas. Recognizing that personalized cancer medicine requires multidisciplinary and multi-institutional collaboration, we are also offering a robust regulatory science and policy track with 10 exciting sessions that will be of significant interest to both laboratory and clinical scientists in all subfields and sectors of the cancer field.

 


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Keep this

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Susan Zager's curator insight, April 3, 2014 3:53 PM

Annual Meeting of the AACR will be held April 5-9, 2014, in San Diego, California

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Novel Clinical Trial “Graduates” Two Promising Agents

Novel Clinical Trial “Graduates” Two Promising Agents | Metaplastic Breast Cancer | Scoop.it

"The first results from the I-SPY 2 trial, which is evaluating novel agents in the neoadjuvant treatment of breast cancer, show encouraging possibilities for veliparib (ABT-888) and neratinib (PB272). The study employs a groundbreaking approach that may accelerate and influence the way that oncology drugs are tested and approved in the near future, leading researchers said during the 2013 San Antonio Breast Cancer Symposium.


The approach involves evaluating drugs in small study populations, using advanced statistical techniques that will promptly identify potentially successful cohorts. The investigators have label these drugs the “graduates,” which are then eligible to move into phase III testing, according to Hope S. Rugo, MD, a professor of medicine and director of Breast Oncology and Clinical Trials Education at the Helen Diller Family Comprehensive Cancer Center at the University of California, San Francisco. At the time of the conference, seven experimental regimens had been evaluated.

Rugo presented data on the oral PARP inhibitor veliparib in combination with carboplatin. Veliparib/ carboplatin improved pathologic complete response (pCR) rates in women with triple-negative breast cancer, thus qualifying the drug to move to the next round of clinical trial testing. In January, AbbVie launched a phase III trial in which 620 patients with early-stage, triple-negative breast cancer will be randomized to one of three arms: veliparib in combination with carboplatin and paclitaxel; placebo plus carboplatin/paclitaxel; or placebo plus paclitaxel (NCT02032277). Patients in all arms would follow these regimens with doxorubicin/ cyclophosphamide."
Via Susan Zager
Maria Fowler's insight:

I-SPY 2 trials

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Susan Zager's curator insight, March 19, 2014 2:36 AM

To see the abstract referred to in the article (Abstract S5-02)

go to: http://www.abstracts2view.com/sabcs13/view.php?nu=SABCS13L_1400


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NBCC's Upcoming Clinical Trials for Women with Metastatic Breast Cancer

NBCC's Upcoming Clinical Trials for Women with Metastatic Breast Cancer | Metaplastic Breast Cancer | Scoop.it

"NBCC is currently partnering with BioMarin and Pfizer on three upcoming clinical trials for women with metastatic breast cancer. Intervention offers the potential of improving the length and quality of life for patients already diagnosed with metastatic breast cancer. Trial accrual has begun for all three studies.

NBCC advocates have been involved in many ways on these trials in the development of the protocols, as members of the Date Safety Monitoring Board, as reviewers of educational materials and consent forms and in conducting outreach activities to educate the public about the trials.


Via Susan Zager
Maria Fowler's insight:

The BMN 673 trial is for a PARP inhibitor which may eventually help with metaplastic breast cancer.

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Susan Zager's curator insight, February 19, 2014 4:09 PM


Here are the trials that the NBCC is partnering with Biomarin and Pfizer for Metastatic Breast Cancer:


EMBRACA clinical trial for the PARP inhibitor BMN 673 (BioMarin)

  • Purpose of the study:   To evaluate the efficacy and safety of BMN 673 in the metastatic setting.
  • Eligibility:  Women with the BRCA1 or BRCA 2 mutation and locally advanced or metastatic breast cancer.  Other eligibility criteria and trial details can be found at  http://clinicaltrials.gov/ct2/show/NCT01945775.
PALOMA 2 clinical trial for the CDK 4/6 inhibitor Palbociclib (Pfizer).
  • Purpose of study:  To evaluate the efficacy and safety of Palbociclib with letrozole in the metastatic setting.
  • Eligibility: First-line treatment of postmenopausal women with ER+/HER2- locally advanced or metastatic breast cancer.  Other eligibility criteria and trial details can be found at http://clinicaltrials.gov/show/NCT01740427


PALOMA 3 clinical trial for CDK 4/6 inhibitor Palbociclib (Pfizer).

  • Purpose of study: To evaluate the efficacy and safety of Palbociclib with fulvestrant in the metastatic setting.
  • Eligibility: Women with HR+/HER2- locally advanced or metastatic breast cancer who progressed on or after prior endocrine therapy. Other eligibility criteria and trial details can be found at  http://clinicaltrials.gov/show/NCT01942135 .
For more information contact the NBCC at: clinicaltrials@breastcancerdeadline2020.org
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Biotech Breakthroughs Brings Powerful Cancer Testing and Drugs to Market

Biotech Breakthroughs Brings Powerful Cancer Testing and Drugs to Market | Metaplastic Breast Cancer | Scoop.it

"NEW YORK, Feb. 18, 2014 /PRNewswire/ -- New trial confirms MetaSite Breast test's ability to predict breast cancer metastasis. MetaSite Breast would allow doctors and patients to customize breast cancer treatment based on the cancer's probability of metastasizing.

Life sciences company MetaStat, Inc. (OTCQB: MTST) recently completed a trial of its MetaSite Breast test that confirmed the test's ability to accurately predict whether breast cancer would metastasize. The confirmation paves the way for MetaStat to bring the test to market in 2015. The company predicts that the test could be used to design more customized treatment for 100 percent of the 232,000 newly diagnosed breast cancer patients every year. That represents a $580 million market opportunity for MetaSite Breast test.

The most recent trial followed 481 women who had been diagnosed with breast cancer. Researchers from Albert Einstein College of Medicine and of Yeshiva College and Weill Cornell Medical College used the MetaSite Breast test on each of the 481 women. They found that there was a significant correlation between the tests' predictions and the women whose cancer did metastasize.

MetaSite Breast test is just one of MetaStat's products aimed at identifying cancerous tumors with the potential to metastasize. MenaCalc is a diagnostic test that predicts metastasis based on the amount of Mena protein isoforms that exist in a cancerous tumor sample. That test is scheduled for release between 2015 and 2018 and could be used to predict metastasization in patients with breast, lung, prostate, and colorectal cancer.

MetaStat is one of a handful of biotech companies that are making exciting advances in the world of testing and treating cancer and other deadly diseases. Oxygen Biotherapeutics, Inc. (NASDAQ: OXBT) was recently granted Fast Track status by the Food and Drug Administration for its drug levosimendan, which will reduce moridity in patients who have undergone cardiac surgery. A recent test showed that the drug does successfully provide renal benefits for those undergoing mitral valve surgery."


Via Susan Zager
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Susan Zager's curator insight, February 18, 2014 6:15 PM

Although this article is from the Wall Street Journal it discusses the "MetaSite Breast test", aimed at detecting breast tumors that metastasize. There are different sources about this test and the sponsored study was conducted in collaboration with Albert Einstein College of Medicine of Yeshiva University and Weill Cornell Medical College. Their licensed proprietary platform technologies are based on the identification of a common pathway for the development of metastatic disease in solid epithelial-based tumor. This is a test to watch but is still at early stages. To learn more go to: http://google.brand.edgar-online.com/EFX_dll/EDGARpro.dll?FetchFilingHtmlSection1?SectionID=9322003-11790-94002&SessionID=TQS56vqOgVIdb-7


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New study shows potential for targeting aggressive breast cancers

New study shows potential for targeting aggressive breast cancers | Metaplastic Breast Cancer | Scoop.it

"A new study led by University of Kentucky Markey Cancer Center researcher Peter Zhou shows that targeting Twist, a nuclear protein that is an accelerant of the epithelial-mesenchymal transition (EMT) program in human cells, may provide an effective approach for treating triple-negative breast cancer.

Triple-negative breast cancer has an activated EMT program, which is a process that provides cells with the increased plasticity (or flexibility) to adapt to stressed environments during embryonic development, wound healing, tissue fibrosis and metastasis. EMT provides tumor cells with stem cell-like characteristics, making them resistant to therapeutics and increasing their chances for early metastasis.

Triple-negative breast cancer in particular is associated with an aggressive clinical history, development of recurrence, distant metastasis and shorter patient survival, especially in younger women. It lacks effective targeted therapies and often displays early metastatic spread to brain and lung, sites known to be associated with an estimated 5-year survival of less than 20 percent.


Via Susan Zager
Maria Fowler's insight:

Knowing that there are already BRD4 inhibitors available makes this study even more interesting.

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Downregulation of Smurf2, a tumor-suppressive ubiquitin ligase, in triple-negative breast cancers: Involvement of the RB-microRNA axis

Downregulation of Smurf2, a tumor-suppressive ubiquitin ligase, in triple-negative breast cancers: Involvement of the RB-microRNA axis | Metaplastic Breast Cancer | Scoop.it

"The HECT family ubiquitin ligase Smurf2 regulates cell polarity, migration, division, differentiation and death, by targeting diverse substrates that are critical for receptor signaling, cytoskeleton, chromatin remodeling and transcription. Recent studies suggest that Smurf2 functions as a tumor suppressor in mice.

However, no inactivating mutation of SMURF2 has been reported in human, and information about Smurf2 expression in human cancer remains limited or complicated. Here we demonstrate that Smurf2 expression is downregulated in human breast cancer tissues, especially of the triple-negative subtype, and address the mechanism of Smurf2 downregulation in triple-negative breast cancer cells.

Methods: Human breast cancer tissues (47 samples expressing estrogen receptor (ER) and 43 samples with triple-negative status) were examined by immunohistochemistry for the expression of Smurf2.

Ten widely-studied human breastcancer cell lines were examined for the expression of Smurf2. Furthermore, microRNA-mediated regulation of Smurf2 was investigated in triple-negative cancer cell lines.

Results: Immunohistochemical analysis showed that benign mammary epithelial cells expressed high levels of Smurf2, so did cells in ductal carcinomas in situ.

In contrast, invasive ductal carcinomas showed focal or diffuse decrease in Smurf2 expression, which was observed more frequently in triple-negative tumors than in ER-positive tumors. Consistently, human triple-negative breast cancer cell lines such as BT549, MDA-MB-436, DU-4475 and MDA-MB-468 cells showed significantly lower expression of Smurf2 protein, compared to ER + or HER2+ cell lines."


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Decreased expression of key tumour suppressor microRNAs is associated with lymph node metastases in triple negative breast cancer

Decreased expression of key tumour suppressor microRNAs is associated with lymph node metastases in triple negative breast cancer | Metaplastic Breast Cancer | Scoop.it

"Breast cancer is the most common malignancy that develops in women, responsible for the highest cancer-associated death rates. Triple negative breast cancers represent an important subtype that have an aggressive clinical phenotype, are associated with a higher likelihood of metastasis and are not responsive to current targeted therapies.

miRNAs have emerged as an attractive candidate for molecular biomarkers and treatment targets in breast cancer, but their role in the progression of triple negative breast cancer remains largely unexplored.

Methods: This study has investigated miRNA expression profiles in 31 primary triple negative breast cancer cases and in 13 matched lymph node metastases compared with 23 matched normal breast tissues to determine miRNAs associated with the initiation of this disease subtype and those associated with its metastasis.

Results: 71 miRNAs were differentially expressed in triple negative breast cancer, the majority of which have previously been associated with breast cancer, including members of the miR-200 family and the miR-17-92 oncogenic cluster, suggesting that the majority of miRNAs involved in the initiation of triple negative breast cancer are not subtype specific. However, the repertoire of miRNAs expressed in lymph node negative and lymph node positive triple negative breast cancers were largely distinct from one another.

In particular, miRNA profiles associated with lymph node negative disease tended to be up-regulated, while those associated with lymph node positive disease were down-regulated and largely overlapped with the profiles of their matched lymph node metastases. From this, 27 miRNAs were identified that are associated with metastatic capability in the triple negative breast cancer subtype."


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Melatonin shows potential to slow tumor growth in certain breast cancers

Melatonin shows potential to slow tumor growth in certain breast cancers | Metaplastic Breast Cancer | Scoop.it

"An early stage study shows melatonin – a hormone that regulates the body's sleep and awake cycles – may have the potential to help slow the growth of certain breast cancer tumors, according to researchers from Henry Ford Hospital in Detroit and Foundation for Research Support of the State of São Paulo.

The study, published online in the journal PLoS One, finds that melatonin may inhibit tumor growth and cell production, as well as block the formation of new blood vessels in ER-negative breast cancer models.

"These early stage research results with the melatonin drug in a triple-negative breast cancer animal models achieved in our lab has not been seen anywhere else," says study co-author Adarsh Shankar, a research assistant in the Department of Radiology at Henry Ford Hospital.

"The key finding of the study is that we now know that we can trace this drug and its effect on tumor growth, which opens the door for more research on this topic."

Melatonin is a hormone naturally produced by the brain's pineal gland in response to darkness, and it is also available as a man-made supplement.

Because of melatonin's suspected antioxidant properties, some believe it may suppress the growth of some types of cancer cells, especially when combined with certain anti-cancer drugs, according to the American Cancer Society."


Via Susan Zager
Maria Fowler's insight:

I would love to find out it was as simple as melatonin.

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Susan Zager's curator insight, January 28, 2014 3:26 PM

This is a very early study not yet tested in human clinical trials. To see the abstract go to: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3887041/


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The Silent Gene // News // College of Science // University of Notre Dame

The Silent Gene // News // College of Science // University of Notre Dame | Metaplastic Breast Cancer | Scoop.it
University of Notre Dame, College of Science, undergraduate science education, research

 

Jenifer Prosperi, a researcher at the Harper Cancer Research Institute, is studying how to treat breast cancers that evolve when a crucial tumor suppressor gene goes silent.


Over the past 15 years, the scientific community has come to understand that breast cancer is a monster with many faces.

Some cancers have one of three special indicator molecules (HER2, estrogen receptors and progesterone receptors) that can guide targeted anti-cancer treatments. But another set of breast cancers, the “triple-negative” types, lack those three indicator molecules that can guide treatment. And even now, the question remains: How can doctors better target and treat triple-negative cancers? And how can they keep up the treatment when breast cancers fight back?

Maria Fowler's insight:

There are very few actual studies being conducted on Metaplastic Breast Cancer. This study of the APC gene looks at why the gene is sometimes silent allowing cancers to replicate uncontrolled.

It's is always exciting when work is being conducted on our specific tumor types.

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